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Enterococci are tough gut commensals that turn into stubborn hospital pathogens. Their virulence runs on the metal manganese, which the host tries to starve them of using calprotectin.
Enterococcus is a genus of hardy Gram-positive gut commensals, led by Enterococcus faecalis and the vancomycin-resistant Enterococcus faecium, that act as major opportunistic hospital pathogens. Enterococcal virulence depends on acquiring the metal manganese, which the host withholds through calprotectin.
Microbiome-targeted interventions (MBTIs) are validated using a dual-evidence logical framework. First, the intervention must realign the condition’s microbiome signature by increasing beneficial taxa that are consistently depleted and reducing pathogenic taxa that are consistently enriched. Second, the intervention must demonstrate measurable clinical benefit. Concordance of these effects in the same context validates the intervention as an MBTI and supports the clinical relevance of the microbiome signature.
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreEnterococcus is a genus of Gram-positive, facultatively anaerobic gut commensals that double as major opportunistic hospital pathogens. It is led by Enterococcus faecalis, the most common clinical species, and Enterococcus faecium, the most antibiotic-resistant and the "E" of the ESKAPE pathogens.[1] On this database the genus appears as a differentially abundant gut taxon across many human microbiome studies.
Enterococci colonize the gut of most people and cause disease, urinary tract infections, bacteremia, and endocarditis, mainly in hospitalized and immunocompromised patients, with vancomycin-resistant strains (VRE) driving rising, higher-fatality bloodstream infections.[1][2] Their metal dependence is on manganese rather than nickel: enterococcal virulence requires active manganese acquisition, and the host counters with calprotectin-mediated manganese and zinc withholding, the nutritional immunity lens this database reads pathogens through.[3]
Enterococcus species are Gram-positive cocci that grow in pairs and chains and are exceptionally hardy, tolerating bile, high salt, and a wide pH and temperature range.[2] That robustness underlies their persistence on hospital surfaces and in the gut.[2]
The genus is opportunistic rather than obligately pathogenic. Gut colonization is common and usually harmless, but in vulnerable patients enterococci cause urinary, bloodstream, and heart-valve infections, frequently after translocating from the gut.[2] Vancomycin resistance, most prominent in E. faecium, makes invasive disease difficult to treat and more often fatal.[1]
Enterococci combine hardiness with metal acquisition and formidable antibiotic resistance.
| Factor | Description and role |
|---|---|
| Vancomycin resistance (VanA/VanB) | Remodels the drug's cell-wall target to resist vancomycin, the defining VRE trait driving hard-to-treat infection.[1] |
| Manganese acquisition | High-affinity manganese transport is essential for enterococcal virulence and to resist host metal withholding (detailed under Metallomics).[3] |
| Biofilm and capsule | Biofilm and capsule help enterococci colonize catheters and tissue and survive host defenses.[2] |
| Intrinsic hardiness | Tolerance of bile, salt, and disinfectant stress supports persistence and spread in hospitals.[2] |
Unlike the nickel-driven pathogens elsewhere on this site, Enterococcus is built around manganese: its virulence hinges on acquiring manganese against a host that actively withholds it.
| Metal / ion | Key features in Enterococcus |
|---|---|
| Manganese (Mn) | Manganese acquisition is essential for virulence; the transporters EfaCBA, MntH1, and MntH2 work together to sustain growth and infection, and disabling them causes drastic loss of cellular manganese and of virulence in infection models.[3] |
| Calprotectin Mn/Zn withholding | The host protein calprotectin chelates manganese and zinc to starve enterococci; strains lacking their manganese transporters become acutely sensitive, marking manganese uptake as a promising drug target.[3] |
The manganese systems that let enterococci cause disease are also their openings.
| Weak point | Why it is exploitable |
|---|---|
| Manganese dependence | Because manganese acquisition is essential for virulence, manganese-uptake inhibitors and reinforcing host metal withholding attack a load-bearing system.[3] |
| Last-line antibiotics | VRE is treated with linezolid and daptomycin, but enterococci can evolve tolerance under treatment.[2][1] |
| Gut-reservoir control | Because invasive disease starts with gut colonization, limiting the reservoir and translocation reduces infection.[2] |
Clinical infection is managed by clinicians; the entries below are classified by our validation method and are not medical advice. The microbiome through-line is manganese restriction.
| Intervention | Class | Status |
|---|---|---|
| Antibiotic therapy for enterococcal / VRE infection | Drug | Validated |
| Manganese-uptake inhibition | Concept | Validation In Progress |
| Gut decolonization and stewardship | Practice | Validation In Progress |
| Intervention | Mechanism |
| Antibiotic therapy | Susceptible enterococci are treated with standard agents; VRE needs last-line drugs such as linezolid and daptomycin, to which tolerance can evolve.[2] |
| Manganese-uptake inhibition | Blocking manganese transporters starves an essential virulence system and heightens sensitivity to host calprotectin.[3] |
| Decolonization and stewardship | Reducing the gut reservoir and antibiotic pressure limits the source of invasive enterococcal disease.[2][1] |
Untargeted dietary manganese loading. Because enterococcal virulence depends on acquiring manganese, excess manganese that overwhelms host calprotectin sequestration is a candidate route by which metal exposure could support pathogenicity.[3]
Where Enterococcus (NCBI:txid1350) appears as a differentially abundant taxon across the Microbiome Medicine corpus. Each row aggregates every experiment in which the genus moved in a given condition; direction is its change in the case/exposure group, and grade is the strongest single study's methodology weight (A·D·S·C·R), the same engine that grades every signature on this site.
Across 193 conditions and 258 studies, the signal is genuinely mixed: enriched in 106, depleted in 47, and direction-conflicting in 40 (directional agreement 0.69). Because Enterococcus is a low-abundance gut colonizer that blooms under antibiotics and dysbiosis, its differential signal usually reflects that expansion rather than a stable community role, so the aggregate evidence tier is Low.
How to read these. Enterococcus is typically a minor gut resident that overgrows under antibiotic pressure and dysbiosis, and genus-level detection groups E. faecalis with E. faecium. A differential signal, particularly enrichment, most often marks that bloom, which is why direction can conflict between cohorts and the aggregate tier stays Low.
Internal summaries of the 258 studies we reviewed in which Enterococcus was a differential taxon across this corpus.
This study examined the fecal microbiome of children newly diagnosed with Crohn's disease (CD) before any treatment was started. The researchers compared microbial composition between these CD patients and children with functional gastrointestinal disorders. They also looked at whether specific microbial patterns correlated with the severity of CD, as measured by the Pediatric Crohn's Disease Activity Index (PCDAI).
The cohort included 43 newly diagnosed, treatment-naive pediatric CD patients. They were compared against 139 age- and sex-matched controls who had other functional gastrointestinal disorders rather than CD. All participants were pediatric patients, and the comparison group was matched specifically to isolate microbial differences attributable to CD rather than age or sex.
Microbial richness and diversity were significantly lower in children with CD compared to controls. Taxonomic analysis showed enrichment of pro-inflammatory bacteria, specifically Fusobacteria and Proteobacteria, alongside depletion of favorable taxa, Firmicutes and Verrucomicrobia. Higher PCDAI scores (indicating greater disease activity) were linked to enrichment of pro-inflammatory genera, Hungatella and Veillonella, and depletion of protective Lachnospiraceae.
The findings support fecal microbiome profiling as a potential tool for distinguishing CD from other functional gastrointestinal disorders in children at diagnosis. The correlation between specific microbial shifts and disease activity suggests the microbiome could help track or predict clinical course. This could ultimately aid clinicians in making more informed treatment decisions for a disease whose course is otherwise unpredictable.
This randomized, double-blind, placebo-controlled trial tested whether daily supplementation with two specific probiotic strains, Bifidobacterium animalis subsp. lactis XLTG11 and Lactiplantibacillus plantarum CCFM8661, could reduce recurrent respiratory tract infections (RRTIs) in children. Over 180 days, the study tracked infection frequency and duration alongside changes in gut microbiota composition, functional metabolic pathways, and immune biomarkers. The design allowed the researchers to link clinical respiratory outcomes to underlying shifts in the gut microbial community and immune regulation.
The study enrolled 120 children who had been diagnosed with recurrent respiratory tract infections. Participants were randomly assigned to receive either the probiotic combination or a matched placebo daily for 180 days. The abstract does not provide further demographic details such as age range or sex distribution.
Children receiving the probiotics had significantly reduced duration and frequency of fever, cough, upper respiratory tract infections, trachea or bronchitis, pneumonia, and overall RRTI recurrence compared with placebo (all p < 0.05). Gut microbiota profiling at day 180 showed clear community differences between groups, with the probiotic group showing greater abundance of beneficial commensal taxa and the placebo group showing more opportunistic genera. Functional pathway analysis pointed to enhanced metabolic stability in the probiotic recipients, and immune biomarker patterns showed comparatively stable IgG, IgM, and complement C3 levels, suggesting a more regulated humoral immune response. Growth trajectories remained normal in both groups.
These findings support strain-defined probiotic supplementation as a viable adjunct strategy for reducing the burden of recurrent respiratory infections in children. The parallel shifts in gut microbial composition, metabolic function, and humoral immune stability suggest the respiratory benefit may be mediated through gut-immune axis modulation rather than a direct respiratory-tract effect. Because growth remained normal, the intervention appears well tolerated over a six-month period, supporting its potential for longer-term pediatric preventive use pending further confirmatory trials.
Helminth infections are consistently associated with reduced cardiovascular disease (CVD) risk, yet the biological mechanisms underlying this relationship remain unclear. The gut microbiome and metabolome are key regulators of cardiometabolic health and may mediate infection-associated effects on host physiology. Here we show that Schistosoma mansoni infection associates with distinct gut microbial and metabolic profiles linked to CVD risk in people living in Uganda. In a cross-sectional study of 209 individuals living in communities with contrasting S. mansoni endemicity, we profile the gut microbiome using 16S rRNA gene sequencing and the faecal metabolome using liquid chromatography-mass spectrometry. S. mansoni infection associates with increased gut microbial diversity and distinct taxonomic signatures, including enrichment of taxa such as Treponema and depletion of Prevotella and Streptococcus. Several infection-associated microbial taxa statistically mediate the relationships between S. mansoni infection and cardiovascular disease risk. Faecal metabolomic profiling identifies infection-associated metabolites, and integrative analyses showed linked microbe-metabolite networks associated with cardiovascular risk.These findings identify gut microbiome and metabolome signatures associated with S. mansoni infection and cardiovascular disease risk in Uganda. Although causality cannot be inferred, this work provides insight into host-parasite-microbiome interactions and highlights microbial and metabolic pathways relevant to cardiometabolic health.
Physiological and pathological changes associated with aging contribute to deteriorating disease prognosis in sepsis. However, the mechanisms by which these disturbances exacerbate inflammation remain underexplored. In this study, fecal samples were collected from aged and young septic patients and mice and subsequently transplanted into young pseudo-germ-free mice via fecal microbiota transplantation. Fecal, colon tissue, and blood samples were collected to be used 16S rDNA sequencing to characterize the gut microbiota, histopathological examination, enzyme-linked immunosorbent assay and FITC-dextran intestinal permeability assay to assess gut injury and gut barrier function. Additionally, nontargeted and targeted metabolomics were used to identify differential metabolites in the feces of aged and young septic mice. To further validate the roles of specific bacterial strains and their metabolites in sepsis, genetically engineered bacteria were used in both in vivo and in vitro experiments. The results showed that an increased abundance of Klebsiella aerogenes (K. aero) in aged hosts, which led to elevated histamine (HA) production and exacerbated intestinal barrier dysfunction. Importantly, K. aero strains carrying a histidine decarboxylase gene variant were identified as major HA producers. Mechanistically, HA was shown to drive intestinal barrier dysfunction by inhibiting Nlrp6 expression and its subsequent binding to LC3, thereby impairing autophagy. Treatments that modulated HA levels or overexpressed Nlrp6 ameliorated inflammation in septic mice. These findings suggest that targeting the HA-Nlrp6-LC3 axis could offer a novel therapeutic approach for managing sepsis, particularly in aged populations.
UNLABELLED: Antiphospholipid syndrome (APS) is a systemic autoimmune disease that contributes substantially to recurrent pregnancy loss, fetal death, intrauterine growth restriction, and preeclampsia, posing major threats to maternal and fetal health. These obstetric complications exhibit clinical similarities to those resulting from vaginal dysbiosis, yet the vaginal microbiota in APS pregnancies has not been systematically investigated. In this study, we characterized the vaginal microbiome in 33 pregnant women with APS and 90 healthy controls using 16S rRNA gene sequencing. We identified a unique microbial signature in APS pregnancies that differed from the commonly observed pattern of increased microbial diversity and Lactobacillus depletion seen in classical vaginal dysbiosis. Specifically, while overall alpha diversity and Lactobacillus dominance were preserved, we observed distinct compositional restructuring characterized by selective depletion of Lactobacillus johnsonii and marked enrichment of Bifidobacterium dentium. A logistic regression model integrating the relative abundances of these microbial biomarkers demonstrated robust diagnostic performance in differentiating pregnancies with APS from healthy pregnancies, with risk scores significantly correlating with clinical parameters and pregnancy outcomes. This study demonstrates that pregnant women with APS display a distinct vaginal microbiome pattern defined by species-specific compositional restructuring rather than global dysbiosis. These microbial alterations may contribute to APS-related pregnancy morbidity, highlighting vaginal microbial signatures as promising noninvasive biomarkers for risk stratification and potential therapeutic targets in obstetric APS management. IMPORTANCE: Antiphospholipid syndrome (APS) is an autoimmune disease that causes recurrent miscarriage, fetal death, and pregnancy complications in women of reproductive age. While coagulation dysfunction is a known contributing factor, whether APS is accompanied by vaginal microbiota alterations and their role in adverse outcomes remains unclear. We discovered that pregnant women with antiphospholipid syndrome harbor a unique vaginal microbial community: they exhibit depletion of the protective species Lactobacillus johnsonii while showing enrichment of Bifidobacterium dentium, a bacterium typically found in the gut. Unlike typical vaginal infections that display widespread microbial dysbiosis, antiphospholipid syndrome induces only selective alterations in specific bacterial species. These microbial signatures correlated with hematological parameters and adverse pregnancy histories, including prior miscarriages. Our findings suggest that monitoring vaginal microbiota could provide a simple, noninvasive approach to identify high-risk pregnancies in women with antiphospholipid syndrome and may guide novel screening strategies for pregnancy-related disorders targeting the vaginal microbiome.
Our prior research revealed that dietary nitrate (NO₃⁻) may mitigate alcohol-induced cognitive impairment through oral microbiota modulation and attenuation of inflammatory responses in mice. While alcohol use disorder (AUD) is known to associate with cognitive decline and gut dysbiosis, the therapeutic potential of nitrate supplementation in ameliorating these effects remains to be elucidated. In this randomized, double-blind, placebo-controlled pilot trial (NCT05963659), 70 AUD patients received either nitrate-rich beetroot juice or placebo for 14 days. Primary outcomes were spatial memory measured by Cambridge Neuropsychological Test Battery. Oral and gut microbiota were analyzed before and after intervention by 16S rRNA sequencing. To establish causality, germ-free (GF) mice were colonized with pre- and post-nitrate intervention saliva samples from AUD patients, followed by microbiota profiling across gastrointestinal regions. The mean difference in Delayed Matching to Sample (all delays) change between the nitrate consumption group and the placebo group after intervention was 9.784 (95%[CI], 1.85-17.72, P = 0.016), as analyzed using a generalized linear mixed model. Nitrate supplementation induced distinct shifts in oral microbiota, while gut microbiota exhibited less pronounced changes. GF mice receiving pre-intervention microbiota exhibited elevated Klebsiella abundance throughout the gut. Mechanistically, nitrate attenuated systemic inflammation, enhanced intestinal barrier integrity, and improved cognitive performance in mice. Dietary nitrate enhances cognitive function in AUD patients, partially mediated by ectopic colonization of oral microbiota. Our findings identify specific oral bacteria (e.g., Klebsiella) as key contributors to alcohol-induced cognitive impairment and suggest promising therapeutic potential for microbiota-targeted interventions in AUD.
Investigating the tissue-associated microbiota after surgically induced remission may help to understand the mechanisms initiating intestinal inflammation in Crohn's disease.
Patients with Crohn's disease undergoing ileocolic resection were prospectively recruited in 6 academic centers. Biopsy samples from the neoterminal ileum, colon, and rectosigmoid were obtained from colonoscopies performed after surgery. Microbial DNA was extracted for 16S rRNA gene sequencing. Microbial diversity and taxonomic differential relative abundance were analyzed. A random forest model was applied to analyze the performance of clinical and microbial features to predict recurrence. A Rutgeerts score ≥i2 was deemed as endoscopic recurrence.
A total of 349 postoperative colonoscopies and 944 biopsy samples from 262 patients with Crohn's disease were analyzed. Ileal inflammation accounted for most of the explained variance of the ileal and colonic mucosa-associated microbiota. Samples obtained from 97 patients who were in surgically induced remission at first postoperative colonoscopy who went on to develop endoscopic recurrence at second colonoscopy showed lower diversity and microbial deviations when compared with patients who remained in endoscopic remission. Depletion of genus Anaerostipes and increase of several genera from class Gammaproteobacteria at the 3 biopsy sites increase the risk of further recurrence. Gut microbiome was able to predict future recurrence better than clinical features.
Ileal and colonic mucosa-associated microbiome deviations precede development of new-onset ileal inflammation after surgically induced remission and show good predictive performance for future recurrence. These findings suggest that targeted microbial modulation is a plausible modality to prevent postoperative Crohn's disease recurrence.
The aim of the study was to explore the alteration of microbiota and SCFA in gut and inflammation in acute exacerbation chronic obstructive pulmonary disease (AECOPD) patients, and to test the hypothesis that a disorder of gut microbiota will lead to the alteration of SCFA, which will aggravate inflammation in AECOPD patients.
24 patients with AECOPD and 18 healthy volunteers were included in the study. Gut microbiota were analyzed by 16S rDNA and serum was used to detect levels of inflammatory factors by ELISA. Fatty acid concentrations were determined in lumen via gas chromatography-mass spectrometry. The richness and diversity of gut microbiota were decreased in AECOPD patients. β-diversity analysis revealed differences between AECOPD patients and healthy controls. p_Bacteroidetes, g_Paraprevotella, g_Ruminococcus2, g_Parasutterella, o_Rhodospirillales, and g_Romboutsia in the healthy controls and p_Firmicutes, o_Actinomycetales, f_Actinomycetadeae, g_Actinomyces, g_Mogibacterium, f_Veillonellaceae, f_Enterococcaceae, and g_Enterococcus in AECOPD patients were the most abundant microbiota. SCFA levels were decreased in patients with AECOPD. In addition, the results demonstrated that except for a reduction in IL-6, there was no change in inflammatory markers in AECOPD patients.
In AECOPD patients, the gut microbiota-SCFA-inflammation axis is augmented, with decreased diversity and abundance of gut microbiota, leading to a reduction in SCFA and an imbalance of inflammation.
Common variable immunodeficiency (CVID) is characterized by hypogammaglobulinemia and recurrent infections. Significant morbidity and mortality are caused by immune dysregulation complications (CVIDid), which affect around one-third of CVID patients and have a poorly understood etiology. Here, we investigate the hypothesis that gut microbial dysbiosis contributes to the inflammation underlying CVIDid.
Bacterial invasion of colonic crypts was observed in CVID (3/15) and X-linked agammaglobulinemia (XLA, 1/3), but not in healthy control (HC, 0/9) biopsies. Fecal gut microbiota was characterized using 16S rRNA-targeted amplicon sequencing. Increased bacterial load, decreased alpha diversity and distinct beta diversity were observed in CVIDid (n = 42) compared to HC (n = 48), and similar results were seen in CVID with IgA deficiency (n = 40) compared to HC. CVIDid and CVID-IgA showed enrichment of the genus Enterococcus, and in vitro studies confirmed the inflammatory potential of Enterococcus gallinarum and Enterococcus hirae in patient monocytes.
This study further supports the hypothesis that a dysregulated gut microbiota, with IgA deficiency as an important driving factor, contributes to systemic inflammation in primary antibody deficiency, and introduces enterococci as potential pathobionts in CVIDid. Video Abstract.
Functional constipation (FC) significantly impacts children's health. This study investigates the prevalence and microbiota characteristics of FC in children aged 0-4 years in Zunyi area.
From October to December 2023, 2039 children aged 0-4 years in Zunyi were selected using stratified sampling and cross-sectional survey methods. A questionnaire based on Rome IV diagnostic criteria was used. Twenty-nine children with FC were randomly selected as the functional constipation group (FCG), and 26 healthy children, matched for age, sex, and area, were selected as the control group (CG).
A total of 2051 questionnaires were collected, with 2039 valid responses. Among them, 151 children had FC, resulting in a prevalence rate of 7.4%. The prevalence rates in boys and girls were 6.6% and 8.5%, respectively, with no significant gender difference (P > 0.05). Alpha diversity analysis revealed higher richness and diversity of intestinal flora in the FCG compared to the CG. At the phylum level, Actinobacteria, Firmicutes, Proteobacteria, and Bacteroidetes were dominant in both groups. The FCG showed a higher relative abundance of Firmicutes, Actinobacteria, and Proteobacteria compared to the CG (P < 0.05).
The prevalence of FC in children aged 0-4 years in Zunyi is 7.4%. Disease characteristics vary with age and living environment but are unrelated to gender. The gut microbiota of children with FC shows significant alterations, with higher diversity and specific phyla abundance.
This study profiled the fecal virome, bacteriome, and blood metabolome together in schizophrenia, testing whether gut viruses (mainly bacteriophages) shape the disease-associated bacterial community and whether those shifts reach the host through circulating metabolites.
Forty-nine first-episode schizophrenia patients, most drug-naive or treated for fewer than five days, and 49 age-, sex-, and BMI-matched healthy controls at West China Hospital, Sichuan University (2021 to 2022). Fecal shotgun sequencing covered 95 participants and untargeted plasma metabolomics 92, with age, sex, BMI, and medication days controlled.
Bacterial beta-diversity separated patients from controls at the family, genus, and species levels while alpha-diversity did not differ, and combining MaAsLin2 with ANCOM-BC flagged 7, 14, and 45 differentially abundant taxa respectively. The healthy viral-bacterial transkingdom correlation network was largely lost in schizophrenia, and the co-occurring metabolites were enriched in bile-acid and eicosanoid pathways linked to inflammation. A serial-mediation model supported a gut viruses to bacteria to metabolites to schizophrenia chain, with metabolites carrying most of the indirect effect.
The results frame schizophrenia-associated dysbiosis as a virome-bacteriome-metabolome system rather than a bacterial shift alone, and highlight bile-acid and eicosanoid (COX and prostaglandin) metabolism as microbiota-linked, potentially treatable inflammatory routes. As a small cross-sectional study, it establishes associations and candidate biomarkers, not causation.
The human microbiome plays a vital role in human health, mediated by the gut-brain axis, with a large diversity of functions and physiological benefits. The dynamics and mechanisms of meditations on oral and gut microbiome modulations are not well understood. This study investigates the short-term modulations of the gut and oral microbiome during an Arhatic Yoga meditation retreat as well as on the role of microbiome in improving well-being through a possible gut-brain axis.
A single-arm pilot clinical trial was conducted in a controlled environment during a 9-day intensive retreat of Arhatic Yoga meditation practices with vegetarian diet. Oral and fecal samples of 24 practitioners were collected at the start (Day0: T1), middle (Day3: T2), and end (Day9:T3) of the retreat. Targeted 16S rRNA gene amplicon sequencing was performed for both oral and gut samples. Functional pathway predictions was identified using phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2). DESeq2 was used to identify the differential abundant taxa. Various statistical analyses were performed to assess the significant changes in the data.
Our findings revealed that Arhatic Yoga meditation together with a vegetarian diet led to changes in the oral and gut microbiome profiles within the 9-day retreat. Oral microbiome profile showed a significant (p < 0.05) difference in the species richness and evenness at the end of study, while non-metric multidimensional scaling (NMDS) confirmed the shift in the gut microbiome profile of the practitioners by T2 timepoint, which was further supported by PERMANOVA analysis (p < 0.05). Health-benefiting microbes known to improve the gastrointestinal and gut-barrier functions, immune modulation, and gut-brain axis were enriched. Gut microbiome of both beginner and advanced Arhatic Yoga practitioners showed similar trends of convergence by the end of study. This implies a strong selection pressure by Arhatic Yoga meditation together with a vegetarian diet on the beneficial gut microbiome.
This pilot study demonstrates that Arhatic Yoga meditation practices combined with a vegetarian diet during a short intensive retreat resulted in enrichment of known health-promoting microbes. Such microbial consortia may be developed for potential health benefits and used as probiotics to improve the gastrointestinal and immune systems, as well as functions mediated by the gut-brain axis.
This study investigated whether alterations in the gut microbiome are associated with allograft rejection in kidney transplant (KT) recipients. Researchers used 16S rRNA gene amplicon sequencing to characterize gut microbiome composition and function over time. They tracked how the microbiome changed from the pre-transplant, chronic kidney disease (CKD) state through recovery, and examined shifts occurring before and after rejection events. Functional analysis focused on the microbiome's capacity to produce short-chain fatty acids, including propionate and butyrate.
The study analyzed 562 samples collected from 245 individuals as part of a multicenter prospective study. Of these participants, 217 had received a kidney transplant. This design allowed comparison of microbiome trajectories across the CKD-to-post-transplant recovery period and around the time of graft rejection events.
Overall, gut microbiome composition gradually recovered after transplantation, mirroring the CKD-to-health transition, as shown by increasing Shannon diversity. However, prior to graft rejection, microbial diversity decreased along with a reduction in short-chain fatty acid-producing taxa. Functional analysis confirmed a decreased potential for short-chain fatty acid production before rejection, and this was validated using quantitative PCR targeting propionate and butyrate production potential. After rejection, these microbiome features normalized again, and the alterations preceding rejection partially overlapped with microbiome signatures previously reported in CKD patients.
The findings suggest that gut microbiome changes, particularly loss of diversity and short-chain fatty acid-producing taxa, may precede and potentially help predict graft rejection in kidney transplant recipients. This raises the possibility that monitoring microbiome composition and short-chain fatty acid production capacity could serve as an early warning signal for clinicians. Because these pre-rejection alterations partially resemble CKD-associated microbiome signatures, they may reflect a shared pathway of microbial dysfunction linked to immune dysregulation. This work supports further exploration of the gut microbiome as a noninvasive biomarker source and a potential target for interventions to support graft survival.
Clinical data on oral fecal microbiota transplantation (FMT), a promising therapy for Crohn's disease (CD), are limited. Herein, we determined the short-term safety and feasibility of FMT for pediatric patients with active CD.
In this open-label, parallel-group, single-center prospective trial, patients with active CD were treated with oral FMT capsules combined with partial enteral nutrition (PEN) (80%). The control group comprised pediatric patients with active CD treated with PEN (80%) and immunosuppressants. Thirty-three patients (11.6 ± 1.82 years)-17 in the capsule and 16 in the control groups-were analyzed. Data regarding the adverse events, clinical reactions, intestinal microbiome composition, and biomarker parameters were collected and compared post-treatment.
At week 10, the clinical and endoscopic remission rates did not differ between the two groups. By week 10, the mean fecal calprotectin level, C-reactive protein level, erythrocyte sedimentation rate, simple endoscopic score for CD, and pediatric CD activity index decreased significantly in the capsule group (all P < 0.05). The main adverse event was mild-to-moderate constipation. Core functional genera, Agathobacter, Akkermansia, Roseburia, Blautia, Subdoligranulum, and Faecalibacterium, were lacking pre-treatment. Post-treatment, the implantation rates of these core functional genera increased significantly, which positively correlated with the anti-inflammatory factor, interleukin (IL)-10, and negatively correlated with the pro-inflammatory factor, IL-6. The combination of these six functional genera distinguished healthy children from those with CD (area under the curve = 0.96).
Oral FMT capsules combined with PEN (80%) could be an effective therapy for children with active CD. The six core functional genera identified here may be candidate biomarkers for identifying children with CD.
This study aimed to explore the distinct characteristics of the gut microbiota in tuberculosis (TB) patients who experienced liver injury following anti-TB treatment compared with those who did not.
We employed a nested case-control study design, recruiting newly diagnosed pulmonary TB patients at Tangshan Infectious Disease Hospital. Participants were categorized into the Antituberculosis Drug-Induced Liver Injury (ADLI) group and the Non-ADLI group based on the occurrence of liver injury after treatment. Both groups received identical anti-TB regimens. Stool samples were collected from patients who developed liver injury within 2-3 weeks of starting treatment, alongside matched controls during the same timeframe. The samples underwent 16S rDNA sequencing, and clinical data and blood samples were also collected for further analysis. At the same time, we constructed mouse models to explore the effects of different anti-tuberculosis drugs on gut microbiota.
Following anti-TB treatment, we observed a decrease in microbial diversity and significant structural changes in the gut microbiota of TB patients (P < 0.05). At T1, the Non_ADLI_T1 group presented relatively high levels of Phascolarctobacterium, Anaerofustis and Mailhella. In contrast, the ADLI_ T1 group presented elevated levels of Bacteroides, Veillonella, Clavibacter, Corynebacterium, Anaerococcus, Gardnerella, Peptostreptococcus and Lautropia. At T2, the ADLI_T2 group presented increased levels of Enterococcus, Faecalibacterium, unclassified_f__Burkholderiaceae, Cardiobacterium, Ruminococcus_gnavus_group and Tyzzerella_4 than did the Non_ADLI_T2 group. Additionally, the ADLI_T2 group presented decreased levels of Prevotella_9, Akkermansia, Erysipelotrichaceae_UCG-003, Rubrobacter and norank_f__Desulfovibrionaceae than did the Non_ADLI_T2 group. In animal experiments, similar changes to those in the human population were observed in the mouse model compared to the control group. Any single anti-tuberculosis drug or two-drug combination or three-drug combination can cause dysbiosis of the mouse gut microbiota. The signature genera between groups are different and related to the type of anti-tuberculosis drug.
Anti-tuberculosis treatment induces dysbiosis in the gut microbiota of TB patients. Notably, there are significant differences in microbiota characteristics between TB patients with and without liver injury at both onset and during treatment. There are some differences in the characteristics of bacterial flora in liver injury caused by different drugs.
Aging is a key contributor of morbidity and mortality during acute viral pneumonia. The potential role of age-associated dysbiosis on disease outcomes is still elusive. In the current study, we used high-resolution shotgun metagenomics and targeted metabolomics to characterize SARS-CoV-2-associated changes in the gut microbiota from young (2-month-old) and aged (22-month-old) hamsters, a valuable model of COVID-19. We show that age-related dysfunctions in the gut microbiota are linked to disease severity and long-term sequelae in older hamsters. Our data also reveal age-specific changes in the composition and metabolic activity of the gut microbiota during both the acute phase (day 7 post-infection, D7) and the recovery phase (D22) of infection. Aged hamsters exhibited the most notable shifts in gut microbiota composition and plasma metabolic profiles. Through an integrative analysis of metagenomics, metabolomics, and clinical data, we identified significant associations between bacterial taxa, metabolites and disease markers in the aged group. On D7 (high viral load and lung epithelial damage) and D22 (body weight loss and fibrosis), numerous amino acids, amino acid-related molecules, and indole derivatives were found to correlate with disease markers. In particular, a persistent decrease in phenylalanine, tryptophan, glutamic acid, and indoleacetic acid in aged animals positively correlated with poor recovery of body weight and/or lung fibrosis by D22. In younger hamsters, several bacterial taxa (Eubacterium, Oscillospiraceae, Lawsonibacter) and plasma metabolites (carnosine and cis-aconitic acid) were associated with mild disease outcomes. These findings support the need for age-specific microbiome-targeting strategies to more effectively manage acute viral pneumonia and long-term disease outcomes.
Accumulating evidence indicates that antibiotic exposure may lead to impaired vaccine responses1-4; however, the mechanisms underlying this association remain poorly understood. Here we prospectively followed 191 healthy, vaginally born, term infants from birth to 15 months, using a systems vaccinology approach to assess the effects of antibiotic exposure on immune responses to vaccination. Exposure to direct neonatal but not intrapartum antibiotics was associated with significantly lower antibody titres against various polysaccharides in the 13-valent pneumococcal conjugate vaccine and the Haemophilus influenzae type b polyribosylribitol phosphate and diphtheria toxoid antigens in the combined 6-in-1 Infanrix Hexa vaccine at 7 months of age. Blood from infants exposed to neonatal antibiotics had an inflammatory transcriptional profile before vaccination; in addition, faecal metagenomics showed reduced abundance of Bifidobacterium species in these infants at the time of vaccination, which was correlated with reduced vaccine antibody titres 6 months later. In preclinical models, responses to the 13-valent pneumococcal conjugate vaccine were strongly dependent on an intact microbiota but could be restored in germ-free mice by administering a consortium of Bifidobacterium species or a probiotic already widely used in neonatal units. Our data suggest that microbiota-targeted interventions could mitigate the detrimental effects of early-life antibiotics on vaccine immunogenicity.
Endometriosis is a chronic inflammatory gynecological disease. Previous studies have explored relationships between endometriosis and the microbiota, but none have focused on differences in gut microbiota between early-stage and late-stage endometriosis patients or their connections to dysmenorrhea symptoms. This study compared gut microbiota compositions between early-stage and late-stage endometriosis patients using amplicon sequencing and further analyzed their dysmenorrhea symptoms.
To minimize seasonal and dietary impacts, we recruited Guangdong residents hospitalized for surgery at Zhujiang Hospital. Participants underwent preoperative screening based on enrollment criteria and fecal samples were collected. Endometriosis was classified according to the American Society for Reproductive Medicine (ASRM) staging system based on surgincal and pathological findings. Stage I-II cases were designated as early-stage endometriosis, and Stage III-IV as late-stage endometriosis.
A total of 112 patient fecal samples were collected, with 75 (median age, 32 years [range, 18-49 years]) meeting the enrollment criteria, including 39 early-stage (32 Stage I and 7 Stage II) and 36 late-stage (16 Stage III and 20 Stage IV) patients. The gut microbiota structure and functions in early-stage patients significantly differed from those in late-stage cases. Dysmenorrhea was associated with specific microbial traits. Late-stage patients with dysmenorrhea displayed distinctly different gut profiles compared to other endometriosis groups. Bartonella, Snodgrassella, and other taxa were enriched in late-stage cases, while Bacteroides, and Prevotella were decreased.
The gut microbial community structure in early-stage endometriosis patients significantly differs from that in late-stage cases, with late-stage patients experiencing dysmenorrhea displaying particularly distinct gut profiles. Predicted functional analysis indicated suppressed steroid biosynthesis pathways in the gut of late-stage endometriosis patients. In conclusion, it is plausible that the multiple effects of steroids on the lower gastrointestinal tract may involve microbiota alterations, suggesting the need for further investigations.
The present study aimed to characterize the salivary microbiota in patients with catathrenia and to longitudinally validate potential biomarkers after treatment with mandibular advancement devices (MAD).
Twenty-two patients with catathrenia (12 M/10 F, median age 28 y) and 22 age-matched control volunteers (8 M/14 F, median age 30 y) were included in the cross-sectional study. Video/audio polysomnography was conducted for diagnosis. All patients received treatment with custom-fit MAD and were followed for one month. Ten patients (6 M/4 F) underwent post-treatment PSG. Salivary samples were collected, and microbial characteristics were analyzed using 16S rRNA gene sequencing. The 10-fold cross-validated XGBoost and nested Random Forest Classifier machine learning algorithms were utilized to identify potential biomarkers.
In the cross-sectional study, patients with catathrenia had lower α-diversity represented by Chao 1, Faith's phylogenetic diversity (pd), and observed species. Beta-diversity based on the Bray-Curtis dissimilarities revealed a significant inter-group separation (p = 0.001). The inter-group microbiota distribution was significantly different on the phylum and family levels. The treatment of MAD did not alter salivary microbiota distribution significantly. Among the most important genera in catathrenia and control classification identified by machine learning algorithms, four genera, Alloprevotella, Peptostreptococcaceae_XI_G1, Actinomyces and Rothia, changed significantly with MAD treatment. Correlation analysis revealed that Alloprevotella was negatively related to the severity of catathrenia (r2= -0.63, p < 0.001).
High-throughput sequencing revealed that the salivary microbiota composition was significantly altered in patients with catathrenia. Some characteristic genera (Alloprevotella, Peptostreptococcaceae_XI_G1, Actinomyces, and Rothia) could be potential biomarkers sensitive to treatment. Future studies are needed to confirm and determine the mechanisms underlying these findings. Catathrenia (nocturnal groaning) is a rare, under-diagnosed sleep-related breathing disorder. The characteristics of salivary microbiota have emerged as a potential biomarker for sleeping disorders.This study utilized the 16S rRNA sequencing technique to characterize the salivary microbiota in patients with catathrenia, identified marker bacteria using machine learning algorithms, and validated the genera longitudinally after treatment with mandibular advancement devices (MAD).The results revealed clear differences in the diversity and composition of salivary microbiota between catathrenia and non-snoring control. Four genera, including Alloprevotella, Peptostreptococcaceae_XI_G1, Actinomyces and Rothia, changed significantly with MAD treatment and were correlated with groaning events.
This study investigated the gut microbiota of older adults with sarcopenic obesity (SO) and sarcopenia without obesity (Sar), compared with age-matched controls. Researchers used 16S rRNA gene sequencing targeting the V3-V4 regions to characterize microbial composition and diversity. The goal was to determine whether gut dysbiosis is associated with the development and progression of sarcopenia and sarcopenic obesity, a link previously suspected but not well documented.
The sample was drawn from a community-based cohort of 1558 older adults (age 65 and older) in Shanghai, China, who underwent sarcopenia screening with the SARC-F questionnaire. Of these, 351 completed further assessment, and 60 participants were ultimately categorized using the Asian Working Group for Sarcopenia 2019 criteria and World Health Organization obesity criteria. The final groups were sarcopenic obesity (n=20), sarcopenia without obesity (n=18), and controls (n=22).
Gut microbiota diversity and composition differed significantly between the sarcopenic obesity, sarcopenia, and control groups. Alpha diversity, measured by the Chao1 and ACE indices, was reduced specifically in the sarcopenic obesity group. Beta diversity, assessed by unweighted UniFrac PCoA, also differed significantly among the three groups, and LEfSe analysis identified 39 taxa with differential abundance across groups.
The findings support the idea that gut microbiota alterations are distinctly linked to sarcopenic obesity rather than sarcopenia alone, with reduced diversity marking the combined obesity and muscle-loss phenotype. This suggests the gut microbiome could serve as a distinguishing biomarker between these related but distinct conditions in older adults. Identifying these taxa-level differences may help guide future microbiome-targeted approaches for prevention or management of sarcopenic obesity in aging populations.
This case-control study characterized the gut microbiome in older adults with Alzheimer disease (AD) and mild cognitive impairment (MCI), comparing them to cognitively normal controls. Researchers extracted DNA from fecal samples and sequenced PCR products using Nanopore technology. They applied diversity indices, principal coordinate analysis, PERMANOVA, and LEfSe to identify microbial differences among the three groups. The study aimed to determine whether gut microbiome composition and diversity differ across the cognitive spectrum from healthy aging to dementia.
The study recruited 104 participants aged 60 years and older from urban and rural populations in Uganda. Participants were categorized into AD, MCI, and control groups based on Montreal Cognitive Assessment (MoCA) scores and ICD-11/DSM-V diagnostic criteria. This design allowed comparison of gut microbiome features across a spectrum of cognitive status within an African population, a group underrepresented in prior microbiome-dementia research.
Gut microbiome diversity, measured by the Chao1 and Shannon indices, was significantly reduced in patients with AD compared to the other groups. This reduced diversity aligns with prior findings that AD is associated with altered abundance of specific microbial taxa. The abstract text provided ends before detailing which specific taxa were enriched or depleted in the AD group, so those specifics cannot be reported here.
The findings support the idea that reduced gut microbial diversity is linked to Alzheimer disease and may reflect disruption of the gut-brain axis, including increased intestinal permeability, systemic inflammation, and oxidative stress. Because this research was conducted in Uganda, it extends microbiome-dementia evidence to an African population, broadening the generalizability of prior findings from other regions. These results reinforce the potential of gut microbiome diversity as a marker of neurodegenerative risk and support further investigation into the microbiome as a target for aging-related cognitive health interventions.
The association of disturbance in gut microbiota with hypertension (HTN) defined on three separate occasions among children and adolescents remains unclear. In this study, we aimed to compare the differences in gut microbiota composition and diversity between children with HTN and those with normal blood pressure (BP).
Data and stool samples were collected from the second follow-up of a childhood cardiovascular health cohort study in 2021. 16 S ribosomal RNA gene sequencing was conducted to determine the relative abundance of microbial taxa in 51 children aged 10-14 years with HTN and 51 children with normal BP.
Compared with children with normal BP, those with HTN had decreased gut microbiome diversity. At the genus level, after adjusting for the false discovery rate (FDR), the proportions of several gut microbiota such as Blautia (PFDR=0.042), Coprococcus (PFDR=0.042), Eubacterium_ventriosum_group (PFDR=0.027), Christensenellaceae_R-7_group (PFDR=0.027), and norank_f__Lachnospiraceae (PFDR=0.015) significantly decreased in children with HTN compared to those with normal BP. Receiver operating characteristic analysis, net reclassification improvement (NRI) and integrated discrimination improvement (IDI) were performed and showed that the genera norank_f__Lachnospiraceae and Dorea significantly enhanced the ability of body mass index to differentiate between children with HTN and those with normal BP (area under the receiver operating characteristic curve: 0.95, 95% confidence interval 0.91-0.99; NRI > 0; IDI = 0.12, P < 0.05). Phylogenetic Investigation of Communities by Reconstruction of Unobserved States showed that the mean proportions of cofactors and vitamins metabolism pathway and the glycan anabolism pathway were higher in children with HTN.
Disturbances in the abundance and diversity of gut microbiota may contribute to the development of HTN in children. Gut microbiota biomarkers may be of significant importance in the early identification and diagnosis of childhood HTN.
Gastrointestinal acute graft-versus-host disease (GI-aGVHD) is one of the main complications of patients undergoing allogenic haematopoietic stem cell transplantation (allo-HSCT). A deeper understanding of the mechanisms of sustaining intestinal homeostasis is essential. Here, we investigated micro-organisms and microbial metabolites that were crucial for intestinal homeostasis in the context of GI-aGVHD management.
We profiled the gut microbiota, immune indices and gut metabolism of 71 patients undergoing allo-HSCT. Initially, we set up a mouse aGVHD model to confirm the effect of Bacteroides fragilis type VI secretion system (T6SS) on aGVHD progression. Subsequently, we applied 16S amplicon sequencing and metabolic profiling to reveal the function of B. fragilis T6SS on microbial structure intestinal and metabolome. Finally, the mediation package was used to validate our findings in clinical samples.
A higher abundance of Bacteroides spp contributes to reducing the incidence of GI-aGVHD, and the T6SS is required for Bacteroides spp protection on aGVHD. T6SS-mediated antagonism regulates the structure and composition of gut microbiota, affecting the entire gut metabolome, particularly the bile acids metabolism, subsequently reducing inflammation response in the intestine and protecting intestinal barrier integrity. Notably, accumulating primary bile acids such as chenodeoxycholic acid exacerbated aGVHD by enhancing the activation of T cells. Mediation analysis further validated that T6SS affects the incidence of GI-aGVHD through its effect on primary bile acid metabolism.
T6SS in commensal bacteria could modulate bile acid metabolism, potentially impacting aGVHD outcomes and offering a novel target for therapeutic interventions.
Recent studies have revealed associations between gut microbiota and glioma. However, the underlying mechanisms remain poorly understood. This study primarily aims to elucidate the impact of altered gut microbiota on tumor progression in glioma-bearing mice.
Fecal samples were collected from glioma patients and healthy controls to compare the effects of human-derived gut microbiota on glioma development in mice. We also analyzed the associations between these microbiota profiles and plasma metabolites.
Significant differences were observed in both the composition and diversity of the gut microbiota between glioma patients and healthy controls. Mice transplanted with gut microbiota from high-grade glioma patients (HGG-FMT) exhibited accelerated glioma progression compared to those transplanted with microbiota from healthy individuals (HC-FMT). Specifically, Eisenbergiella, Mailhella, and Merdimonas were significantly enriched in HGG-FMT mice, while Limosilactobacillus and Anaerospora increased in HC-FMT mice. Furthermore, Merdimonas showed a positive correlation with sphingosine, sphingosine 1-phosphate, and D-sphingosine in HGG-FMT mice. Conversely, Limosilactobacillus was positively correlated with stearidonic acid and eicosapentaenoic acid in HC-FMT mice.
Our findings demonstrate that gut microbiota from high-grade glioma patients can promote glioma progression in mice, potentially through mechanisms involving sphingosine 1-phosphate. This metabolite may enter the bloodstream and accelerate glioma growth, offering novel insights into glioma pathogenesis and potential treatment options.
The human gut microbiota is an important modulator of host immune responses and has a crucial role in the development of tuberculosis (TB). Evidences suggest that metabolites may function as a bridge between gut microbiome and TB progression in children. However, the underlying interactive mechanisms are not well explored. The results may provide useful insight into the role played by the gut microbiome in pulmonary TB in children.
To explore the gut bacterial features and its interaction with plasma lipid metabolisms in children with TB. We enrolled children aged younger than 14 years old from Beijing Children’s Hospital and West China Second Hospital between January 2020 and June 2021. We investigated the gut bacterial community using 16S rRNA sequencing of 98 children with active TB, 37 other infectious diseases, and 80 healthy children. The plasma lipids were further analyzed using ultra-high-performance liquid chromatography coupled with mass spectrometry.
Children with TB showed decreased diversity and species richness indices compared to healthy children. Significant increases in the abundance of Firmicutes and Actinobacteriota combined with a decrease in the abundance of Bacteroidetes and Proteobacteria were also observed in TB children when compared with healthy controls. Among children with TB, gut bacterial composition differed in subgroups with pulmonary and extrapulmonary TB, or subgroups with different Mycobacterium tuberculosis (MTB) load. Children with TB had a higher risk of fever (OR = 3.02, P = 0.005) and poor appetite (OR = 2.96, P = 0.02) than the controls. Several bacterial genera were associated with severe illness and clinical indices, such as aspartate aminotransferase levels and fever. The plasma lipids showedc difference between TB patients and the children with other infectious diseases. Eight genera with the highest relative abundance strongly correlated with the plasma lipids.
The gut microbiome is compromised in TB children, with a correlation with the plasma lipid metabolites and clinical presentations. Integrating analysis of microbiome and metabolism may help improve precise diagnosis, treatment, and mechanism study for TB in children.
This observational study examined whether the gut microbiota influences functional recovery three months after acute ischemic stroke. Researchers used shotgun metagenomic sequencing on stool samples collected from patients treated at a tertiary stroke centre between January 2020 and March 2022. They compared microbial community structure, diversity, and functional gene pathways between patients with favorable versus unfavorable outcomes on the modified Rankin Scale. They also used two-sample Mendelian randomization with GWAS summary statistics to test whether specific bacteria have a causal relationship with post-stroke outcomes.
The study population consisted of 128 patients with acute ischemic stroke recruited from a single tertiary stroke centre. Outcomes were stratified using modified Rankin Scale scores at three months post-stroke, with scores of 0 to 2 classified as favorable and 3 to 6 classified as unfavorable. The abstract does not provide further demographic details such as age, sex distribution, or stroke severity at baseline.
Beta-diversity analysis showed a clear separation in overall microbial community structure between patients with favorable and unfavorable outcomes, and alpha-diversity measures showed greater bacterial richness in the favorable outcomes group. Taxonomic profiling found that a greater abundance of pathogenic bacteria, including Pseudomonas, Finegoldia, and Porphyromonas, was associated with unfavorable functional outcomes. Functional profiling of the metagenomic data revealed differences between groups in the ethylbenzene degradation pathway and in 16S rRNA (uracil1498-N3)-methyltransferase. The abstract text provided is truncated before the Mendelian randomization results are reported in full, so the specific causal findings from that analysis cannot be summarized here.
The findings suggest that gut microbial diversity and composition may help explain some of the unexplained variability in functional recovery after ischemic stroke. Lower bacterial richness and higher abundance of pathogenic taxa appear linked to worse three-month outcomes, pointing to the gut microbiota as a potential prognostic marker or modifiable target after stroke. The use of Mendelian randomization suggests the authors aimed to move beyond association toward establishing whether specific bacteria causally affect recovery, which could inform future microbiome-targeted interventions. This abstract does not mention Faecalibacterium prausnitzii, butyrate, or anti-inflammatory commensals specifically, so the study's implications should be understood on its own terms as centered on pathogenic bacterial abundance and overall community diversity rather than on any single beneficial organism.
This study examined how dietary patterns shape the gut resistome, the collection of antimicrobial resistance genes (ARGs) carried by gut bacteria. Researchers compared the effects of a high-fat/low-fiber diet against a high-fiber/low-fat diet, using comparative metagenomic analysis. They tracked changes in ARG abundance, virulence genes (VGs), and mobile genetic elements (MGEs) as diets shifted away from a normal baseline diet. Network analysis was also used to identify which gut bacteria act as hosts for these resistance and virulence genes.
The core experiments were conducted in mice, whose diets were shifted from a normal diet to either a high-fat/low-fiber or a high-fiber/low-fat diet. The abstract also references a human comparison showing a similar trend, though it does not specify the human cohort size or characteristics. Based on the available text, the human data appear to come from a separate metagenomic dataset or cohort used to corroborate the mouse findings.
The high-fat/low-fiber diet significantly increased the relative abundance of the resistome (from 0.14 to 0.25), virulence genes (0.56 to 0.91), and mobile genetic elements (0.20 to 1.66), all with p < 0.001. In contrast, the high-fiber/low-fat diet decreased these same measures, including the resistome (0.14 to 0.09) and virulence genes (0.58 to 0.50), with p < 0.05. Bacteroides, Parabacteroides, and Alistipes were identified as key bacterial hosts of ARGs and VGs, with their abundance shifts closely tracking changes in resistance and virulence gene levels. Mobile genetic elements such as Tn916, ISBf10, IS91, and intl1 were linked to these changes, including genes conferring vancomycin resistance and capsule-related virulence genes. A similar pattern, higher resistome levels with high-fat diets and lower levels with high-fiber diets, was also observed in humans.
These findings suggest that diet, particularly fat and fiber content, is a modifiable driver of antimicrobial resistance gene burden in the gut microbiome. The consistency between mouse and human data strengthens the case that high-fiber, low-fat dietary patterns could help suppress the spread of resistance and virulence genes. Because specific gut bacteria and mobile genetic elements were identified as mediators of this effect, the results point to potential microbial and genetic targets for reducing the gut's role as a reservoir for antimicrobial resistance.
This study characterized the microbial DNA profile present in organ preservation solution (OPS) used during liver transplantation, using 16S rRNA sequencing. The researchers asked whether specific microbial taxa detected in the OPS, reflecting the intrahepatic graft's native microbiota, are associated with short-term clinical outcomes after transplant. They also built machine learning models to predict outcomes from these microbial features and used RNA sequencing of matched liver biopsies to validate host-microbiome interactions.
The discovery cohort consisted of 110 liver transplant donors, with an independent validation cohort of 29 additional donors. Microbial signatures were derived from the organ preservation solution collected in association with each donor's liver, rather than from patient stool or blood samples. Clinical outcome data for recipients were linked to these donor-derived OPS samples using MaAsLin2-adjusted statistical models.
The microbial DNA signature detected in the OPS closely resembled known liver and bile microbiome profiles and was dominated by Proteobacteria. Specific bacterial genera, including Bacillus and Prevotella, were differentially abundant and statistically associated with adverse post-transplant outcomes, being hyperabundant in cases with worse results. Gene pathway enrichment analysis and RNA sequencing of matched liver biopsies were used to explore host-microbiome interactions underlying these associations.
This work suggests that the intrahepatic graft's own microbiota, detectable in the preservation solution at the time of transplant, carries prognostic information that has previously been overlooked in favor of gut microbiota studies. Machine learning models built on these OPS-derived microbial features could enable early risk stratification for liver transplant recipients before complications arise. If validated further, this approach could support a practical, minimally invasive tool for predicting short-term transplant outcomes.
Preterm infants (<37 weeks' gestation) are commonly given broad-spectrum antibiotics due to their risk of severe conditions like necrotising enterocolitis and sepsis. However, antibiotics can disrupt early-life gut microbiota development, potentially impairing gut immunity and colonisation resistance. Probiotics (e.g., certain Bifidobacterium strains) may help restore a healthy gut microbiota. In this study, we investigated the effects of probiotics and antibiotics on the gut microbiome and resistome in two unique cohorts of 34 very-low-birth-weight, human-milk-fed preterm infants - one of which received probiotics. Within each group, some infants received antibiotics (benzylpenicillin and/or gentamicin), while others did not. Using shotgun metagenomic sequencing on 92 longitudinal faecal samples, we reconstructed >300 metagenome-assembled genomes and obtained ~90 isolate genomes via targeted culturomics, allowing strain-level analysis. We also assessed ex vivo horizontal gene transfer (HGT) capacity of multidrug-resistant (MDR) Enterococcus using neonatal gut models. Here we show that probiotic supplementation significantly reduced antibiotic resistance gene prevalence, MDR pathogen load, and restored typical early-life microbiota profile. However, persistent MDR pathogens like Enterococcus, with high HGT potential, underscore the need for continued surveillance. Our findings underscore the complex interplay between antibiotics, probiotics, and HGT in shaping the neonatal microbiome and support further research into probiotics for antimicrobial stewardship in preterm populations.
This study examined cocoa (Theobroma cacao L.) bean fermentation, the spontaneous process that shapes the final flavour of chocolate. The researchers investigated how abiotic factors (pH and temperature) and biotic factors (bacterial and fungal microbiota) interact to produce key flavour attributes in premium chocolate. They used genome-resolved metagenomics to identify the metabolic traits within the fermentation microbial community responsible for flavour development. They then tested whether a defined microbial consortium could reproduce those fine flavour attributes under controlled conditions.
The study drew on cocoa bean fermentation samples collected from farms in Colombia. From these samples, the researchers characterized the natural bacterial and fungal community and used genome-resolved metagenomics to build a picture of the metabolic capacities present. They then assembled a separate, defined and metabolically competent microbial consortium, rather than studying a human or animal cohort, to test controlled fermentation. A trained tasting panel was also used to evaluate the resulting chocolate.
The pH, temperature, and combined bacterial and fungal microbiota composition of the fermentation samples all influenced key flavour attributes of the resulting premium chocolate. Genome-resolved metagenomics showed that the metabolic traits needed for flavour development were redundantly encoded across multiple members of the fermentation community, not confined to a single organism. Using a defined microbial consortium built from this information, the researchers replicated fine flavour attributes of chocolate under controlled conditions. This was confirmed through omics analyses, metabolic network modeling, and evaluation by a trained tasting panel.
These findings show that the flavour-relevant functions of spontaneous cocoa fermentation can be captured in a defined, reproducible microbial consortium rather than relying on uncontrolled natural fermentation. This provides a basis for designing standardized fermentation starters that can reliably reproduce fine chocolate flavour characteristics. Such starters could help cocoa producers achieve consistent premium quality across batches and locations. The approach also demonstrates a model for linking metagenomic and metabolic data to sensory outcomes in food fermentation more broadly.
The gut microbiota plays a pivotal role in developing colorectal cancer (CRC) through interactions with host immunity, metabolism, and inflammation. However, microbiome-based studies remain scarce in Middle Eastern populations, limiting regional insights into microbial signatures associated with CRC. This study aimed to characterize the gut microbiota profiles of Jordanian CRC patients using 16S rRNA gene sequencing and compare them to those of healthy controls from the GutFeeling KnowledgeBase (GutFeelingKB). Stool samples from 50 CRC patients were analyzed using Illumina iSeq targeting the V3-V4 region. Taxonomic profiling was conducted with a standardized 16S metagenomics pipeline and compared with GutFeelingKB reference data. CRC samples were enriched in Streptococcus, Enterococcus, Klebsiella, Escherichia, Citrobacter, Veillonella, Megamonas, and Eggerthella, while beneficial butyrate-producing genera such as Roseburia, Ruminococcus, Akkermansia, Faecalibacterium, and Bacteroides were significantly depleted. The absence of Fusobacterium nucleatum and Bacteroides fragilis-commonly seen in global studies-suggests region-specific microbial patterns. This study is the first metagenomic study profiling CRC-associated microbiota in Jordan. The findings reveal a dysbiotic microbial signature that reflects both global changes associated with CRC and local ecological influences. This research emphasizes the importance of population-specific microbiome studies and highlights the need to include appropriately matched controls in future investigations.
What is the composition of bacterial communities at various genital sites and are there potential interactions between partners' microbiota?
This observational study involved metagenomic analyses of samples collected from male and female partners of couples undergoing fertility treatment. Samples included vaginal and penile swabs, as well as follicular fluid and semen, which were analysed using next-generation sequencing.
The bacterial community profiles of different genital tract niches were distinct, niche-specific compositions, with female samples predominantly featuring Lactobacillus species and male samples displaying greater microbial diversity, including genital-specific and skin-associated taxa. Significant differences were observed between the sample types and intra-couple comparisons, which suggested potential microbiota interactions between partners. Differential abundance analyses further identified genera specifically enriched in female versus male samples, and correlations between partner samples point towards possible microbial transmission or shared influences on genital microbiota composition.
Despite advances in reproductive medicine, many infertility cases remain idiopathic, prompting exploration into how the genital microbiota (both in female and male reproductive tracts) might influence reproductive success. Our findings reveal that, although female samples were predominantly colonized by Lactobacillus species, particularly in the lower genital tract, male samples had greater microbial diversity (including bacteria linked to bacterial vaginosis), with only limited evidence of inter-partner microbiota transmission, underscoring the need for further longitudinal studies on the effect of sexual activity on microbial dynamics.
This study examined whether rifaximin, a gut-specific non-absorbable antibiotic, could reduce gut-derived systemic inflammation in severe acute pancreatitis (SAP). The researchers combined murine experimental models with a single-center, open-label randomized controlled trial (ChiCTR2100049794). They assessed pancreatic injury, systemic inflammatory markers, and gut microbiota composition, and tested whether rifaximin's effects depended on modulating the microbiota by using antibiotic-treated and germ-free mice.
The animal component used murine models of severe acute pancreatitis, including antibiotic-treated and germ-free mice used to probe the mechanism. The clinical component enrolled 60 patients with predicted severe acute pancreatitis, randomized to receive rifaximin or standard control treatment. No further demographic details are given in the abstract.
In mice, rifaximin reduced pancreatic injury and systemic inflammation and decreased mucin-degrading gut genera such as Akkermansia, but its protective effects persisted even in antibiotic-treated and germ-free mice, indicating mechanisms beyond microbiota modulation. In patients, rifaximin significantly lowered systemic inflammation, with white blood cell count falling from a median of 11.50 x10^9/L to 8.49 x10^9/L and TNF-alpha falling from 15.05 pg/mL to 11.00 pg/mL. However, the rate of culture-confirmed infection was identical between rifaximin and control groups (13.3% vs 13.3%), and adverse events were comparable between groups.
The findings suggest rifaximin can dampen systemic inflammation in severe acute pancreatitis through mechanisms that are not solely dependent on reshaping the gut microbiota, pointing to a possible direct anti-inflammatory or barrier-protective effect. Because inflammation markers improved without any change in infection risk, rifaximin may offer a safe adjunct for controlling inflammatory injury in SAP without added infectious risk. This supports further investigation of rifaximin as a therapeutic strategy for gut-derived inflammation in acute pancreatitis, alongside continued study of its non-microbiota-dependent mechanisms.
The maternal microbiome during pregnancy and the peripartum period plays a critical role in maternal health outcomes and establishing the neonatal gut microbiome, with long-term implications for offspring health. However, a healthy microbiome during these key periods has not been definitively characterized. This longitudinal study examines maternal and neonatal microbiomes using 16S rRNA amplicon sequencing in a Japanese cohort throughout pregnancy and the postpartum period. Forty-two mothers and their forty-five offspring participate in the study. The maternal vaginal microbiome remains relatively stable during pregnancy but significantly changes in the postpartum period. Among Lactobacillus species, the Lactobacillus crispatus group is predominant. A higher abundance of Lactobacillus early in pregnancy is associated with a favorable gestational period. The maternal gut microbiome is associated with the vaginal microbiome throughout pregnancy. The neonatal gut microbiome substantially changes in early life, with bacterial composition influenced by delivery mode. Over time, bacteria shared with the maternal gut microbiome become dominant in the neonatal gut. This study provides insights into microbiome dynamics in Japanese mothers and their offspring during pregnancy and the postpartum period. Identification of common patterns across diverse populations may help define keystone microbes essential for human health and inform the development of microbiome-based interventions.
This study examined whether person-to-person transmission of gut microbes, not just diet, helps explain why traditional microbiomes shift toward an industrialized pattern after immigration. Researchers used germ-free mice colonized with human donor stool to test how sharing air and physical contact between mice carrying different donor microbiomes affects microbial composition. They then exposed the resulting microbiomes to dietary ingredients and food additives common in industrialized diets to see how composition changes translated into metabolic outcomes, including weight gain.
The study did not involve human subjects directly. Instead, germ-free mice were colonized with human donor stool collected from the United States and from Thailand, creating humanized mouse models representing an industrialized and a traditional microbiome. Transmission and metabolic effects were then measured in these colonized mice under shared-air or co-housing conditions.
Both shared air and physical contact enabled bidirectional microbial transmission between the U.S. and Thai humanized mice. U.S. mucus-degrading taxa such as Akkermansia transferred into Thai microbiomes, while potentially health-promoting Thai-derived bacteria colonized U.S. microbiomes, with the host's baseline microbiome shaping how much remodeling occurred. When exposed to industrialized dietary ingredients and food additives, the U.S. microbiome responded differently than the Thai microbiome, with food additives reducing Akkermansia and the U.S. microbiome showing a predisposition toward weight gain under these dietary conditions.
The findings suggest that shared living environments, not diet alone, are an underappreciated route by which industrialized-style microbiomes and their metabolic consequences spread between people. Notably, sharing air supply or co-housing with a Thai-derived microbiome mitigated the U.S. microbiome's predisposition toward diet-induced weight gain, pointing to a protective effect of microbial transmission from traditional microbiomes. This implies that interventions aimed at preventing microbiome-related metabolic disease may need to consider household and community-level microbial exposure alongside dietary changes.
Adaptation of species represents the outcome of interactions between organisms and their environment, as well as a product of natural selection and evolution.
To elucidate how East China sika deer in TNNR respond to seasonal climatic selection pressures in the mid-lower Yangtze River basin, we investigated their seasonal adaptive strategies via analyses of dietary nutrition and the gut microbiome, using high-throughput sequencing of the trnL P6-loop of chloroplast and 16S rRNA.
In summer, sika deer consumed 174 plant species belonging to 183 genera and 107 families, exhibiting pronounced dietary generalization. Conversely, in winter, they fed on 130 species from 173 genera and 90 families, characterized by dietary specialization. The nutritional composition and availability of plants differed between the two seasons, driven by seasonal changes, which led to corresponding adjustments in foraging strategies. Notably, sika deer maintained a stable balance in nutrient intake across seasons. and industrialization of sika deer breeding in eastern China, whereas α-diversity was higher in winter. Microbiota in both seasons exhibited distinct correlations with consumed plant species and nutrients, but their microbial functions were predominantly enriched in metabolic processes. This pattern indicates that sika deer can flexibly reshape the structural and interaction networks of gut microbiota to enhance adaptive capacity to seasonal shifts. Overall, we demonstrated seasonal dynamics and provided new insights into understanding the diet diversity and nutrition components associated with gut microbiota in the adaptation of sika deer. These results will further facilitate genetic resource conservation, habitat improvement, food plant breeding, wild rescue, and industrialization of sika deer breeding in eastern China.
This study examined how ethnicity and geography each relate to fecal microbiota composition and dietary habits among Tibeto-Burman-speaking hill-tribe populations in Northern Thailand. Researchers used quantitative PCR to characterize gut microbiota and applied multivariate statistical methods, including multiple factor analysis and partial least squares discriminant analysis, to link microbiota composition with ethnicity, geographic location, dietary behaviors, and other host variables. The goal was to disentangle whether ethnic identity or regional residence is the stronger driver of gut microbiota variation, a question the abstract notes is understudied in Thailand.
The study population consisted of 102 individuals from Tibeto-Burman hill-tribe ethnic groups, specifically the Akha, Lahu, and Lisu peoples. These participants resided in two provinces of Northern Thailand, Chiang Mai and Chiang Rai, allowing comparisons both across ethnic groups and across geographic locations. The abstract does not provide further demographic detail such as age or sex distribution.
Both ethnicity and geography were associated with gut microbiota composition and dietary patterns, but geography showed a stronger association with microbiota variation than ethnicity did. Ethnicity, by contrast, was primarily linked to differences in dietary habits rather than directly to microbiota composition. Notably, microbiota profiles were more similar among different ethnic groups sharing the same location than among the same ethnic group split across different regions, and the diet-microbiota relationship itself varied by ethnic and geographic group. Host factors other than diet, ethnicity, and geography had a comparatively minor influence on microbiota composition.
The findings suggest that shared environment and geography can outweigh shared ethnic ancestry in shaping the gut microbiota, at least among closely related hill-tribe populations living in the same region. This implies that microbiome studies should account for local geographic and environmental exposures rather than treating ethnicity alone as the key explanatory variable. The results also highlight that diet, rather than ethnicity per se, may be the more direct pathway linking population identity to microbiota differences, which is relevant for designing future studies of diet-microbiome relationships in diverse populations.
Fecal microbiota transplantation (FMT) has emerged as a widely used treatment for various diseases. While previous efforts have focused on selecting "super donors", the precise modulation of donor microbiota to enhance FMT efficacy remains a critical challenge. This study aimed to develop strategies to modify donor microbiota to promote gastrointestinal development and maturation in germ-free mice. Probiotic Pediococcus pentosaceus Li05 (Li05) was used as gut microbiota modulator to establish a healthier donor fecal microbiota, and a microencapsulation method was applied to ensure high bacterial viability during gastrointestinal tract transition.
Probiotic intervention initially altered the stability of the gut microbiota but eventually fostered a more complex bacterial interaction network and established a new equilibrium within 14 days. Transplantation of encapsulated Li05-modulated fecal microbiota significantly promoted epithelial development, improved barrier function, and altered the colonic transcriptome profile. These effects were found to be more dependent on the abundance of some bacterial genera instead of their co-occurrence network, and the key functional bacterial genera associated with these benefits were believed to be Parabacteroides, Parasutterella, Lachnoclostridium, Muribaculum and Desulfovibrio. Notably, both encapsulation and probiotic modulation played critical roles in enhancing the functional efficacy of these key bacterial genera, and the community composed of key functional bacteria demonstrated an antagonistic relationship with other bacterial communities. Moreover, encapsulated Li05-modulated fecal microbiota induced dramatical changes in host lipid metabolism, especially the bile acids and their derives. Sporobiota gained the function of promoting epithelium development gene expression only after Li05-modulation since high abundance of Lachnoclostridium was introduced.
These findings underscore the importance of encapsulation and donor microbiota modulation in FMT and provide valuable strategies for improving transplantation precision and outcomes.
This study investigated the relationship between intestinal microbiota and abdominal fat deposition in meat ducks. Researchers used a combined multi-omics approach, including 16S rRNA gene sequencing, metagenomics, and whole transcriptomics, to compare ducks with high and low abdominal fat rates. They profiled multiple intestinal segments, including the duodenum, jejunum, ileum, rectum, and cecum, to identify which region and which microbial features were most associated with fat accumulation.
The subjects were an F2 population of meat ducks derived from a cross between Cherry Valley Ducks (male) and Runzhou Crested White Ducks (female), evaluated at 42 days of age. Ducks were sorted into a low abdominal fat (LF) group, with an abdominal fat rate of 0 to 0.75 percent, and a high abdominal fat (HF) group, with a rate of 1.5 to 2.25 percent. This was an animal-based comparative cohort rather than a human or purely computational dataset.
The cecum showed the highest microbial diversity of all intestinal segments examined and was significantly enriched in carbohydrate metabolism pathways, underscoring its central role in nutrient utilization and growth. Because of this, the cecum was selected for deeper analysis. Metagenomic analysis of cecal contents revealed significantly different microbial beta diversity between the high and low abdominal fat rate groups, indicating that overall cecal community composition differs by fat status.
The findings point to the cecum as the key intestinal segment linking gut microbiota to abdominal fat deposition in ducks, largely through its role in carbohydrate metabolism. This positions cecal microbial composition and function as a potential target for strategies to improve feed efficiency and reduce excess fat in meat duck production. The multi-omics design also offers a model for tracing host-microbe interactions underlying fat storage in poultry more broadly.
Increasing evidence support the association between the oral microbiome and human systemic diseases. This association may be attributed to the ability of many oral microbes to influence the inflammatory microenvironment. Herein, we focused our attention on the bidirectional relationship between periodontitis and type 2 diabetes using high-resolution whole metagenomic shotgun analysis to explore the composition and functional profile of the subgingival microbiome in diabetics and non-diabetics subjects with different periodontal conditions. In the present study, the abundance of metabolic pathways encoded by oral microbes was reconstructed from the metagenome, and we identified a set of dysregulated metabolic pathways significantly enriched in the periodontitis and/or diabetic patients. These pathways were mainly involved in branched and aromatic amino acids metabolism, fatty acid biosynthesis and adipocytokine signaling pathways, ferroptosis and iron homeostasis, nucleotide metabolism, and finally in the peptidoglycan and lipopolysaccharides synthesis. Overall, the results of the present study provide evidence in favor of the hypothesis that during the primary inflammatory challenge, regardless of whether it is induced by periodontitis or diabetes, endotoxemia and/or the release of inflammatory cytokines cause a change in precursor and/or in circulating innate immune cells. Dysbiosis and inflammation, also via oral-gut microbiome axis or adipose tissue, reduce the efficacy of the host immune response, while fueling inflammation and can induce that metabolic/epigenetic reprogramming of chromatin accessibility of genes related to the immune response. Moreover, the presence of an enhanced ferroptosis and an imbalance in purine/pyrimidine metabolism provides new insights into the role of ferroptotic death in this comorbidity.
Symbiotic microbial communities affect the host immune system and produce molecules contributing to the odor of an individual. In many mammalian species, saliva and vaginal fluids are important sources of chemical signals that originate from bacterial metabolism and may act as honest signals of health and reproductive status. In this study, we aimed to define oral and vaginal microbiomes and their dynamics throughout the estrous cycle in wild house mice. In addition, we analyzed a subset of vaginal proteomes and metabolomes to detect potential interactions with microbiomes. 16S rRNA sequencing revealed that both saliva and vagina are dominated by Firmicutes and Proteobacteria but differ at the genus level. The oral microbiome is more stable during the estrous cycle and most abundant bacteria belong to the genera Gemella and Streptococcus, while the vaginal microbiome shows higher bacterial diversity and dynamics during the reproductive cycle and is characterized by the dominance of Muribacter and Rodentibacter. These two genera cover around 50% of the bacterial community during estrus. Proteomic profiling of vaginal fluids revealed specific protein patterns associated with different estrous phases. Highly expressed proteins in estrus involve the keratinization process thus providing estrus markers (e.g., Hrnr) while some proteins are downregulated such as immune-related proteins that limit bacterial growth (Camp, Clu, Elane, Lyz2, and Ngp). The vaginal metabolome contains volatile compounds potentially involved in chemical communication, for example, ketones, aldehydes, and esters of carboxylic acids. Data integration of all three OMICs data sets revealed high correlations, thus providing evidence that microbiomes, host proteomes, and metabolomes may interact.IMPORTANCEOur data revealed dynamic changes in vaginal, but not salivary, microbiome composition during the reproductive cycle of wild mice. With multiple OMICs platforms, we provide evidence that changes in microbiota in the vaginal environment are accompanied by changes in the proteomic and metabolomics profiles of the host. This study describes the natural microbiota of wild mice and may contribute to a better understanding of microbiome-host immune system interactions during the hormonal and cellular changes in the female reproductive tract. Moreover, analysis of volatiles in the vaginal fluid shows particular substances that can be involved in chemical communication and reproductive behavior.
UNLABELLED: The relationship between COVID-19 and nasopharyngeal (NP) microbiota has been investigated mainly in the adult population. We explored the NP profile of children affected by COVID-19, compared to healthy controls (CTRLs). NP swabs of children with COVID-19, collected between March and September 2020, were investigated at the admission (T0), 72 h to 7 days (T1), and at the discharge (T2) of the patients. NP microbiota was analyzed by 16S rRNA targeted-metagenomics. Data from sequencing were investigated by QIIME 2.0 and PICRUSt 2. Multiple machine learning (ML) models were exploited to classify patients compared to CTRLs. The NP microbiota of COVID-19 patients (N = 71) was characterized by reduction of α-diversity compared to CTRLs (N = 59). The NP microbiota of COVID-19 cohort appeared significantly enriched in Streptococcus, Haemophilus, Staphylococcus, Veillonella, Enterococcus, Neisseria, Moraxella, Enterobacteriaceae, Gemella, Bacillus, and reduced in Faecalibacterium, Akkermansia, Blautia, Bifidobacterium, Ruminococcus, and Bacteroides, compared to CTRLs (FDR < 0.001). Exploiting ML models, Enterococcus, Pseudomonas, Streptococcus, Capnocytopagha, Tepidiphilus, Porphyromonas, Staphylococcus, and Veillonella resulted as NP microbiota biomarkers, in COVID-19 patients. No statistically significant differences were found comparing the NP microbiota profile of COVID-19 patients during the time-points or grouping patients on the basis of high, medium, and low viral load (VL). This evidence provides specific pathobiont signatures of the NP microbiota in pediatric COVID-19 patients, and the reduction of anaerobic protective commensals. Our data suggest that the NP microbiota may have a specific disease-related signature since infection onset without changes during disease progression, regardless of the SARS-CoV-2 VL. IMPORTANCE: Since the beginning of pandemic, we know that children are less susceptible to severe COVID-19 disease. A potential role of the nasopharyngeal (NP) microbiota has been hypothesized but to date, most of the studies have been focused on adults. We studied the NP microbiota modifications in children affected by SARS-CoV-2 infection showing a specific NP microbiome profile, mainly composed by pathobionts and almost missing protective anaerobic commensals. Moreover, in our study, specific microbial signatures appear since the first days of infection independently from SARS-CoV-2 viral load.
This study examined the tumor-associated microbiome in colorectal cancer (CRC), comparing young-onset CRC (yoCRC, diagnosed under age 50) to average-onset CRC (aoCRC, diagnosed over age 60). Researchers used 16S rRNA amplicon sequencing on tumor tissue and paired adjacent non-malignant tissue to characterize microbial composition. They applied multiple bioinformatics tools (Phyloseq, microbiomeSeq, metagenomeSeq, and NetComi) alongside statistical tests including PERMANOVA, ANOVA, and Wilcoxon tests to assess differences in microbial diversity and community structure between the two groups.
The study included fresh frozen tumor and paired adjacent non-malignant tissue specimens prospectively collected from 136 patients with young-onset CRC and 140 patients with average-onset CRC. The yoCRC group was defined as patients diagnosed before age 50, while the aoCRC group consisted of patients diagnosed after age 60. Clinical and tumor characteristics, such as tumor location and stage, were also recorded for both cohorts.
yoCRC tumors were more often left-sided, rectal, and diagnosed at stage IV compared to aoCRC tumors. yoCRC tumors also showed significantly higher microbial alpha diversity and distinct beta diversity patterns relative to aoCRC tumors. Akkermansia and Bacteroides were enriched in yoCRC tumors, whereas aoCRC tumors showed greater relative abundances of Bacillus, Staphylococcus, Listeria, Enterococcus, Pseudomonas, Fusobacterium, and Escherichia/Shigella (the Enterobacteriaceae-associated Escherichia/Shigella group).
These findings suggest that yoCRC has a distinct intratumoral microbial profile compared to aoCRC, indicating that age of onset may be linked to different microbial dysbiosis patterns in CRC development. The clinical differences in tumor location and stage, paired with microbial differences, imply that yoCRC may represent a biologically distinct disease process rather than simply an earlier-onset version of aoCRC. This raises the possibility that microbiome-informed diagnostics or risk stratification could eventually help address the rising incidence of yoCRC.
This study examined the oral and gut microbiota of rats to explore a possible microbiological basis for major depressive disorder. Researchers induced depression-like symptoms using chronic unpredictable mild stress (CUMS), a validated animal model of stress-triggered depression. They then used 16S rRNA sequencing to characterize the diversity and composition of bacterial communities at both body sites. The goal was to identify microbial features that distinguish depressed rats from unstressed controls.
The subjects were laboratory rats divided into a CUMS-exposed group and a control group. Depression-like status was confirmed through body weight measurements and behavioral testing after the stress protocol was applied. The abstract does not specify the exact number of animals, strain, or sex used. This was an animal model study rather than a human cohort.
Rats in the CUMS group showed significant differences from controls in both alpha and beta diversity of the oral microbiota. In the oral cavity, Rothia, Psychrobacter, and Streptococcus were the most abundant genera, with Rothia significantly decreased and Psychrobacter-related taxa significantly increased in the CUMS group. In the gut, Lactobacillus, Ruminococcus, and Oscillospira predominated, with Ruminococcus significantly decreased in CUMS rats. Spearman correlation analysis linked these differentially abundant taxa to depression-like behavioral measures, though the abstract does not report Desulfovibrio, sulfate-reducing bacteria, or hydrogen sulfide findings.
The findings suggest that chronic stress and depression-like states are accompanied by measurable, site-specific shifts in both oral and gut bacterial communities, not just gut microbiota alone. The consistent decrease of Rothia orally and Ruminococcus in the gut points to candidate microbial markers worth investigating further in depression research. Because oral samples are easier to collect than gut samples, this raises the possibility of oral microbiota as a less invasive proxy for studying depression-related microbial changes. These are preclinical rat findings, so translation to human MDD etiology or diagnostics would require further validation.
Adequate consumption of fiber has a positive effect on health. The crossover study examined the effect of a pectin-enriched smoothie on gut microbiota and health parameters. During 3 weeks, 31 adults consumed two smoothies (11.6 or 4.8 g of fiber/day), alternating with washout periods in different order. At the end of each period, weekly food diaries, blood samples, and stool microbiota were collected. Changes in the microbiota during smoothie consumption were associated with baseline fiber intake. A greater proportion of up- (Lachnospira, Colidextribacter, and Bacteroides) or down-shifts (Streptococcus, Holdemanella) was observed in low-fiber (n = 22) compared to high-fiber consumers (n = 9). In both groups, the pectin-enriched smoothie reduced the number of the Ruminococcus torques group bacteria. Our results showed that the short-term approach is effective to estimate relationships between food components and gut bacteria.
Previous studies have shown that the gut microbiota and its metabolites are associated with the success of organ transplantation. However, the specific changes in the gut microbiota of lung transplant patients remain unclear. Hence, this study aimed to elucidate the interplay between the gut microbiota, metabolome, and lung transplantation outcomes. Using 16S metagenomics sequencing and untargeted metabolic profiling, we conducted a comprehensive analysis of gut microbial and metabolic alterations in lung transplant recipients relative to non-transplant group. Our findings revealed the predominance of Enterococcus and Streptococcus genera within the lung transplant cohort, accompanied by the significant reduction in Bacteroides, Epulopiscium, Faecalibacterium, and Prevotella abundance. In addition, a significant reduction in ATRA (all-trans retinoic acid) levels and suppression of IgA production were observed in lung transplant recipients, which were found to be closely associated with the Enterococcus genus. It was speculated that the association might have implications for the prognosis of lung transplant patients. Notably, the differences in gut microbial composition and metabolomic profiles between successful transplant recipients and those experiencing chronic rejection were not statistically significant. These novel insights shed light on the putative implications of the gut microbiota and metabolome in shaping lung transplantation outcomes, and provide a foundation for future investigations and targeted therapeutic interventions.
This study examined the microbial composition and temporal dynamics of the human microbiome at four body sites: stool, oral, skin, and nasal. The researchers tracked how these microbial communities changed over time and how they related to host multi-omics data, immune markers, and clinical features. The goal was to understand how the microbiome behaves dynamically during both health and disease.
The study followed 86 participants over a period of 6 years, sampling microbiomes from four body sites in each person. The abstract does not specify additional demographic details such as age range or sex distribution. Some participants in the cohort were insulin-resistant, allowing comparison between metabolically healthy and metabolically disrupted individuals.
Microbiome stability and individuality were found to be body-site specific and strongly shaped by the host, with the stool and oral microbiomes proving more stable than the skin and nasal microbiomes, likely due to differing levels of interaction with the host and external environment. The researchers identified both individual-specific and commonly shared bacterial taxa, and individualized taxa showed greater stability over time. Notably, microbiome dynamics were correlated across different body sites, pointing to systemic patterns driven by host-microbial-environment interactions. Insulin-resistant individuals showed altered microbial stability and disrupted associations among microbiome composition, molecular markers, and clinical features.
The findings suggest that microbiome stability is not uniform across the body and that host factors play a central role in shaping which microbial communities remain stable versus dynamic over time. The correlation of microbiome dynamics across separate body sites implies a systemic, whole-body relationship between host and microbiota rather than site-isolated behavior. The disrupted microbiome-host associations seen in insulin resistance suggest that metabolic disease may involve a breakdown in normal host-microbial coupling, offering a potential angle for understanding or monitoring metabolic disease through longitudinal microbiome tracking.
The study examined how peripheral neurons connected to the gastrointestinal tract influence the gut microbiome and gut physiology. Researchers activated choline acetyltransferase (ChAT)-expressing or tyrosine hydroxylase (TH)-expressing gut-associated neurons in mice. They then measured effects on intestinal microbial communities, microbial metabolites (including bile acid profiles), and host physiological responses using multi-omics approaches.
The subjects were mice in which ChAT+ or TH+ gut-associated neurons were experimentally activated. The abstract does not give a specific sample size or strain detail, so no cohort numbers can be stated. This was an animal model study, not a human cohort, and it generated multi-omics datasets from these mice rather than drawing on a public metagenomic dataset.
Activating either ChAT+ or TH+ neurons reshaped the structure of the intestinal microbiome, including changes to bile acid profiles and fungal colonization. Physiologically, activation of either neuron type increased fecal output, showing a shared downstream effect on gut transit. Only ChAT+ neuron activation additionally increased colonic contractility and produced diarrhea-like fluid secretion, indicating that these two neuronal subtypes act through distinct physiological pathways despite some overlapping effects.
The findings show that distinct subsets of peripheral, gut-associated neurons can independently shape microbiome composition and gastrointestinal physiology without requiring signals from the brain. This suggests the enteric and peripheral nervous system directly sculpts microbial ecology, including bacterial and fungal populations and bile acid metabolism, rather than the microbiome being shaped only by diet or host genetics. Because different neuron subtypes produce different physiological outcomes (fecal output alone versus contractility and diarrhea-like secretion), this points to neuron-specific pathways as potential targets for understanding or treating GI motility and secretory disorders.
This study tested whether Parkinson's disease alters the periodontitis-associated oral microbiome. Researchers collected unstimulated saliva samples and stool samples and profiled microbial communities using next-generation sequencing of the 16S ribosomal RNA gene (V1-V3 regions). Clinical, periodontal, and neurological parameters were recorded, including the severity of Parkinson's disease motor dysfunction.
Three groups were enrolled: patients with periodontitis and Parkinson's disease (PA+P), patients with periodontitis but without Parkinson's disease (P), and systemically and periodontally healthy individuals used as controls (HC). The abstract does not give exact group sizes. The PA+P group had mild to moderate motor dysfunction, and plaque scores were comparable between the PA+P and P groups, indicating similarly effective oral hygiene.
Beta diversity in saliva differed significantly between HC and PA+P, between HC and P, and between P and PA+P groups, showing that both periodontitis and the presence of Parkinson's disease reshape the oral microbial community. Saliva and fecal microbial profiles were distinct from each other. Mycoplasma faucium, Tannerella forsythia, Parvimonas micra, and Saccharibacteria (TM7) were increased in the P group, while Prevotella pallens, Prevotella melaninogenica, and Neisseria multispecies were more abundant in the PA+P group. In fecal samples from the P group, Ruthenibacterium lactatiformans, Dialister succinatiphilus, Butyrivibrio crossotus, and Alloprevotella tannerae were detected.
The findings support the hypothesis that Parkinson's disease is associated with a distinct periodontitis-related oral microbial signature, separate from periodontitis alone. Because oral and gut microbial profiles diverged between groups despite similar oral hygiene, the results suggest disease-associated shifts rather than simple hygiene differences drive these community changes. This points to the oral-gut microbiome axis as a potential area for further investigation in Parkinson's disease and periodontitis.
Graves' disease (GD), characterized by immune aberration, is associated with gut dysbiosis. Despite the growing interest, substantial evidence detailing the precise impact of gut microbiota on GD's autoimmune processes remains exceedingly rare. This study was designed to investigate the influence of gut microbiota on immune dysregulation in GD.
It encompassed 52 GD patients and 45 healthy controls (HCs), employing flow cytometry and enzyme-linked immunosorbent assay to examine lymphocyte and cytokine profiles, alongside lipopolysaccharide (LPS) levels. Gut microbiota profiles and metabolic features were assessed using 16S rRNA gene sequencing and targeted metabolomics.
Our observations revealed a disturbed B-cell distribution and elevated LPS and pro-inflammatory cytokines in GD patients compared to HCs. Significant differences in gut microbiota composition and a marked deficit in short-chain fatty acid (SCFA)-producing bacteria, including ASV263(Bacteroides), ASV1451(Dialister), and ASV503(Coprococcus), were observed in GD patients. These specific bacteria and SCFAs showed correlations with thyroid autoantibodies, B-cell subsets, and cytokine levels. In vitro studies further showed that LPS notably caused B-cell subsets imbalance, reducing conventional memory B cells while increasing naïve B cells. Additionally, acetate combined with propionate and butyrate showcased immunoregulatory functions, diminishing cytokine production in LPS-stimulated cells.
Overall, our results highlight the role of gut dysbiosis in contributing to immune dysregulation in GD by affecting lymphocyte status and cytokine production.
Recent studies have suggested that periodontal disease and alterations in the oral microbiome may be associated with cognitive decline and Alzheimer's disease (AD) development. Here, we report a case-control study of oral microbiota diversity in AD patients compared to healthy seniors from Central Asia. We have characterized the bacterial taxonomic composition of the oral microbiome from AD patients (n = 64) compared to the healthy group (n = 71) using 16S ribosomal RNA sequencing. According to our results, the oral microbiome of AD has a higher microbial diversity, with an increase in Firmicutes and a decrease in Bacteroidetes in the AD group. LEfSe analysis showed specific differences at the genus level in both study groups. A region-based analysis of the oral microbiome compartment in AD was also performed, and specific differences were identified, along with the absence of differences in bacterial richness and on the functional side. Noteworthy findings demonstrated the decrease in periodontitis-associated bacteria in the AD group. Distinct differences were revealed in the distribution of metabolic pathways between the two study groups. Our study confirms that the oral microbiome is altered in AD. However, a comprehensive picture of the complete composition of the oral microbiome in patients with AD requires further investigation.
This study examined the early development of the human gut microbiome by comparing infants to their mothers and grandmothers within the same family lines. Researchers used a multi-omics approach combining metagenomics (16S rRNA gene and shotgun sequencing) with two independent metabolomics platforms, gas chromatography and capillary electrophoresis coupled to mass spectrometry. The goal was to characterize differences in microbial populations, function, and metabolite output across three generations.
Fecal samples were collected from 200 individuals spanning three generations of the same families. This included infants aged 0 to 12 months (55% female, 45% male) along with their respective mothers and grandmothers. The design allowed direct comparison of gut microbiota and metabolome across a shared generational line.
Infants showed markedly less diverse gut microbiota than their mothers and grandmothers, along with distinct microbial population and functional profiles. The infant metabolome also differed substantially from the adults, particularly in short- and branched-chain fatty acids. These metabolite shifts were linked to corresponding differences in bacterial populations between infants and elders.
The findings offer biochemical insight into how the gut microbiome is shaped during infancy within a single family lineage. Because dysregulation of the gut microbiome at this early stage may contribute to disease later in life, understanding these generational differences could inform strategies to support healthy microbiome development in infants. The authors suggest this multi-omics approach could ultimately help improve childhood health outcomes.
Schizophrenia (SCZ), as a neurodevelopmental disorder and devastating disease, affects approximately 1% of the world population. Although numerous studies have attempted to elucidate the causes of SCZ occurrence, it is not clearly understood. Recently, the emerging roles of the gut microbiota in a range of brain disorders, including SCZ, have attracted much attention. While the molecular mechanism of gut microbiota in regulating the pathogenesis of SCZ is still lacking. Here, we first confirmed the difference of gut microbiome between SCZ patients and healthy controls, and then, we performed fecal microbiota transplantation (FMT) to clarify the roles of SCZ patients-derived microbiota in a specific pathogen free (SPF) mice model. 16 S rDNA sequencing confirmed that a significant difference of gut microbiome was present between two groups of FMT mice, which has a similar trend with the above human gut microbiome. Furthermore, we found that transplantation of fecal microbiota from SCZ patients into SPF mice was sufficient to induce schizophrenia-like (SCZ-like) symptoms, such as deficits in sociability and hyperactivity. Furthermore, the brains of mice colonized with SCZ microbiota displayed dysregulated transcript response and alternative splicing of SCZ-relevant genes. Moreover, 10 key genes were identified to be correlated with SCZ by an integrative transcriptome data analysis. Finally, 4 key genes were identified to be correlated with the 12 differential genera between two groups of FMT mice. Our results thus demonstrated that the gut microbiome might modify the transcriptomic profile in the brain, thereby modulating social behavior, and our present study can help better understand the link between gut microbiota and SCZ pathogenesis through the gut-brain axis.
To investigate the vaginal microbiota signature of patients with gynecologic cancer and evaluate its diagnostic biomarker potential. We incorporated vaginal 16S rRNA-seq data from 529 women and utilized VSEARCH to analyze the raw data. α-Diversity was evaluated utilizing the Chao1, Shannon, and Simpson indices, and β-diversity was evaluated through principal component analysis using Bray-Curtis distances. Linear discriminant analysis effect size (LEfSe) was utilized to determine species differences between groups. A bacterial co-abundance network was constructed utilizing Spearman correlation analysis. A random forest model of gynecologic tumor risk based on genus was constructed and validated to test its diagnostic efficacy. In gynecologic cancer patients, vaginal α-diversity was significantly greater than in controls, and vaginal β-diversity was significantly separated from that of controls; there was no correlation between these characteristics and menopause status among the subject women. Women diagnosed with gynecological cancer exhibited a reduction in the abundance of vaginal Firmicutes and Lactobacillus, while an increase was observed in the proportions of Bacteroidetes, Proteobacteria, Prevotella, Streptococcus, and Anaerococcus. A random forest model constructed based on 56 genus achieved high accuracy (area under the curve = 84.96%) in gynecological cancer risk prediction. Furthermore, there were discrepancies observed in the community complexity of co-abundance networks between gynecologic cancer patients and the control group. Our study provides evidence that women with gynecologic cancer have a unique vaginal flora structure and microorganisms may be involved in the gynecologic carcinogenesis process. A gynecological cancer risk prediction model based on characteristic genera has good diagnostic value.
Gastric cancer is one of the global health concerns. A series of studies on the stomach have confirmed the role of the microbiome in shaping gastrointestinal diseases. Delineation of microbiome signatures to distinguish chronic gastritis from gastric cancer will provide a non-invasive preventative and treatment strategy. In this study, we performed whole metagenome shotgun sequencing of fecal samples to enhance the detection of rare bacterial species and increase genome sequence coverage. Additionally, we employed multiple bioinformatics approaches to investigate the potential targets of the microbiome as an indicator of differentiating gastric cancer from chronic gastritis.
A total of 65 patients were enrolled, comprising 33 individuals with chronic gastritis and 32 with gastric cancer. Within each group, the chronic gastritis group was sub-grouped into intestinal metaplasia (n = 15) and non-intestinal metaplasia (n = 18); the gastric cancer group, early stage (stages 1 and 2, n = 13) and late stage (stages 3 and 4, n = 19) cancer. No significant differences in alpha and beta diversities were detected among the patient groups. However, in a two-group univariate comparison, higher Fusobacteria abundance was identified in phylum; Fusobacteria presented higher abundance in gastric cancer (LDA scored 4.27, q = 0.041 in LEfSe). Age and sex-adjusted MaAsLin and Random Forest variable of importance (VIMP) analysis in species provided meaningful features; Bacteria_caccae was the most contributing species toward gastric cancer and late-stage cancer (beta:2.43, se:0.891, p:0.008, VIMP score:2.543). In contrast, Bifidobacterium_longum significantly contributed to chronic gastritis (beta:-1.8, se:0.699, p:0.009, VIMP score:1.988). Age, sex, and BMI-adjusted MasAsLin on metabolic pathway analysis showed that GLCMANNANAUT-PWY degradation was higher in gastric cancer and one of the contributing species was Fusobacterium_varium.
Microbiomes belonging to the pathogenic phylum Fusobacteria and species Bacteroides_caccae and Streptococcus_anginosus can be significant targets for monitoring the progression of gastric cancer. Whereas Bifidobacterium_longum and Lachnospiraceae_bacterium_5_1_63FAA might be protection biomarkers against gastric cancer.
This pilot prospective cohort study examined whether ethnicity influences gut microbiome dysbiosis in pregnancies complicated by gestational diabetes mellitus (GDM). The researchers also investigated whether diet and lifestyle modifications made after a GDM diagnosis could modulate the gut microbiome. Fecal samples were collected at two time points, 24 to 28 weeks and 36 to 40 weeks of gestation, and analyzed using targeted 16S rRNA gene-based amplicon sequencing. Statistical comparisons between groups used PERMANOVA, differential abundance testing used DeSeq2, and functional predictions were generated with PICRUSt2.
The cohort included 53 women with GDM and 16 women without GDM, all residing in Singapore. Participants belonged to three Asian ethnic groups: Chinese, Malay, and Indian. This design allowed comparison of gut dysbiosis patterns both across GDM status and across ethnic background within the same population.
Among women with GDM, gut microbiomes from the different ethnic groups shared common features rather than diverging by ethnicity. This suggests that GDM-related dysbiosis is a relatively consistent phenomenon across the Chinese, Malay, and Indian groups studied. The abstract indicates that ethnicity was not a major driver of the microbiome differences observed in these GDM pregnancies.
If GDM-associated gut dysbiosis is largely independent of Asian ethnic background, microbiome-targeted strategies for GDM may generalize across these ethnic groups rather than needing ethnicity-specific approaches. This supports the idea that dietary and lifestyle interventions after a GDM diagnosis could be evaluated and applied similarly across diverse populations. As a pilot study, these findings point to the need for larger cohorts to confirm whether microbiome-based interventions can be standardized across ethnicities.
This study examined whether the traditional Chinese medicine formula Shenling Baizhu San (SLBZS) could prevent or treat non-alcoholic fatty liver disease (NAFLD) at the preclinical level. Researchers induced NAFLD using a western diet combined with CCl4 injection, then treated mice with SLBZS for six weeks. They measured body weight, energy intake, liver enzymes, pro-inflammatory factors, and hepatic steatosis. They also tracked gut microbiota and metabolite changes using 16S rRNA gene sequencing and untargeted metabolomics, alongside serotonin-pathway markers TPH1, 5-HT, HTR2A, and HTR2B.
The study used male C57BL/6J mice, a standard inbred laboratory mouse strain, divided into three groups. One group received a normal diet, a second received a western diet plus CCl4 injection to induce NAFLD, and a third received the same NAFLD-inducing regimen plus SLBZS intervention. No human subjects were studied; this was an animal model investigation.
SLBZS intervention for six weeks reduced serum and liver lipid levels, blood glucose, and pro-inflammatory factors, while improving insulin resistance and liver function indexes, effectively alleviating NAFLD in the mice. The treatment also produced significant changes in intestinal TPH-1, 5-HT, liver 5-HT, and the related receptors HTR2A and HTR2B. Gut microbiota analysis via 16S rRNA sequencing showed SLBZS altered the composition of the gut microbiota, linking these microbial shifts to the observed metabolic and serotonergic changes.
The findings suggest SLBZS may offer a multi-target approach to NAFLD prevention and treatment by simultaneously improving liver function, metabolic markers, gut microbiota composition, and gut-liver serotonin signaling. This supports further investigation of traditional Chinese medicine formulas as adjunct or alternative therapies for NAFLD. Because this work was conducted in mice, human clinical studies are needed before drawing conclusions about efficacy in people.
Resistance to antibiotics in newborns is a huge concern as their immune system is still developing, and infections and resistance acquisition in early life have short- and long-term consequences for their health. Bifidobacterium species are important commensals capable of dominating the infant gut microbiome and are known to be less prone to possess antimicrobial resistance genes than other taxa that may colonize infants. We aimed to study the association between Bifidobacterium-dominated infant gut microbiota and the antibiotic resistant gene load in neonates, and to ascertain the perinatal factors that may contribute to the antibiotic resistance acquisition. Two hundred infant fecal samples at 7 days and 1 month of age from the MAMI birth cohort were included in the study and for whom maternal-neonatal clinical records were available. Microbiota profiling was carried out by 16S rRNA amplicon sequencing, and targeted antibiotic resistance genes (ARGs) including tetM, tetW, tetO, blaTEM, blaSHV and ermB were quantified by qPCR. Infant microbiota clustered into two distinct groups according to their Bifidobacterium genus abundance: high and low. The main separation of groups or clusters at each time point was performed with an unsupervised non-linear algorithm of k-means partitioning to cluster data by time points based on Bifidobacterium genus relative abundance. Microbiota composition differed significantly between both groups, and specific bifidobacterial species were enriched in each cluster. Lower abundance of Bifidobacterium in the infant gut was associated with a higher load of antibiotic resistance genes. Our results highlight the relevance of Bifidobacterium genus in the early acquisition and establishment of antibiotic resistance in the gut. Further studies are needed to develop strategies to promote a healthy early colonization and fight against the spread of antibiotic resistances.
Graphene-based warm uterus acupoint paste (GWUAP) is an emerging non-drug alternative therapy for the treatment of primary dysmenorrhea (PD), but the underlying mechanism is still unclear. SD female rats were randomly divided into control group, model group and treatment group to explore the mechanism of GWUAP in the treatment of PD. Combined with 16S rDNA and fecal metabolomics, the diversity of microbiota and metabolites in each group was comprehensively evaluated. In this study, GWUAP reduced the torsion score of PD model rats, improved the pathological morphology of uterine tissue, reduced the pathological damage score of uterine tissue, and reversed the expression levels of inflammatory factors, pain factors and sex hormones. The 16 S rDNA sequencing of fecal samples showed that the abundance of Lactobacillus in the intestinal flora of the model group decreased and the abundance of Romboutsia increased, while the abundance of Lactobacillus in the intestinal flora of the treatment group increased and the abundance of Romboutsia decreased, which improved the imbalance of flora diversity in PD rats. In addition, 32 metabolites related to therapeutic effects were identified by metabolomics of fecal samples. Moreover, there is a close correlation between fecal microbiota and metabolites. Therefore, the mechanism of GWUAP in the treatment of PD remains to be further studied.
This study examined the relationship between faecal microbiota and nutritional status in schoolchildren using a double-blinded cluster-randomized controlled trial. Researchers tested the impact of six months of consumption of rice fortified with two different levels of vitamins and minerals. The faecal microbiota was characterized using 16S rRNA sequencing and analyzed against nutritional, micronutrient, inflammatory, and parasitic infection markers. The trial was registered with ClinicalTrials.gov (NCT01706419).
The study population consisted of 380 Cambodian schoolchildren enrolled in a cluster-randomized trial. Participants were assessed for age, sex, nutritional status (including underweight and stunting), and micronutrient status covering iron, zinc, and vitamin A deficiencies. Additional measures included anaemia, iron deficient anaemia, hemoglobinopathy, systemic and gut inflammation, and parasitic infection status.
The faecal microbiota of these schoolchildren showed a surprisingly high proportion of Lactobacillaceae. Deficiencies in specific micronutrients, namely iron and vitamin A, correlated with particular microbiota profiles, while zinc deficiency showed no such association. The six-month rice fortification intervention altered both the composition and the predicted functions of the microbiota, with the two rice treatments producing different effects. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, or sulfur metabolism.
These findings suggest that specific micronutrient deficiencies, rather than micronutrient status broadly, are linked to distinct gut microbiota signatures in children. The differential response of microbiota composition and function to two fortification formulations indicates that the type of nutrient fortification matters, not just its presence. This work supports further investigation into how targeted nutritional interventions might be designed to favorably shape childhood gut microbiota and, in turn, nutritional and inflammatory outcomes.
Fecal microbiota transplantation (FMT) and fecal virome transplantation (FVT, sterile filtrated donor feces) have been effective in treating recurrent Clostridioides difficile infections, possibly through bacteriophage-mediated modulation of the gut microbiome. However, challenges like donor variability, costly screening, coupled with concerns over pathogen transfer (incl. eukaryotic viruses) with FMT or FVT hinder their wider clinical application in treating less acute diseases.
To overcome these challenges, we developed methods to broaden FVT's clinical application while maintaining efficacy and increasing safety. Specifically, we employed the following approaches: (1) chemostat-fermentation to reproduce the bacteriophage FVT donor component and remove eukaryotic viruses (FVT-ChP), (2) solvent-detergent treatment to inactivate enveloped viruses (FVT-SDT), and (3) pyronin-Y treatment to inhibit RNA virus replication (FVT-PyT). We assessed the efficacy of these processed FVTs in a C. difficile infection mouse model and compared them with untreated FVT (FVT-UnT), FMT, and saline.
FVT-SDT, FVT-UnT, and FVT-ChP reduced the incidence of mice reaching the humane endpoint (0/8, 2/7, and 3/8, respectively) compared to FMT, FVT-PyT, and saline (5/8, 7/8, and 5/7, respectively) and significantly reduced the load of colonizing C. difficile cells and associated toxin A/B levels. There was a potential elimination of C. difficile colonization, with seven out of eight mice treated with FVT-SDT testing negative with qPCR. In contrast, all other treatments exhibited the continued presence of C. difficile. Moreover, the results were supported by changes in the gut microbiome profiles, cecal cytokine levels, and histopathological findings. Assessment of viral engraftment following FMT/FVT treatment and host-phage correlations analysis suggested that transfer of phages likely were an important contributing factor associated with treatment efficacy.
This proof-of-concept study shows that specific modifications of FVT hold promise in addressing challenges related to donor variability and infection risks. Two strategies lead to treatments significantly limiting C. difficile colonization in mice, with solvent/detergent treatment and chemostat propagation of donor phages emerging as promising approaches. Video Abstract.
Systemic inflammatory response syndrome (SIRS) is a severe inflammatory response that can lead to organ dysfunction and death. Modulating the gut microbiome is a promising therapeutic approach for managing SIRS. This study assesses the therapeutic potential of the Xuanfei Baidu (XFBD) formula in treating SIRS. The results showed that XFBD administration effectively reduced mortality rates and inflammation in SIRS mice. Using 16S rRNA sequencing and fecal microbiota transplantation (FMT), we substantiated that the therapeutic effects of XFBD are partly attributed to gut microbiota modulation. We conducted in vitro experiments to accurately assess the gut microbiome remodeling effects of 51 compounds isolated from XFBD. These compounds exhibited varying abilities to induce a microbial structure that closely resembles that of the healthy control group. By quantifying their impact on microbial structure and clustering their regulatory patterns, we devised multiple gut microbiome remodeling compound (GMRC) cocktails. GMRC cocktail C, comprising aucubin, gentiopicroside, syringic acid, gallic acid, p-hydroxybenzaldehyde, para-hydroxybenzoic acid, and isoimperatorin, demonstrated superior efficacy in treating SIRS compared to a single compound or to other cocktails. Finally, in vitro experiments showcased that GMRC cocktail C effectively rebalanced bacteria composition in SIRS patients. This study underscores XFBD's therapeutic potential in SIRS and highlights the importance of innovative treatment approaches for this disease by targeting the gut microbiota.IMPORTANCEDeveloping effective treatment strategies for systemic inflammatory response syndrome (SIRS) is crucial due to its severe and often life-threatening nature. While traditional treatments like dexamethasone have shown efficacy, they also come with significant side effects and limitations. This study makes significant strides by demonstrating that the Xuanfei Baidu (XFBD) formula can substantially reduce mortality rates and inflammation in SIRS mice through effective modulation of the gut microbiota. By quantitatively assessing the impact of 51 compounds derived from XFBD on the gut microbiome, we developed a potent gut microbiome remodeling compound cocktail. This cocktail outperformed individual compounds and other mixtures in efficacy against SIRS. These findings highlight the potential of XFBD as a therapeutic solution for SIRS and underscore the critical role of innovative strategies targeting the gut microbiota in addressing this severe inflammatory condition.
The gut microbiota of infants in low- to middle-income countries is underrepresented in microbiome research. This study explored the faecal microbiota composition and faecal cytokine profiles in a cohort of infants in a rural province of Cambodia and investigated the impact of sample storage conditions and infant environment on microbiota composition. Faecal samples collected at three time points from 32 infants were analysed for microbiota composition using 16S rRNA amplicon sequencing and concentrations of faecal cytokines. Faecal bacterial isolates were subjected to whole genome sequencing and genomic analysis. We compared the effects of two sample collection methods due to the challenges of faecal sample collection in a rural location. Storage of faecal samples in a DNA preservation solution preserved Bacteroides abundance. Microbiota analysis of preserved samples showed that Bifidobacterium was the most abundant genus with Bifidobacterium longum the most abundant species, with higher abundance in breast-fed infants. Most infants had detectable pathogenic taxa, with Shigella and Klebsiella more abundant in infants with recent diarrhoeal illness. Neither antibiotics nor infant growth were associated with gut microbiota composition. Genomic analysis of isolates showed gene clusters encoding the ability to digest human milk oligosaccharides in B. longum and B. breve isolates. Antibiotic-resistant genes were present in both potentially pathogenic species and in Bifidobacterium. Faecal concentrations of Interlukin-1alpha and vascular endothelial growth factor were higher in breast-fed infants. This study provides insights into an underrepresented population of rural Cambodian infants, showing pathogen exposure and breastfeeding impact gut microbiota composition and faecal immune profiles.
This study examined how the gut microbiome and serum metabolome differ between people with lactose intolerance (LI) and those without it. The researchers combined a paired-sample analysis of American Gut Project (AGP) data with metagenomic and untargeted metabolomic analyses in a separate cohort. They also performed fecal microbiota transplantation (FMT) experiments to test whether the LI-associated gut microbiome could influence inflammatory outcomes. The goal was to characterize the interaction between gut microbiota and circulating metabolites in LI.
The study drew on two data sources: paired samples from the American Gut Project (AGP), a large public microbiome dataset, and a Chinese cohort in which metagenomic and metabolomic profiling was performed. The abstract does not give exact sample sizes for either group. FMT experiments were also conducted, implying an animal model component, though further details are not specified in the abstract.
Fourteen microbial genera differed significantly between LI and control individuals in the AGP data. In the Chinese cohort, a machine learning approach identified seven bacterial species and nine metabolites that could distinguish the two groups. Notably, increased Escherichia coli in the LI group was negatively correlated with several metabolites, including PC (22:6/0:0), indole, and Lyso PC, while reduced levels of Faecalibacterium prausnitzii and Eubacterium rectale were positively associated with other metabolic changes.
The findings suggest that lactose intolerance is accompanied by a distinct gut microbial and metabolic signature, not just a lactase enzyme deficiency. The rise in Escherichia coli alongside depletion of beneficial short-chain-fatty-acid producers like Faecalibacterium prausnitzii and Eubacterium rectale points to a shift toward a more pro-inflammatory microbial community. This raises the possibility that microbiome-targeted interventions could help manage LI-related gastrointestinal symptoms, and the FMT experiments support a causal link between this altered microbiome and inflammatory outcomes.
This study characterized gastrointestinal microbial communities involved in gastric carcinogenesis by pooling 16S rRNA sequencing data across 11 independent published and open datasets. The researchers compared both intratumoral (gastric biopsy) and fecal microbiota between gastric cancer patients and non-cancer individuals. They used tools including VSEARCH, QIIME, and R packages such as vegan, phyloseq, cooccur, and random forest for diversity analysis, network analysis, and biomarker identification, with PICRUSt used to predict functional pathways.
The analysis drew on 1,642 gastric biopsy samples and 394 stool samples aggregated across 11 independent studies. The abstract does not give demographic details such as age, sex, or geographic origin of the underlying cohorts. This was a meta-analysis of existing sequencing data rather than a newly recruited single-site cohort.
Alpha-diversity of the intratumoral microbiota differed significantly between gastric cancer patients and non-cancer patients, while fecal microbiota diversity showed no significant difference between groups. Network analysis revealed that positive correlations among gastric cancer-enriched bacteria increased, while positive correlations among gastric cancer-depleted bacteria decreased, compared to healthy individuals. Functional prediction analyses pointed to alterations in pathways related to carbohydrate metabolism, though the abstract text describing these functional results was truncated.
The findings suggest that local, tumor-site microbial signatures may be more informative for gastric cancer detection than stool-based sampling, since diversity differences were seen intratumorally but not fecally. The shifting co-occurrence network structure around cancer-enriched and cancer-depleted bacteria points to microbial community reorganization as a feature of gastric carcinogenesis. By pooling data across 11 studies, this work moves toward identifying more reproducible microbial markers for early gastric cancer detection across populations.
This study examined how laparoscopic sleeve gastrectomy (LSG), a form of bariatric surgery, affects cognitive function through the microbiota-gut-brain axis (MGBA). Researchers integrated fecal 16S microbiota profiling, serum metabolomics, cognitive assessment scales, and resting-state functional connectivity MRI (rs-fMRI) to capture changes across the gut, blood, and brain simultaneously. Correlation-based statistical methods, including Spearman correlation and Co-inertia analysis, were used to link microbiota shifts and metabolite changes to changes in brain connectivity and cognitive scores.
The cohort consisted of 39 obese patients who underwent laparoscopic sleeve gastrectomy. Each patient was assessed at two time points, before surgery and six months after, using demographic data, serum samples, fecal samples, cognitive testing, and rs-fMRI scans. The abstract does not specify age, sex distribution, or geographic location of the cohort.
LSG produced substantial weight loss, with reductions of up to 28% of body weight at six months. The surgery was accompanied by measurable changes in gut microbiota composition, serum metabolite profiles, and brain functional connectivity networks identified through rs-fMRI. The abstract indicates that these multi-omics changes were statistically correlated with alterations in cognitive assessment scores, suggesting coordinated shifts across the gut-brain axis, though the specific taxa, metabolites, and brain regions most strongly implicated are not detailed in the available text.
The findings support the idea that bariatric surgery's cognitive benefits may be mediated in part by changes in gut microbiota and their downstream metabolic effects on the brain, rather than weight loss alone. This multi-omics approach, linking microbiota, serum metabolomics, and neuroimaging, offers a framework for identifying specific microbial and metabolic targets that could explain or potentially enhance post-surgical cognitive improvement. Further work identifying the exact bacterial taxa and metabolites involved could inform future non-surgical interventions aimed at the same gut-brain pathways.
This prospective cohort pilot study investigated whether oral, vaginal, and stool microbial communities could serve as non-invasive diagnostic biomarkers for endometriosis. Researchers self-collected samples from each of the three body sites at a single time point, then performed 16S rRNA amplicon sequencing followed by bioinformatics analysis. Diversity analyses and LEfSe were used to compare microbial composition and identify differentially abundant taxa across groups.
The study enrolled sixty-four age- and sex-matched subjects recruited at Nepean Hospital and the UNSW Microbiome Research Centre in Australia. Participants were divided into three cohorts: 19 healthy controls, 24 non-endometriosis patients, and 21 patients with confirmed endometriosis. All participants other than healthy controls underwent laparoscopic surgical assessment, with histology performed on excised lesions to confirm diagnosis.
Oral microbiota composition differed significantly between the three cohorts, as did stool microbiota composition. LEfSe analysis identified differentially abundant taxa distinguishing each group. Notably, Fusobacterium was enriched in the oral samples of patients with moderate or severe disease.
These findings suggest that oral and stool microbial signatures, rather than vaginal samples alone, may carry diagnostic signal for distinguishing endometriosis from non-endometriosis and healthy states. The enrichment of Fusobacterium in more severe disease raises the possibility that microbial shifts track with disease severity. If validated in larger cohorts, this approach could support development of a non-invasive diagnostic test that reduces reliance on laparoscopic surgery for endometriosis diagnosis.
This study examined whether iron overload in thalassemia patients is linked to gut dysbiosis and cognitive impairment through the gut-brain axis. Researchers assessed iron burden, cognitive function, and both gut and blood microbiome composition across different blood-transfusion regimens. The goal was to determine whether specific microbial shifts track with iron accumulation and cognitive status in this population.
Sixty participants were recruited, comprising healthy controls, transfusion-dependent thalassemia (TDT) patients, and non-transfusion-dependent thalassemia (NTDT) patients. TDT patients receive more frequent blood transfusions and, consistent with this, showed greater iron overload than NTDT patients. This design allowed comparisons of gut and blood microbiota across a spectrum of iron-overload severity within the same disease population.
Most thalassemia patients developed gut dysbiosis, and about 25% developed minor cognitive impairment. Both TDT and NTDT groups showed increased Fusobacteriota and Verrucomicrobiota with decreased Fibrobacterota, and TDT patients had more abundant Verrucomicrobia, described as beneficial bacteria. Iron overload correlated with cognitive impairment, and increased Butyricimonas with decreased Paraclostridium was associated with higher cognitive function. No blood microbiota was detected, and blood bacterial profiles did not differ significantly between thalassemia patients and controls.
The findings suggest that iron overload in thalassemia is associated with gut microbial imbalance that may relate to cognitive outcomes through the gut-brain axis. Specific gut taxa such as Butyricimonas and Paraclostridium emerge as candidate markers linked to cognitive function, while the blood compartment appears not to harbor a distinct microbiome signal in this context. This points to the gut, rather than blood, as the more relevant site for future investigation of microbiome-cognition relationships in iron-overloaded thalassemia patients.
Microbiome-directed dietary interventions such as microbiota-directed fibers (MDFs) have a proven track record in eliciting responses in beneficial gut microbes and are increasingly being promoted as an effective strategy to improve animal production systems. Here we used initial metataxonomic data on fish gut microbiomes as well as a wealth of a priori mammalian microbiome knowledge on α-mannooligosaccharides (MOS) and β-mannan-derived MDFs to study effects of such feed supplements in Atlantic salmon (Salmo salar) and their impact on its gut microbiome composition and functionalities. Our multi-omic analysis revealed that the investigated MDFs (two α-mannans and an acetylated β-galactoglucomannan), at a dose of 0.2% in the diet, had negligible effects on both host gene expression, and gut microbiome structure and function under the studied conditions. While a subsequent trial using a higher (4%) dietary inclusion of β-mannan significantly shifted the gut microbiome composition, there were still no biologically relevant effects on salmon metabolism and physiology. Only a single Burkholderia-Caballeronia-Paraburkholderia (BCP) population demonstrated consistent and significant abundance shifts across both feeding trials, although with no evidence of β-mannan utilization capabilities or changes in gene transcripts for producing metabolites beneficial to the host. In light of these findings, we revisited our omics data to predict and outline previously unreported and potentially beneficial endogenous lactic acid bacteria that should be targeted with future, conceivably more suitable, MDF strategies for salmon.
This study investigated the microbial and metabolic profile of the gut-lung axis in children with pulmonary arterial hypertension associated with congenital heart disease (PAH-CHD). The researchers used an integrated multi-omics approach, analyzing metabolites and microbiota from both the gut and lower respiratory tract. Their goal was to characterize how gut and pulmonary microbiome and metabolome profiles relate to each other in PAH-CHD and to explore the potential diagnostic value of these profiles.
The study recruited 15 healthy individuals and 15 patients with pulmonary arterial hypertension due to congenital heart disease. Participants were drawn from Fuwai Yunnan Hospital, Chinese Academy of Medical Sciences, and Kunming Children's Hospital. This design allowed direct comparison of gut and lower respiratory tract samples between affected children and healthy controls.
The gut and pulmonary microbiota of children with PAH-CHD showed an increased abundance of beneficial symbionts compared to healthy individuals. These microbial shifts were closely linked to accompanying metabolite changes, indicating coordinated alterations across the gut-lung axis. The abstract does not specify particular taxa such as Salmonella, Salmonella enterica, typhoid-associated organisms, or the Enterobacteriaceae, so no claims about those groups can be made from this study.
The findings support the idea that the gut-lung axis is disrupted in pediatric PAH-CHD and may play a role in disease progression through immune and metabolic pathways. Because distinct microbiome and metabolome signatures were identified, these profiles could potentially serve as aids in diagnosing PAH-CHD. Further validation would be needed before such profiles could be used clinically, but the results point toward the microbiome as a relevant factor in this cardiopulmonary condition.
Constipation is a common symptom in maintenance hemodialysis patients and greatly affects the quality of survival of hemodialysis patients. Fecal microbiota transplantation and probiotics are feasible treatments for functional constipation, but there is still a gap in the research on the characteristics of gut flora in patients with maintenance hemodialysis combined with constipation. The aim of this study is to clarify the characteristics of the intestinal flora and its changes in maintenance hemodialysis patients with constipation.
Fecal samples were collected from 45 participants, containing 15 in the maintenance hemodialysis constipation group,15 in the maintenance hemodialysis non-constipation group and 15 in the healthy control group. These samples were analyzed using 16S rRNA gene sequencing. The feature of the intestinal microbiome of maintenance hemodialysis constipation group and the microbiome differences among the three groups were elucidated by species annotation analysis, α-diversity analysis, β-diversity analysis, species difference analysis, and predictive functional analysis.
The alpha diversity analysis indicated that maintenance hemodialysis constipation group was less diverse and homogeneous than maintenance hemodialysis non-constipation group and healthy control group. At the genus level, the top ten dominant genera in maintenance hemodialysis constipation group patients were Enterococcus, Escherichia-Shigella, Bacteroides, Streptococcus, Bifidobacterium, Ruminococcus_gnavus_group, Lachnospiraceae_unclassified, Faecalibacterium, Akkermansia and UCG-002. Compared with non-constipation group, the Enterococcus, Rhizobiales_unclassified, Filomicrobium, Eggerthella, Allobaculum, Prevotella_7, Gordonibacter, Mitochondria_unclassified, Lachnoanaerobaculum were significantly higher in constipation group (p<0.05). Compared with non-constipation group, the Kineothrix, Rhodopirellula, Weissella were significantly lower in constipation group (p<0.05). The predictive functional analysis revealed that compared with non-constipation group, constipation group was significantly enriched in pathways associated with pyruate metabolism, flavonoid biosynthesis.
This study describes for the first time the intestinal microbiome characteristics of maintenance hemodialysis patients with constipation. The results of this study suggest that there is a difference in the intestinal flora between maintenance hemodialysis patients with constipation and maintenance hemodialysis patients without constipation.
Background/Objectives: The prevalence of food allergy (FA) in children is increasing. Dysbiosis of the microbiome has been linked to FA but needs to be better understood. We aimed to characterize the gut and skin microbiome of young food-allergic children over time and within different types of immunoglobulin E (IgE)-mediated FA. Methods: We studied 23 patients, as a pilot study of an ongoing prospective multicenter cohort study including children < 2y with newly diagnosed IgE-mediated FA. Samples (feces/skin swabs) were collected at enrollment and at 1-year follow-up and sequenced for the bacterial 16S rRNA gene (hypervariable v1–v2 region). Results: Gut and skin bacterial diversity was significantly higher in patients compared with controls and increased over time (beta test, Shannon diversity, p < 0.01). Within different types of IgE-mediated FA, bacterial diversity was similar. Community composition differed significantly over time and within IgE-mediated FA types (PERMANOVA: p < 0.01). Several significantly different genus abundances were revealed. We observed a positive correlation between high total IgE and a high abundance of the genus Collinsella in patients with a higher number of allergies/sensitizations (≥3), and patients with tree nut and/or peanut allergy. Conclusions: This study revealed an increased bacterial diversity in children with FA compared with non-atopic children. Importantly, the gut and skin microbiome differed in their composition over time and within different types of IgE-mediated FA. These findings contribute to the understanding of microbiome changes in children with FA and indicate the potential of the genus Collinsella as a biomarker for tree nut and/or peanut allergy and possibly for allergy persistence.
Gut microbiota are associated with the pathological features and development of colorectal cancer (CRC); however, how gut microbiota changes in patients with CRC is unknown. This study investigated the role of gut microbiota in the development and progression of CRC by retrospectively comparing the structural differences between the gut microbiota of patients with CRC and healthy individuals.
Together with clinical data, we collected fecal samples from patients with CRC (n = 18) and healthy controls (n = 18) and performed 16S rRNA gene sequencing and alpha and beta diversity analysis to compare microbiota richness and diversity. Based on the differences in microbiota between the CRC and control groups, we identified disease-specific microbial communities after relevant factors. PICRUSt2 software was used to predict the differential microbial functions.
The CRC and control groups differed in both composition and abundance of intestinal microbiota. Firmicutes and Bacteroidetes were the most abundant phyla in both groups, while Verrucomicrobi was significantly more abundant in the CRC group. Megamonas, Lachnospira, and Romboutsia were more abundant in the control group; 18 genera differed significantly in abundance between the groups, which were found to involve 21 metabolic pathways. The distribution and abundance of gut microbiota differed significantly between patients with CRC with and without lymph node metastasis; at the genus level, the abundance of Rothia and Streptococcus was significantly higher and that of Bacteroides, Parabacteroides, and Oscillibacter was significantly lower in patients with lymph node metastasis.
The gut microbiota is altered in CRC patients compared with healthy individuals, with specific changes in the microbiota associated with clinical and pathological features such as tumor stage, lymph node involvement, and tumor differentiation. Our findings elaborate to some extent on the link between the gut microbiota and CRC.
This study examined how gut microbiome composition and function differ across subtypes of irritable bowel syndrome (IBS), including IBS with diarrhea (IBS-D), IBS with constipation (IBS-C), and unclassified IBS (IBS-U). Researchers used 16S sequencing data to compare taxonomic and functional profiles of gut bacteria between these IBS subtypes and matched non-IBS controls. They also examined how clinical characteristics, dietary factors, and depression status related to microbial composition within IBS.
The study drew on deeply phenotyped individuals enrolled in the American Gut Project, a large public microbiome dataset with associated clinical and dietary information. A total of 942 subjects with IBS (spanning IBS-D, IBS-C, and IBS-U) were included and matched by age, gender, body mass index, geography, and dietary patterns with 942 non-IBS controls. This design allowed comparison of microbiome features across IBS subtypes while controlling for major demographic and lifestyle confounders.
Subjects with IBS-D or IBS-U, but not IBS-C, showed significantly reduced bacterial diversity compared to controls. Each IBS subtype was associated with a distinct bacterial signature and corresponding functional shifts tied to disease pathogenesis. Notably, IBS-D was linked to an increased hydrogen sulfide production pathway, while IBS-C was linked to increased palmitoleate biosynthesis. Among IBS subjects, those with depression showed lower Bifidobacterium, Sutterella, and Butyricimonas and higher Proteus than those without depression, and short-chain fatty acid production pathways were reduced in affected patients.
These findings support treating IBS as a heterogeneous condition with subtype-specific microbial and metabolic signatures rather than a single uniform disorder. The elevated hydrogen sulfide production pathway identified in IBS-D points to sulfur metabolism, potentially involving sulfate-reducing bacterial activity, as a mechanistic feature worth further investigation in diarrhea-predominant disease. The link between depression and specific bacterial taxa also suggests that mental health status should be considered when characterizing IBS microbiome profiles. Together, these results could inform more precise, subtype-tailored approaches to diagnosing and managing IBS.
Metabolites secreted by the gut microbiota may play an essential role in microbiota-gut-central nervous system crosstalk. In this study, we explored the changes occurring in the gut microbiota and their metabolites in patients with spinal cord injury (SCI) and analyzed the correlations among them.
The structure and composition of the gut microbiota derived from fecal samples collected from patients with SCI (n = 11) and matched control individuals (n = 10) were evaluated using 16S rRNA gene sequencing. Additionally, an untargeted metabolomics approach was used to compare the serum metabolite profiles of both groups. Meanwhile, the association among serum metabolites, the gut microbiota, and clinical parameters (including injury duration and neurological grade) was also analyzed. Finally, metabolites with the potential for use in the treatment of SCI were identified based on the differential metabolite abundance analysis.
The composition of the gut microbiota was different between patients with SCI and healthy controls. At the genus level, compared with the control group, the abundance of UBA1819, Anaerostignum, Eggerthella, and Enterococcus was significantly increased in the SCI group, whereas that of Faecalibacterium, Blautia, Escherichia-Shigella, Agathobacter, Collinsella, Dorea, Ruminococcus, Fusicatenibacter, and Eubacterium was decreased. Forty-one named metabolites displayed significant differential abundance between SCI patients and healthy controls, including 18 that were upregulated and 23 that were downregulated. Correlation analysis further indicated that the variation in gut microbiota abundance was associated with changes in serum metabolite levels, suggesting that gut dysbiosis is an important cause of metabolic disorders in SCI. Finally, gut dysbiosis and serum metabolite dysregulation was found to be associated with injury duration and severity of motor dysfunction after SCI.
We present a comprehensive landscape of the gut microbiota and metabolite profiles in patients with SCI and provide evidence that their interaction plays a role in the pathogenesis of SCI. Furthermore, our findings suggested that uridine, hypoxanthine, PC(18:2/0:0), and kojic acid may be important therapeutic targets for the treatment of this condition.
This study examined the faecal microbiota profiles of young children affected by acute gastroenteritis (AGE), a major cause of childhood illness marked by diarrhoea, abdominal pain, fever, and vomiting. Researchers focused on the composition and structure of the gut microbial community, comparing children with AGE to healthy children. The work aimed to characterize disease-associated microbial changes in an African setting, where such data have been limited.
The study population was Ghanaian children aged five years and below. It included children diagnosed with acute gastroenteritis as well as healthy controls for comparison. The abstract does not specify an exact sample size or recruitment sites beyond this age-defined, Ghana-based pediatric cohort.
Children with AGE showed altered faecal microbiota composition and structure compared with healthy controls. Consistent with prior evidence linking AGE to gut microbial disruption, the pattern described involves increased presence of pathogenic or opportunistic microbes alongside reduced beneficial taxa. The abstract does not report specific taxa, effect sizes, or statistical values for the Ghanaian cohort itself, so these findings should be read as a confirmed shift in overall community composition and structure rather than itemized taxon-level results.
The findings extend understanding of AGE-associated gut microbiota disruption to an African pediatric population, an area where evidence was previously limited. Documenting these microbial alterations in Ghanaian children supports the broader view that early-life microbiome disruption may increase susceptibility to infectious diarrhoeal disease. This regional data can inform future research into microbiota-targeted approaches for preventing or managing childhood gastroenteritis in developing-country settings.
This study examined the relationship between gastrointestinal (GI) microbial composition and GI symptoms in patients with systemic sclerosis (SSc). It also compared GI symptoms and microbial composition between SSc patients following a low FODMAP diet versus those not following a low FODMAP diet. Stool specimens underwent bacterial 16S rRNA gene sequencing, and microbial differences were assessed using alpha diversity (species richness, evenness, phylogenetic diversity) and beta diversity (overall composition). Differential abundance analysis was used to identify specific bacterial genera linked to the SSc-GI phenotype and to diet group.
The study included 66 adult patients with systemic sclerosis who were consecutively recruited and provided stool samples. Patients also completed the UCLA Scleroderma Clinical Trial Consortium Gastrointestinal Tract Instrument (GIT 2.0) to assess GI symptoms and the Diet History Questionnaire (DHQ) II to assess dietary intake. Based on their reported intake, patients were classified as adhering to a low or non-low FODMAP diet.
The abstract provided does not include the specific results, so the detailed findings on microbial diversity, differential genera, or symptom associations cannot be reported here. The study design indicates that both alpha diversity and beta diversity metrics were used to compare gut microbial composition across SSc-GI phenotypes and across diet groups. Differential abundance analysis was intended to pinpoint particular bacterial genera associated with GI symptoms and with FODMAP diet status in this SSc cohort.
By pairing validated GI symptom instruments with dietary history and 16S rRNA sequencing, this approach helps disentangle whether GI microbial alterations in systemic sclerosis are driven by disease-related changes, dietary patterns, or both. Clarifying this distinction could inform whether dietary interventions such as a low FODMAP diet meaningfully influence gut microbial composition and symptom burden in SSc patients. This kind of design lays groundwork for future studies testing whether dietary modification can be used as a targeted strategy to manage SSc-associated GI symptoms.
This study examined the bacterial tear film microbiome in aqueous-deficient dry eye, comparing Sjogren's syndrome (SS) and non-Sjogren's syndrome (NSS) dry eye to healthy eyes. Researchers sequenced the V3-V4 region of the 16S rRNA gene from tear film DNA samples using the Illumina HiSeq2500 platform. Taxa were assigned using the QIIME pipeline, and alpha and beta diversity were assessed statistically in R. Differences between groups were further characterized using principal coordinate analysis (PCoA), differential abundance testing, and network analysis.
The study included tear film samples from 33 healthy individuals, 17 individuals with Sjogren's syndrome dry eye, and 28 individuals with non-Sjogren's syndrome dry eye, for a total of 78 participants. The abstract does not provide further demographic details such as age, sex, or geographic location of the cohorts.
The phyla Actinobacteria, Firmicutes, and Bacteroidetes showed significant changes in both SS and NSS dry eye compared to healthy eyes, while Lactobacillus and Bacillus were the predominant genera across all three groups. PCoA and heat map analyses revealed that SS and NSS samples formed distinct clusters separate from the healthy cohort. Several genera, including Prevotella, Coriobacteriaceae UCG-003, Enterococcus, Streptomyces, Rhodobacter, Ezakiella, and Microbacterium, were significantly increased in the disease groups relative to healthy eyes.
These findings suggest that aqueous-deficient dry eye, whether associated with Sjogren's syndrome or not, is accompanied by a distinct shift in the ocular surface microbiome rather than a uniform or random change. The clear separation between disease and healthy clusters indicates the tear microbiome could potentially serve as a biomarker to help distinguish dry eye subtypes. This work supports further investigation into whether these microbial shifts contribute to, or result from, the inflammatory processes seen in aqueous-deficient dry eye.
Effects of antibiotics on gut bacteria have been widely studied, but very little is known about the consequences of such treatments on the fungal microbiota (mycobiota). It is commonly believed that fungal load increases in the gastrointestinal tract following antibiotic treatment, but better characterization is clearly needed of how antibiotics directly or indirectly affect the mycobiota and thus the entire microbiota.
We used samples from humans (infant cohort) and mice (conventional and human microbiota-associated mice) to study the consequences of antibiotic treatment (amoxicillin-clavulanic acid) on the intestinal microbiota. Bacterial and fungal communities were subjected to qPCR or 16S and ITS2 amplicon-based sequencing for microbiota analysis. In vitro assays further characterized bacterial-fungal interactions, with mixed cultures between specific bacteria and fungi.
Amoxicillin-clavulanic acid treatment triggered a decrease in the total fungal population in mouse feces, while other antibiotics had opposite effects on the fungal load. This decrease is accompanied by a total remodelling of the fungal population with the enrichment in Aspergillus, Cladosporium, and Valsa genera. In the presence of amoxicillin-clavulanic acid, microbiota analysis showed a remodeling of bacterial microbiota with an increase in specific bacteria belonging to the Enterobacteriaceae. Using in vitro assays, we isolated different Enterobacteriaceae species and explored their effect on different fungal strains. We showed that Enterobacter hormaechei was able to reduce the fungal population in vitro and in vivo through yet unknown mechanisms.
Bacteria and fungi have strong interactions within the microbiota; hence, the perturbation initiated by an antibiotic treatment targeting the bacterial community can have complex consequences and can induce opposite alterations of the mycobiota. Interestingly, amoxicillin-clavulanic acid treatment has a deleterious effect on the fungal community, which may have been partially due to the overgrowth of specific bacterial strains with inhibiting or competing effects on fungi. This study provides new insights into the interactions between fungi and bacteria of the intestinal microbiota and might offer new strategies to modulate gut microbiota equilibrium. Video Abstract.
Gut microecosystem has been shown to play an important role in human health. In recent years, the concept of the gut-kidney axis has been proposed to explain the potential association between gut microbiota and chronic kidney disease (CKD). Here, a cohort of fecal samples collected from patients with CKD (n = 13) were involved. The composition of gut microbial communities and clinical features in CKD and end-stage renal disease (ESRD) were characterized. Our study focused on the changes in gut microbiome and the correlation with clinical features in patients with CKD and ESRD by analyzing high-throughput sequencing results of collected feces. We elucidated the alterations of gut microbiota in CKD patients at different stages of disease and initially identified the gut microbiota associated with CKD progression. We also combined correlation analysis to identify clinical features closely related to the gut microbiome. Our results offered the possibility of using non-invasive gut microbiome in the early diagnosis of course from CKD to ESRD and provide new insights into the association between clinical features and gut microbiota in CKD.
Constipation is a common disease affecting humans. Bifidobacterium longum is reportedly effective in relieving constipation. Current studies generally focus on the dose–response relationship of oral doses; however, the dose–effect relationship of B. longum in the colon, which is the primary site where B. longum exerts constipation-relieving effects, to treat constipation has not been studied. Herein, three strains of B. longum (FGSZY6M4, FJSWXJ10M2, and FSDJN6M3) were packaged in colon-released capsules to explore the dose–effect relationship in the colon. For each strain, three groups of capsules (104, 106, and 108 CFU/capsule, respectively) and one group of free probiotics (108 CFU/mL) were used to explore the colonic dose effect of B. longum. The results showed that the three strains of B. longum improved fecal water content and promoted intestinal motility by regulating gastrointestinal peptide (MTL, GAS, and VIP), aquaporin-3, and 5-hydroxytryptamine levels while promoting gastrointestinal motility and relieving constipation by regulating the intestinal flora composition of constipated rats and changing their metabolite content (short-chain fatty acids). Among the three free bacterial solution groups (108 CFU/mL), FGSZY6M4 was the most effective in relieving constipation caused by loperamide hydrochloride in rats. The optimal effective dose of each strain was 6M4 (104 CFU/day), 10M2 (106 CFU/day), and S3 (108 CFU/day) of the colon-released capsules. Therefore, for some effective strains, the dose of oral probiotics can be reduced by colon-released capsules, and constipation can be relieved without administering a great number of bacterial solutions. Therefore, investigating the most effective dose of B. longum at the colon site can help to improve the efficiency of relieving constipation.
This study examined the gut microbiome and serum metabolome in patients with functional constipation (FC), a common gastrointestinal disorder that significantly affects physical and mental health. The researchers used 16S rRNA microbial genomics to profile gut microbiota composition and non-target metabolomics based on liquid chromatography-mass spectrometry to characterize serum metabolic profiles. The study was designed to address inconsistent prior findings on the gut microbiome and FC, and to better link microbiome changes to host metabolites.
The study included 30 patients with functional constipation and 28 healthy individuals as a comparison group. Fecal samples were used for 16S rRNA gut microbiota analysis and serum samples were used for metabolomic profiling in these participants. The abstract does not specify additional demographic details such as age or sex distribution.
FC patients had distinct gut microbiota structures and serum metabolic profiles compared to healthy individuals. Patients with FC showed increased levels of Bacteroides and of several butyrate-producing bacteria, including Roseburia, Faecalibacterium, and Butyricicoccus. Serum levels of upstream products of host arginine biosynthesis, specifically 2-oxoglutaric acid, L-glutamic acid, N-acetylornithine, and L-ornithine, were significantly reduced in FC patients.
The findings suggest that functional constipation may be associated with an altered gut microbiota, including increased Bacteroidetes, alongside downregulation of host arginine biosynthesis intermediates. This points to a potential link between specific gut bacteria and disrupted host amino acid metabolism in FC. The pairing of microbiome and metabolome data offers a more integrated view of FC pathophysiology than microbiome data alone, which could inform future mechanistic or therapeutic research.
Age-related macular degeneration (AMD) is the leading cause of vision loss in those over the age of 50. Recently, intestinal microbiota has been reported to be involved in the pathogenesis of ocular diseases. The purpose of this study was to discover more about the involvement of the intestinal microbiota in AMD patients.
Fecal samples from 30 patients with AMD (AMD group) and 17 age- and sex-matched healthy controls (control group) without any fundus disease were collected. DNA extraction, PCR amplification, and 16S rRNA gene sequencing of the samples were performed to identify intestinal microbial alterations. Further, we used BugBase for phenotypic prediction and PICRUSt2 for KEGG Orthology (KO) as well as metabolic feature prediction.
The intestinal microbiota was found to be significantly altered in the AMD group. The AMD group had a significantly lower level of Firmicutes and relatively higher levels of Proteobacteria and Bacteroidota compared to those in the control group. At the genus level, the AMD patient group showed a considerably higher proportion of Escherichia-Shigella and lower proportions of Blautia and Anaerostipes compared with those in the control group. Phenotypic prediction revealed obvious differences in the four phenotypes between the two groups. PICRUSt2 analysis revealed KOs and pathways associated with altered intestinal microbiota. The abundance of the top eight KOs in the AMD group was higher than that in the control group. These KOs were mainly involved in lipopolysaccharide biosynthesis.
The findings of this study indicated that AMD patients had different gut microbiota compared with healthy controls, and that AMD pathophysiology might be linked to changes in gut-related metabolic pathways. Therefore, intestinal microbiota might serve as non-invasive indicators for AMD clinical diagnosis and possibly also as AMD treatment targets.
Microbial Dysbiosis is associated with the etiology and pathogenesis of diseases. The studies on the vaginal microbiome in cervical cancer are essential to discern the cause and effect of the condition. The present study characterizes the microbial pathogenesis involved in developing cervical cancer. Relative species abundance assessment identified Firmicutes, Actinobacteria, and Proteobacteria dominating the phylum level. A significant increase in Lactobacillus iners and Prevotella timonensis at the species level revealed its pathogenic influence on cervical cancer progression. The diversity, richness, and dominance analysis divulges a substantial decline in cervical cancer compared to control samples. The β diversity index proves the homogeneity in the subgroups' microbial composition. The association between enriched Lactobacillus iners at the species level, Lactobacillus, Pseudomonas, and Enterococcus genera with cervical cancer is identified by Linear discriminant analysis Effect Size (LEfSe) prediction. The functional enrichment corroborates the microbial disease association with pathogenic infections such as aerobic vaginitis, bacterial vaginosis, and chlamydia. The dataset is trained and validated with repeated k-fold cross-validation technique using a random forest algorithm to determine the discriminative pattern from the samples. SHapley Additive exPlanations (SHAP), a game theoretic approach, is employed to analyze the results predicted by the model. Interestingly, SHAP identified that the increase in Ralstonia has a higher probability of predicting the sample as cervical cancer. New evidential microbiomes identified in the experiment confirm the presence of pathogenic microbiomes in cervical cancer vaginal samples and their mutuality with microbial imbalance.
The World Health Organization recommends untargeted iron supplementation for women of reproductive age (WRA) in countries where anemia prevalence is greater than 40%, such as Cambodia. Iron supplements, however, often have poor bioavailability, so the majority remains unabsorbed in the colon. The gut houses many iron-dependent bacterial enteropathogens; thus, providing iron to individuals may be more harmful than helpful. We examined the effects of two oral iron supplements with differing bioavailability on the gut microbiomes in Cambodian WRA. This study is a secondary analysis of a double-blind, randomized controlled trial of oral iron supplementation in Cambodian WRA. For 12 weeks, participants received ferrous sulfate, ferrous bisglycinate, or placebo. Participants provided stool samples at baseline and 12 weeks. A subset of stool samples (n = 172), representing the three groups, were randomly selected for gut microbial analysis by 16S rRNA gene sequencing and targeted real-time PCR (qPCR). At baseline, 1% of women had iron-deficiency anemia. The most abundant gut phyla were Bacteroidota (45.7%) and Firmicutes (42.1%). Iron supplementation did not alter gut microbial diversity. Ferrous bisglycinate increased the relative abundance of Enterobacteriaceae, and there was a trend towards an increase in the relative abundance of Escherichia-Shigella. qPCR detected an increase in the enteropathogenic Escherichia coli (EPEC) virulence gene, bfpA, in the group that received ferrous sulfate. Thus, iron supplementation did not affect overall gut bacterial diversity in predominantly iron-replete Cambodian WRA, however, evidence does suggest an increase in relative abundance within the broad family Enterobacteriaceae associated with ferrous bisglycinate use. IMPORTANCE To the best of our knowledge, this is the first published study to characterize the effects of oral iron supplementation on the gut microbiomes of Cambodian WRA. Our study found that iron supplementation with ferrous bisglycinate increases the relative abundance of Enterobacteriaceae, which is a family of bacteria that includes many Gram-negative enteric pathogens like Salmonella, Shigella, and Escherichia coli. Using qPCR for additional analysis, we were able to detect genes associated with enteropathogenic E. coli, a type of diarrheagenic E. coli known to be present around the world, including water systems in Cambodia. The current WHO guidelines recommend blanket (untargeted) iron supplementation for Cambodian WRA despite a lack of studies in this population examining iron's effect on the gut microbiome. This study can facilitate future research that may inform evidence-based global practice and policy.
A case-control study was conducted. Fecal microbiota was determined by 16S rDNA sequencing. The cases with CRC or adenoma were subclassified by gut microbiota enterotypes. Multivariate analyses were used to test associations between smoking and the odds of colorectal neoplasm subtypes. Mann-Whitney U tests were used to find differential genera, genes, and pathways between the subtypes.
Included in the study were 130 CRC patients (type I: n=77; type II: n=53), 120 adenoma patients (type I: n=66; type II: n=54), and 130 healthy participants. Smoking increased the odds for type II tumors significantly (all p for trend <0.05) but not for type I tumors. The associations of smoking with increased odds of colorectal neoplasm significantly differed by gut microbiota enterotypes (p<0.05 for heterogeneity). An increase in carcinogenic bacteria (genus Escherichia shigella) and a decrease in probiotics (family Lachnospiraceae and Ruminococcaceae) in type II tumors may drive disease progression by upregulating oncogenic signaling pathways and inflammatory/oxidative stress response pathways, as well as protein phospholipase D1/2, cytochrome C, and prostaglandin-endoperoxide synthase 2 expression.
Smoking was associated with a higher odds of type II colorectal neoplasms but not type I tumors, supporting a potential role for the gut microbiota in mediating the association between smoking and colorectal neoplasms.
This study examined the oral (saliva) microbiome composition of diverse human populations from southwestern Angola and Zimbabwe. It used the non-human sequencing reads recovered from an expanded exome capture approach, repurposing genomic data to characterize salivary bacterial communities. The aim was to add southern African, non-industrialized populations to the global picture of oral microbiome composition and diversity, which remains poorly understood on a broad scale.
The sample comprised 52 individuals drawn from eight ethnolinguistically diverse southern African populations. These included the Kuvale, Kwepe, Himba, Tjimba, Kwisi, Twa, and !Xun from Angola, and the Tshwa from Zimbabwe. The groups represented a range of subsistence strategies, including foragers, food-producers, and peripatetic communities that provide services to dominant neighboring groups.
Neisseria, Streptococcus, Prevotella, Rothia, and Porphyromonas were the five most frequent genera across all southern African groups, consistent with patterns reported in other human populations worldwide. Neither host genetics nor livelihood strategy appeared to shape the overall oral microbiome profile, pointing to a broadly homogeneous core community. However, some individuals from the Tshwa and Twa forager groups showed an enrichment of pathogenic genera belonging to the Enterobacteriaceae family, a family that includes Salmonella and other clinically relevant organisms.
The findings suggest that the human oral microbiome maintains a stable, homogeneous core composition across ethnolinguistically and subsistence-diverse populations, independent of genetic ancestry or lifestyle. This supports the idea that core oral genera are a conserved feature of human biology rather than a product of industrialization or diet alone. The localized enrichment of pathogenic Enterobacteriaceae in specific forager subgroups also highlights that certain communities may carry distinct risks worth further investigation in relation to oral and systemic health.
Chronic granulomatous disease (CGD) is caused by defects in any 1 of the 6 subunits forming the nicotinamide adenine dinucleotide phosphate oxidase complex 2 (NOX2), leading to severely reduced or absent phagocyte-derived reactive oxygen species production. Almost 50% of patients with CGD have inflammatory bowel disease (CGD-IBD). While conventional IBD therapies can treat CGD-IBD, their benefits must be weighed against the risk of infection. Understanding the impact of NOX2 defects on the intestinal microbiota may lead to the identification of novel CGD-IBD treatments. We sought to identify microbiome and metabolome signatures that can distinguish individuals with CGD and CGD-IBD.
We conducted a cross-sectional observational study of 79 patients with CGD, 8 pathogenic variant carriers, and 19 healthy controls followed at the National Institutes of Health Clinical Center. We profiled the intestinal microbiome (amplicon sequencing) and stool metabolome, and validated our findings in a second cohort of 36 patients with CGD recruited through the Primary Immune Deficiency Treatment Consortium.
We identified distinct intestinal microbiome and metabolome profiles in patients with CGD compared to healthy individuals. We observed enrichment for Erysipelatoclostridium spp, Sellimonas spp, and Lachnoclostridium spp in CGD stool samples. Despite differences in bacterial alpha and beta diversity between the 2 cohorts, several taxa correlated significantly between both cohorts. We further demonstrated that patients with CGD-IBD have a distinct microbiome and metabolome profile compared to patients without CGD-IBD.
Intestinal microbiome and metabolome signatures distinguished patients with CGD and CGD-IBD, and identified potential biomarkers and therapeutic targets.
The gut microbiota plays an important role in human health. In this study, we aimed to investigate whether and how gut microbiota communities are altered in patients with immune-mediated necrotizing myopathy (IMNM) and provide new ideas to further explore the pathogenesis of IMNM or screen for its clinical therapeutic targets in the future.
The gut microbiota collected from 19 IMNM patients and 23 healthy controls (HCs) were examined by using 16S rRNA gene sequencing. Alpha and beta-diversity analyses were applied to examine the bacterial diversity and community structure. Welch's t test was performed to identify the significantly abundant taxa of bacteria between the two groups. Spearman correlation analysis was performed to analyze the correlation between gut microbiota and clinical indicators. A receiver operator characteristic (ROC) curve was used to reflect the sensitivity and specificity of microbial biomarker prediction of IMNM disease. P < 0.05 was considered statistically significant.
Nineteen IMNM patients and 23 HCs were included in the analysis. Among IMNM patients, 94.74% (18/19) of them used glucocorticoids, while 57.89% (11/19) of them used disease-modifying antirheumatic drugs (DMARDs), and the disease was accessed by MITAX (18.26 ± 8.62) and MYOACT (20.68 ± 8.65) scores. Participants in the groups were matched for gender and age. The diversity of the gut microbiota of IMNM patients differed and decreased compared to that of HCs (Chao1, Shannon, and Simpson indexes: p < 0.05). In IMNM patients, the relative abundances of Bacteroides, Roseburia, and Coprococcus were decreased, while that of Lactobacillus and Streptococcus were relatively increased. Furthermore, in IMNM patients, Lactobacillus was positively correlated with the levels of anti-signal recognition particle (SRP) antibodies, anti-Ro52 antibodies, and erythrocyte sedimentation rate (ESR), while Streptococcus was positively correlated with anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) antibodies and C-reactive protein (CRP). Roseburia was negatively correlated with myoglobin (MYO), cardiac troponin T (cTnT), ESR, CRP, and the occurrence of interstitial lung disease (ILD). Bacteroides was negatively correlated with ESR and CRP, and Coprococcus was negatively correlated with ESR. Finally, the prediction model was built using the top five differential genera, which was verified using a ROC curve (area under the curve (
We observed a characteristic compositional change in the gut microbiota with an abnormal elevation of Lactobacillus in IMNM patients, which was accompanied by changes in clinical indicators. This suggests that gut microbiota dysbiosis occurs in IMNM patients and is correlated with systemic autoimmune features.
The correlation existing between gut microbiota diversity and survival after allogeneic hematopoietic stem cell transplantation (allo-HSCT) has so far been studied in adults. Pediatric studies question whether this association applies to children as well. Stool samples from a multicenter cohort of 90 pediatric allo-HSCT recipients were analyzed using 16S ribosomal RNA amplicon sequencing to profile the gut microbiota and estimate diversity with the Shannon index. A global-to-local networking approach was used to characterize the ecological structure of the gut microbiota. Patients were stratified into higher- and lower-diversity groups at 2 time points: before transplantation and at neutrophil engraftment. The higher-diversity group before transplantation exhibited a higher probability of overall survival (88.9% ± 5.7% standard error [SE] vs 62.7% ± 8.2% SE; P = .011) and lower incidence of grade 2 to 4 and grade 3 to 4 acute graft-versus-host disease (aGVHD). No significant difference in relapse-free survival was observed between the 2 groups (80.0% ± 6.0% SE vs 55.4% ± 10.8% SE; P = .091). The higher-diversity group was characterized by higher relative abundances of potentially health-related microbial families, such as Ruminococcaceae and Oscillospiraceae. In contrast, the lower-diversity group showed an overabundance of Enterococcaceae and Enterobacteriaceae. Network analysis detected short-chain fatty acid producers, such as Blautia, Faecalibacterium, Roseburia, and Bacteroides, as keystones in the higher-diversity group. Enterococcus, Escherichia-Shigella, and Enterobacter were instead the keystones detected in the lower-diversity group. These results indicate that gut microbiota diversity and composition before transplantation correlate with survival and with the likelihood of developing aGVHD.
The most common toxic side effect after chemotherapy, one of the main treatments for colorectal cancer (CRC), is myelosuppression. To analyze the correlation between gut microbiota and leukopenia after chemotherapy in CRC patients.
Stool samples were collected from 56 healthy individuals and 55 CRC patients. According to the leukocytes levels in peripheral blood, the CRC patients were divided into hypoleukocytes group (n = 13) and normal leukocytes group (n = 42). Shannon index, Simpson index, Ace index, Chao index and Coverage index were used to analyze the diversity of gut microbiota. LDA and Student's t-test(St test) were used for analysis of differences. Six machine learning algorithms, including logistic regression (LR) algorithm, random forest (RF) algorithm, neural network (NN) algorithm, support vector machine (SVM) algorithm, catboost algorithm and gradient boosting tree algorithm, were used to construct the prediction model of gut microbiota with leukopenia after chemotherapy for CRC.
Compared with healthy group, the microbiota alpha diversity of CRC patients was significantly decreased (p < 0.05). After analyzing the gut microbiota differences of the two groups, 15 differential bacteria, such as Bacteroides, Faecalibacterium and Streptococcus, were screened. RF prediction model had the highest accuracy, and the gut microbiota with the highest predictive value were Peptostreptococcus, Faecalibacterium, and norank_f__Ruminococcaceae, respectively. Compared with normal leukocytes group, the microbiota alpha diversity of hypoleukocytes group was significantly decreased (p < 0.05). The proportion of Escherichia-Shigella was significantly decreased in the hypoleukocytes group. After analyzing the gut microbiota differences of the two groups, 9 differential bacteria, such as Escherichia-Shigella, Fusicatenibacter and Cetobacterium, were screened. RF prediction model had the highest accuracy, and the gut microbiota with the highest predictive value were Fusicatenibacte, Cetobacterium, and Paraeggerthella.
Gut microbiota is related to leukopenia after chemotherapy. The gut microbiota may provide a novel method for predicting myelosuppression after chemotherapy in CRC patients.
This retrospective cohort study investigated whether intestinal obstruction caused by colorectal cancer (CRC) is associated with distinct changes in the gut microbiota. Researchers used 16S rRNA sequencing to compare microbiota composition in tumour and adjacent normal tissues between CRC patients with and without obstruction. Patients with and without obstruction were matched using 1:1 propensity score matching to reduce confounding. The study also examined whether obstruction status was linked to differences in survival outcomes.
A total of 313 patients with colorectal cancer were recruited for the study. Total DNA was extracted and amplified from tumour and adjacent normal tissues of 84 patients, along with 36 additional frozen tumour tissue samples. Patients were divided into obstruction and non-obstruction groups and compared after propensity score matching. The abstract does not specify additional demographic details such as age or sex distribution.
Patients with CRC-related intestinal obstruction had shorter overall survival and disease-free survival than those without obstruction. Microbial richness and diversity in tumour tissues were significantly higher in the obstruction group, with both alpha and beta diversity differing significantly between groups (P < 0.05). At the phylum and genus levels, Bacteroidetes were significantly enriched in the tumour tissues of patients with obstruction. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings suggest that intestinal obstruction in colorectal cancer is associated with a distinct, more diverse tumour-associated microbiota dominated by Bacteroidetes, and with worse clinical outcomes. This raises the possibility that microbiota alterations may be a marker of, or contributor to, the more aggressive clinical course seen in obstructed CRC. These associations could inform future research into microbiota-based prognostic markers or risk stratification for CRC patients presenting with obstruction. Further studies would be needed to clarify causality and underlying mechanisms.
Grade C (previously aggressive) periodontitis (GCP) in adolescents is prevalent in certain parts of Africa where it is associated with JP2 genotype, a highly virulent strain of Aggregatibacter actinomycetemcomitans. The aim of this study was to characterize the subgingival bacteriome in Moroccan subjects with GCP positive to A. actinomycetemcomitans JP2 genotype.
Subgingival plaque samples were collected from shallow and deep pockets of 8 subjects with GCP (17.2 ± 1.5 years) and from gingival sulci of 13 controls with no periodontitis (14.6 ± 1.1 years). Identification and genotyping of A. actinomycetemcomitans was performed using PCR analysis of the ltx operon, while bacteriome profiling was done by 16S rRNA gene sequencing (V1-V3 region). Groups were compared in terms of microbial diversity, abundances, and dysbiosis.
The shallow and deep pocket sites from GCP cases had a significantly altered microbial composition compared to controls. Species associated with health included Haemophilus parainfluenzae, Lautropia mirabilis, Streptococcus spp., Gemella spp., and Rothia spp. While known periodontal pathogens, including Porphyromonas gingivalis, Tannerella forsythia, Treponema spp. and Fretibacterium spp., were significantly enriched in GCP, non-conventional taxa, including Pseudomonas oral taxon C61 and Enterobacter cloacae were more abundant and showed stronger association with the disease. Less significant differences in abundances of individual taxa were observed between shallow and deep pockets. Overall dysbiosis measured in terms of Subgingival Microbial Dysbiosis Index (SMDI) differentiated between GCP and no-periodontitis with 95% accuracy.
The results suggest that several periodontal pathogens involved in the adult-type periodontitis also play a role in JP2 genotype-associated GCP. The potential role of non-conventional taxa in the pathogenesis of GCP warrants further investigation.
Orthokeratology (OK) lens wear increases the risk of bacterial infection, but little is known about the microbiota of the conjunctival sac in myopic children wearing OK lenses. This study aimed to investigate the changes of conjunctival microbiota in children after treatment with OK lenses using 16 S rDNA sequencing.
Twenty-eight myopic children who had been continuously wearing OK lenses for 12 to 13 months were enrolled in this prospective study. Twenty-two gender- and age-matched myopic children who had not worn OK lenses or discontinued OK lens wear at least 1 year ago were recruited as controls. Conjunctival swabs from each participant were collected for exploration of the microbiota profiles, targeting the V3-V4 regions of the 16 S rRNA gene by MiSeq sequencing. The differences in the microbial community structure and diversity were also compared between groups.
The bacterial alpha diversity indices in the OK lens group were not different from those in the non-wearer group (P > 0.05, Wilcoxon test), while beta diversity examined using principle coordinate analysis of unweighted UniFrac divided the two groups into different clusters. Proteobacteria, Bacteroidetes, and Firmicutes were the abundant phyla in the conjunctival sac microbiota in both groups (P < 0.05, Mann-Whitney U test). Among children in the OK lens group, the Linear discriminant analysis Effect Size identified the compositional changes in OK lens-associated bacteria. Key functional genera such as Blautia, Parasutterella, and Muribaculum were enriched, whereas Brevundimonas, Acinetobacter, Proteus, and Agathobacter decreased significantly (P < 0.05, Mann-Whitney U test). Phylogenetic investigation of communities by reconstruction of unobserved states also showed altered bacterial metabolic pathways in OK lens-associated microbiota. Moreover, using receiver operating characteristic curves, Brevundimonas, Acinetobacter, Proteus, and Agathobacter alone (the area under the curve was all > 0.7500) or in combination (the area under the curve was 0.9058) were revealed to discriminate OK lens wearers from controls.
The relative abundance of the microbial community in the conjunctival sac of myopic children can alter after OK lens wear. Brevundimonas, Acinetobacter, Proteus, and Agathobacter may be candidate biomarkers to distinguish between OK lens wearers and non-wearers.
This study examined whether gut microbiota composition influences the return of estrus in post-weaning sows by regulating the metabolism of sex steroid hormones. The researchers used 16S rRNA gene sequencing, metagenomic sequencing, and fecal metabolome analysis to link microbial community changes to hormone-related outcomes. They specifically looked at how shifts in gut bacterial species affect the functional capacity for steroid hormone biosynthesis within the gut microbiome.
The study analyzed 207 fecal samples from well-phenotyped sows using 16S rRNA gene sequencing to find associations between gut microbes and estrus return. A subset of 85 fecal samples underwent metagenomic sequencing to identify specific bacterial species tied to estrus return status. The findings were then confirmed in a separate validation cohort of sows.
Metagenomic analysis identified 37 bacterial species significantly associated with estrus return after weaning. Sows that returned to normal estrus had increased abundances of L. reuteri and P. copri, and decreased abundances of B. fragilis, S. suis, and B. pseudolongum, compared to non-returning sows. These microbial shifts significantly altered the gut microbiome's functional capacity for steroid hormone biosynthesis, and metabolome analysis found significant differences in sex steroid hormones and related compounds between normal and non-return sows.
By integrating differential bacterial species, metagenomic function, and fecal metabolome data, the study provides evidence that gut microbiota, including reduced B. fragilis abundance, is linked to normal post-weaning estrus return through effects on sex steroid hormone metabolism. This suggests that specific gut bacteria could serve as biomarkers or targets for improving reproductive efficiency in sows. The findings point toward potential microbiome-based strategies to address delayed or absent estrus return, a costly problem in swine production.
We collected clinical data and stool samples from participants. Bacterial 16S rRNA genes were amplified, sequenced, and clustered into operational taxonomic unit. Alpha diversity was studied by Shannon and Simpson indexes. To study how different the gut microbiota composition is between the different groups, beta diversity estimation was evaluated by principal coordinate analysis (PCoA) using Bray-Curtis dissimilarity. To further analyze differences in microbiome composition we performed a linear discriminant analysis (LDA) effect size (LEfSe).
We included 30 HIV+MASLD+, 30 HIV+MASLD- and 20 HIV-MASLD+ participants. Major butyrate producers, including Faecalibacterium, Ruminococcus, and Lachnospira dominated the microbiota in all three groups. Shannon's and Simpson's diversity metrics were higher among MASLD+ individuals (Kruskal-Wallis p = 0.047). Beta diversity analysis showed distinct clustering in MASLD-, with MASLD+ participants overlapping regardless of HIV status (ADONIS significance <0.001). MASLD was associated with increased homogeneity across individuals, in contrast to that observed in the HIV+NAFDL- group, in which the dispersion was higher (Permanova test, p value <0.001; ANOSIM, p value <0.001). MASLD but not HIV determined a different microbiota structure (HIV+MASLD- vs. HIV+MASLD+, q-value = 0.002; HIV-MASLD+ vs. HIV+MASLD+, q-value = 0.930; and HIV-MASLD+ vs. HIV+MASLD-, q-value < 0.001). The most abundant genera in MASLD- were Prevotella, Bacteroides, Dialister, Acidaminococcos, Alloprevotella, and Catenibacterium. In contrast, the most enriched genera in MASLD+ were Ruminococcus, Streptococcus, Holdemanella, Blautia, and Lactobacillus.
We found a microbiome signature linked to MASLD, which had a greater influence on the overall structure of the gut microbiota than HIV status alone.
Microbiomes have immunoregulatory functions and may be involved in the pathophysiology of eye diseases. However, the effects of microbiomes on uveitic glaucoma (UG) and open-angle glaucoma (OAG) have not been sufficiently investigated. This study analysed differences in eyelid and buccal microbiomes between UG and OAG using metagenomic technology.
Eyelid and buccal specimens were collected from 34 UG and 62 OAG patients. The taxonomic composition of the microbiome was determined via 16S rRNA gene sequencing, operational taxonomic unit analysis and diversity analysis. Differential gene expression analysis (DEG) and principal component analyses (PCoA) determined taxon differences between the microbiomes of the UG and OAG patients. Subgroup analysis according to age and baseline IOP was performed.
There was no significant difference in alpha-diversity between the microbiomes of UG and OAG patients. Further, PCoA revealed no differences in eyelid microbiome between the UG and OAG groups, but significant differences were found in buccal microbiome between the groups, especially in a subgroup of OAG patients with normal IOP. DEG analysis of the eyelid microbiome revealed various taxa differences, including the enrichment of Rhodococcus in UG samples over OAG samples. Taxa such as Lactobacillus and Proteus were significantly depleted (q-value = 9.98e-6 and q-value = 1.38 × 10-4 , respectively) in the buccal microbiome of UG patients, whereas Enterococcus was enriched (q-value = 5.26e-5 ).
This study showed that the buccal microbiome in UG differs from that in OAG; reduced Lactobacillus was observed in UG. These results suggest that apart than OAG, microbiome composition may be a factor in the pathogenesis of UG.
The significance of the relationship between the microbiota and diseases is increasingly being recognized. However, the characterization of tumor microbiome and their precise molecular mechanisms through which microbiota promotes hepatocellular carcinoma (HCC) development are still unclear.
The intrahepatic microbiota was investigated from tumor, normal adjacent tissues in 46 patients with HCC and normal hepatic tissues in 33 patients with hemangioma by 16S rRNA gene sequencing. Taxonomic composition differences in patients were evaluated using Linear discriminant analysis Effect Size (LefSe) and Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) to predict microbial functional pathways. Associations between the most relevant taxa and clinical characteristics of HCC patients were analyzed by Spearman rank correlations. The effects of microbe on hepatic stellate cells (HSCs) activation and HCC progression were examined.
We observed intrahepatic microbiota disturbances by reduced microbial diversity in HCC. The tumor microbiota of the HCC patients with cirrhosis showed higher abundance of Stenotrophomonas maltophilia (S. maltophilia). S. maltophilia provoked senescence-associated secretory phenotype (SASP) in HSCs by activating TLR-4-mediated NF-κB signaling pathway, which in turn induced NLRP3 inflammasome complex formation and secreted various inflammatory factors in the liver, thus facilitating HCC progression in mice. Moreover, signs of SASP were also observed in the HSCs in the area of HCC with higher S. maltophilia enrichment arising in patients with cirrhosis.
Our analysis of the hepatic microbiota revealed for the first time that patients with HCC exhibited a dysbiotic microbial community with higher S. maltophilia abundance, which induced the expression SASP factors of HSCs and cirrhosis in the liver, concurring in the process of hepatocarcinogenesis.
This study examined whether Parkinson's disease (PD) medications themselves, rather than the disease process alone, alter gastrointestinal motility and microbiota composition in the small intestine. The small intestine is the primary site of drug absorption, yet it had not previously been studied in this context. Researchers treated healthy, non-PD rats with dopamine, pramipexole (combined with levodopa-carbidopa), or ropinirole (combined with levodopa-carbidopa) for 14 sequential days. The aim was to determine whether the medications alone could reproduce microbiota changes resembling those reported in human PD patients.
The subjects were healthy, non-PD, wild-type Groningen rats, not human patients or a public dataset. The rats were divided into treatment groups receiving dopamine, pramipexole with levodopa-carbidopa, or ropinirole with levodopa-carbidopa, alongside a vehicle (control) group. The abstract does not specify the exact number of animals per group. Using healthy animals allowed the researchers to isolate the effects of the medications from any confounding effects of PD itself.
Rats treated with dopamine agonists showed significantly reduced small intestinal motility and increased bacterial overgrowth in the distal small intestine. Treated animals also showed significant microbial taxa shifts compared to vehicle controls, including increases in Lactobacillus and Bifidobacterium and decreases in Lachnospiraceae and Prevotellaceae. These shifts closely resembled differences previously reported between human PD patients and healthy controls. Notably, certain Lactobacillus species correlated negatively with systemic levodopa levels, suggesting these bacteria may affect the drug's bioavailability.
The findings suggest that PD medications themselves, not just the underlying disease, can drive gastrointestinal motility changes and microbiota alterations previously attributed to PD pathology. This represents an important confounder that should be accounted for when interpreting microbiome studies in PD patients taking dopaminergic therapy. The negative correlation between certain Lactobacillus species and levodopa levels also raises the possibility that drug-induced microbiota shifts could feed back to affect medication bioavailability. Future PD microbiome research and drug-microbiome interaction studies should account for medication effects independent of disease status.
People with COPD have been reported to bear a distinct airway microbiota from healthy individuals based on bronchoalveolar lavage (BAL) and sputum samples. Unfortunately, the collection of these samples involves relatively invasive procedures and is resource-demanding, limiting its regular use. Non-invasive samples from the upper airways could constitute an interesting alternative, but its relationship with COPD is still underexplored. We examined the merits of saliva to identify the typical profile of COPD oral bacteria and test its association with the disease.
Outpatients with COPD and age-sex matched healthy controls were recruited and characterised based on clinical parameters and 16S rRNA profiling of oral bacteria. A clustering analysis based on patients' oral bacteria beta-diversity and logistic regressions were performed to evaluate the association between oral bacteria composition and COPD.
128 individuals participated (70 patients and 58 controls). Differential abundance analyses showed differences in patients comparable to the ones previously observed in samples from the lower respiratory tract, i.e., an increase in Proteobacteria (particularly Haemophilus) and loss of microbiota diversity. An unsupervised clustering analysis separated patients in two groups based on microbiota composition differing significantly in the frequency of patients hospitalized due to severe acute exacerbation of COPD (AECOPD) and in the frequency of GOLD D patients. Furthermore, a low frequency of Prevotella was associated with a significantly higher risk of recent severe AECOPD and of being GOLD D.
Salivary bacteria showed an association with COPD, particularly with severe exacerbations, supporting the use of this non-invasive specimen for future studies of heterogeneous respiratory diseases like COPD.
This study examined whether dysbiosis of the skin microbiome and the gut microbiome is associated with melanoma growth and progression. The researchers used the MeLiM porcine model, which spontaneously develops melanoma that can progress or regress, to study this relationship. They performed parallel analysis of cutaneous (skin) microbiota and faecal microbiota from the same animals, comparing melanoma tissue to healthy skin and comparing MeLiM piglets to control piglets. Bacterial composition was profiled using high throughput sequencing of the V4-V5 region of the 16S rRNA gene.
The subjects were MeLiM piglets aged 8 to 12 weeks, a porcine model of melanoma progression and spontaneous regression. Skin swabs from melanoma tissue and healthy skin, along with faecal samples, were collected from the same individual animals. A control group of piglets without melanoma was also included for comparison of the faecal microbiome. The abstract does not specify the exact number of animals sampled.
There was a significant difference in microbiome diversity and richness between melanoma tissue and healthy skin, and between the faecal microbiome of MeLiM piglets and control piglets. Principal Coordinate Analysis and Non-metric multidimensional scaling both showed clear dissimilarities between these different bacterial communities. Linear discriminant analysis was used to identify specific bacterial taxa distinguishing the groups, though the abstract text is cut off before naming these taxa. Overall, the findings indicate that melanoma progression is accompanied by detectable shifts in both cutaneous and gut bacterial community composition.
The findings support the idea that skin microbiome alterations, not just gut microbiome alterations, may be relevant to the tumor microenvironment in melanoma. This suggests a potential link between local skin dysbiosis and systemic gut dysbiosis during melanoma progression, an area the authors note had not been previously investigated. Because the gut microbiome has already been shown to modulate response to melanoma immunotherapy, these results raise the possibility that skin microbiota could also influence tumor behavior or serve as an additional biomarker. This porcine model may offer a useful system for further mechanistic study of microbiome-melanoma interactions relevant to human disease.
The gut microbiota is implicated in the adverse developmental outcomes of postnatal iron supplementation. To generate hypotheses on how changes to the gut microbiota by iron adversely affect development, and to determine whether the form of iron influences microbiota outcomes, we characterized gut microbiome and metabolome changes in Sprague-Dawley rat pups given oral supplements of ferrous sulfate (FS), ferrous bis-glycinate chelate (FC), or vehicle control (CON) on postnatal day (PD) 2−14. Iron supplementation reduced microbiome alpha-diversity (p < 0.0001) and altered short-chain fatty acids (SCFAs) and trimethylamine (TMA) in a form-dependent manner. To investigate the long-term effects of iron provision in early life, an additional cohort was supplemented with FS, FC, or CON until PD 21 and then weaned onto standard chow. At ~8 weeks of age, young adult (YA) rats that received FS exhibited more diverse microbiomes compared to CON (p < 0.05), whereas FC microbiomes were less diverse (p < 0.05). Iron provision resulted in 10,000-fold reduced abundance of Lactobacilli in pre-weanling and YA animals provided iron in early life (p < 0.0001). Our results suggest that in pre-weanling rats, supplemental iron form can generate differential effects on the gut microbiota and microbial metabolism that persist into adulthood.
The microbiome could trigger inflammation leading to epigenetic changes and is involved in the pathophysiology of eye diseases; however, its effect on uveitic glaucoma (UG) has not been fully investigated. This study analysed the differences in eyelid and buccal microbiomes in patients with UG using next-generation sequencing.
The eyelid and buccal specimens of 34 UG and 25 control patients were collected. The taxonomic composition of the microbiome was obtained via 16S ribosomal DNA sequencing. Diversity and differential gene expression analyses (DEG) determined taxon differences between the microbiomes of UG and control groups.
In both the eyelid and buccal microbiomes, alpha-diversity was lower in UG patients than controls, while beta-diversity in patients with UG was higher than in controls. DEG analysis of the eyelid microbiome revealed various taxa differences, including enrichment of Paenibacillus and Dermacoccus (p-value, 1.31e-6 and 1.55e-7, respectively) and depletion of Morganella and Lactococcus (p-value, 6.26e-12 and 2.55e-6, respectively) in patients with UG. In the buccal microbiome, taxa such as Lactococcus was significantly depleted (p-value, 1.31e-17), whereas Faecalibacterium was enriched in patients with UG (p-value, 6.12e-8).
The eyelid and buccal microbiomes in patients with UG differ from controls, which raises concerns surrounding environmental influences on the pathogenesis of UG. The reduced Lactococcus in the eyelid and buccal area suggest that microbiota dysbiosis is associated with UG.
Patients with severe pneumonia admitted to the intensive care unit (ICU) have a high risk of mortality, and the microbiome is likely to affect the outcome of such patients. However, the composition of the skin microbiota of ICU patients with severe pneumonia remains unclear. In this study, on the basis of 16S ribosomal ribonucleic acid sequencing, we explored the difference in skin bacterial richness and diversity between the ICU patient group (PG) with severe pneumonia and the healthy control group (CG).
The diversity index and taxonomic distribution of skin bacteria were analyzed using the Quantitative Insights Into Microbial Ecology (QIIME) bioinformatics pipeline. Blood, endotracheal aspirate, and bronchoalveolar lavage fluid samples were collected from the same PG subjects for culture.
Compared with the CG, the diversity of skin bacteria in the PG decreased significantly. Staphylococcus, Acinetobacter, Stenotrophomonas, Enterococcus, Halomonas, and Brevibacillus were differentially abundant in the PG, and most of these bacteria were also identified in the cultures of upper respiratory tract samples of the same PG.
We provide evidence that healthcare-associated infection in ICU patients with severe pneumonia is strongly associated with skin microbiota, which necessitates the prevention and control of skin bacterial pathogens for these patients.
This study examined how delivery mode shapes the early gut microbiota of newborns using high-resolution shotgun sequencing. Researchers tracked the composition and dynamics of the neonatal gut microbiome over the first month of life. The design specifically compared elective cesarean section against vaginal delivery to sidestep the confounding effect of emergency cesareans, which can muddy conclusions about delivery mode's true influence.
The cohort consisted of Tunisian newborns, with stool samples collected from 5 infants born by elective cesarean section and 5 born vaginally. Samples were taken longitudinally at Day 0, Day 15, and Day 30 after birth. This is a small, delivery-mode-stratified newborn cohort rather than a large population sample.
Bacterial richness and diversity were similar between the elective cesarean and vaginally delivered groups, and both showed a shift in microbiota community composition during the first two weeks regardless of delivery mode. Both groups were dominated by Proteobacteria, Actinobacteria, and Firmicutes. However, starting from the second week, cesarean-delivered infants showed an underrepresentation of Bacteroides alongside an enrichment of opportunistic pathogenic species belonging to the ESKAPE group.
The findings suggest that even elective, non-emergency cesarean delivery is associated with a distinct early gut microbiota signature marked by Bacteroides depletion and ESKAPE pathogen enrichment, not merely overall diversity differences. This points to delivery mode as an independent driver of neonatal microbiome composition beyond confounding clinical circumstances. The emergence of opportunistic ESKAPE species by two weeks of age raises questions about potential vulnerability to opportunistic infection in cesarean-born infants that merit further, larger-scale investigation.
This study examined whether changes in the gut microbiome over time are linked to improvement in liver stiffness in people with nonalcoholic steatohepatitis (NASH). Researchers used 16S rRNA gene sequencing to profile gut microbial communities at baseline and again after 24 weeks of study participation. Liver stiffness was measured using magnetic resonance (MR) elastography, and the investigators compared microbial shifts in participants whose liver stiffness measurement (LSM) improved against those whose did not. They also looked at whether microbial changes tracked with secondary outcomes, including reduction in MRI-derived liver fat (MRI-PDFF) and regression of fibrosis on biopsy.
The cohort consisted of 69 adults with biopsy-confirmed NASH and significant fibrosis (stages 2 to 3), enrolled in a multi-center randomized controlled trial evaluating the drug selonsertib alone or combined with simtuzumab. For comparison, fecal samples were also collected from 32 healthy adults. Genus-level multidimensional scaling was used to see whether microbial changes in the NASH participants who improved resembled the composition seen in this healthy comparison group.
The abundance of 36 bacterial taxa shifted differently between participants with and without longitudinal improvement in liver stiffness. Lactobacillus showed a notably large decrease in participants with LSM improvement (log2 fold change of about -4.51, false discovery rate under 0.001), and Enterococcus was also among the taxa with altered abundance. These findings indicate that specific, identifiable shifts in gut bacterial composition accompany improvement in liver stiffness in NASH, rather than liver stiffness changing independently of the microbiome.
By pairing longitudinal microbiome sampling with an objective, imaging-based measure of liver stiffness, this study strengthens the case for a mechanistic link between gut bacteria and NASH fibrosis trajectory. Identifying taxa such as Lactobacillus and Enterococcus as markers of improvement points toward candidate microbial signatures that could eventually help monitor or stratify NASH patients undergoing treatment. Because the design also compared shifts against a healthy reference cohort, the work lays groundwork for testing whether restoring a more typical gut microbial profile could be a therapeutic target in NASH, though this abstract does not itself establish causation.
The microbial population of the intestinal tract and its relationship to specific diseases has been extensively studied during the past decade. However, reports characterizing the bile microbiota are rare. This study aims to investigate the microbiota composition in patients with pancreaticobiliary cancers and benign diseases by 16S rRNA gene amplicon sequencing and to evaluate its potential value as a biomarker for the cancer of the bile duct, pancreas, and gallbladder.
We enrolled patients who were diagnosed with cancer, cystic lesions, and inflammation of the pancreaticobiliary tract. The study cohort comprised 244 patients. We extracted microbiome-derived DNA from the bile juice in surgically resected gallbladders. The microbiome composition was not significantly different according to lesion position and cancer type in terms of alpha and beta diversity. We found a significant difference in the relative abundance of Campylobacter, Citrobacter, Leptotrichia, Enterobacter, Hungatella, Mycolicibacterium, Phyllobacterium and Sphingomonas between patients without and with lymph node metastasis.
There was a significant association between the relative abundance of certain microbes and overall survival prognosis. These microbes showed association with good prognosis in cholangiocarcinoma, but with poor prognosis in pancreatic adenocarcinoma, and vice versa. Our findings suggest that pancreaticobiliary tract cancer patients have an altered microbiome composition, which might be a biomarker for distinguishing malignancy.
This study examined the role of gut microbiota in two autoimmune thyroid conditions, Graves' disease (GD) and Hashimoto's thyroiditis (HT). Researchers used 16S sequencing to characterize fecal bacterial communities and chemiluminescence to measure thyroid function and autoantibodies (FT3, FT4, TSH, TRAb, TGAb, and TPOAb). Thyroid ultrasound was also used, and functional prediction of the microbiota was carried out using KEGG and COG analyses to explore possible mechanisms linking gut bacteria to disease.
Seventy fecal samples were collected in total. These included 27 patients with Graves' disease, 27 patients with Hashimoto's thyroiditis, and 16 samples from healthy volunteers who served as controls.
The overall structure of the gut microbiota in both the GD and HT groups differed significantly from that of the healthy control group. Proteobacteria and Actinobacteria were most abundant in the HT group, while both the GD and HT groups showed higher levels of Erysipelotrichia, Cyanobacteria, and Ruminococcus_2 and lower levels of Bacillaceae and Megamonas compared to controls. Functional analysis linked the ABC transporter pathway strongly to GD and HT, and COG analysis showed enrichment in carbohydrate transport and metabolism, but not amino acid transport and metabolism, in both patient groups.
The findings suggest that gut microbiota alterations, particularly shifts in carbohydrate transport and metabolism pathways, may be mechanistically involved in the development of Graves' disease and Hashimoto's thyroiditis. This supports a role for the gut microbiome in autoimmune thyroid disease pathogenesis and points to specific bacterial taxa and metabolic pathways as potential targets for further mechanistic study. Because the abstract does not specify additional cohort details or long-term outcomes, further research is needed to confirm causality and clinical relevance.
The tsetse flies, biological vectors of African trypanosomes, harbour a variety of bacteria involved in their vector competence that may help in developing novel vector control tools. This study provides an inventory of tsetse bacterial communities in Cameroon and explores their possible associations with trypanosome establishment in Glossina palpalis palpalis. High throughput sequencing of the V3-V4 hypervariable region of the bacterial 16S rRNA gene, with subsequent metagenomic, multivariate, and association analyses, were used to investigate the levels and patterns of microbial diversity in four tsetse species. Overall, 31 bacterial genera and four phyla were identified. The primary symbiont Wigglesworthia dominated almost all the samples, with an overall relative abundance of 47.29%, and seemed to be replaced by Serratia or Burkholderia in some G. tachinoides flies. Globally, significant differences were observed in the microbiome diversity and composition among tsetse species and between teneral and non-teneral flies, or between flies displaying or not displaying mature trypanosome infections. In addition, differential abundance testing showed some OTUs, or some bacteria taxa, associated with trypanosome maturation in tsetse flies. These bacteria could be further investigated for an understanding of their mechanism of action and alternatively, transformed and used to block trypanosome development in tsetse flies.
This study investigated the connection between the oral and gut microbiome in Parkinson's disease (PD) using shotgun metagenomic sequencing. Researchers examined both the taxonomic composition and the functional gene content of these microbial communities. The aim was to determine whether oral microbiome changes relate to gut microbiome changes in PD, and whether these shifts produce functional alterations rather than just compositional differences.
The abstract does not report specific sample sizes, ages, or recruitment details. The study compared PD patients to healthy controls, using paired oral and gut microbiome samples analyzed by shotgun metagenomic sequencing. Beyond the PD-versus-control design, no further cohort characteristics are given in the abstract.
The taxonomic composition of both the oral and gut microbiome differed significantly between PD patients and healthy controls (P = 0.003 and 0.001, respectively). Oral Lactobacillus was more abundant in PD patients and was associated with opportunistic pathogens in the gut (FDR-adjusted P < 0.038). Functionally, microbial gene markers for glutamate and arginine biosynthesis were downregulated, while antimicrobial resistance gene markers were upregulated in PD patients compared to healthy controls (all P < 0.001).
The findings suggest a connection between the oral and gut microbiota in PD that may drive functional, not just compositional, alterations of the microbiome. The rise in oral Lactobacillus alongside opportunistic gut pathogens points to the oral cavity as a potential contributor to gut dysbiosis in PD. Reduced glutamate and arginine biosynthesis and increased antimicrobial resistance gene markers highlight functional microbial pathways that may warrant further investigation as they relate to PD pathophysiology.
Cesarean section scar diverticulum (CSD) has become a formidable obstacle preventing women receiving CS from reproducing. However, the pathogenesis of CSD remains unexplored. In this study, we characterized the cervical microbiota, metabolome, and endometrial transcriptome of women with CSD. Based on the 16s rRNA results of cervical microbes, the microbial diversity in the CSD group was higher than that in the control group. Lactobacillus were significantly decreased in the CSD group and were mutually exclusive with potentially harmful species (Sphingomonas, Sediminbacterium, and Ralstonia) abnormally elevated in CSD. The microbiota in the CSD group exhibited low activity in carbohydrate metabolism and high activity in fatty acid metabolism, as confirmed by the metabolomic data. The metabolomic characterization identified 6,130 metabolites, of which 34 were significantly different between the two groups. In the CSD group, N-(3-hydroxy-eicosanoid)-homoserine lactone and Ternatin were significantly increased, in addition to the marked decrease in fatty acids due to high consumption. N-(3-hydroxy-eicosanoyl)-homoserine lactone is a regulator that promotes abnormal apoptosis in a variety of cells, including epithelial cells and vascular endothelial cells. This abnormal apoptosis of endometrial epithelial cells and neovascularization was also reflected in the transcriptome of the endometrium surrounding the CSD. In the endometrial transcriptome data, the upregulated genes in the CSD group were active in negatively regulating the proliferation of blood vessel endothelial cells, endothelial cells, and epithelial cells. This alteration in the host's endometrium is most likely influenced by the abnormal microbiota, which appears to be confirmed in the results by integrating host transcriptome and microbiome data. For the first time, this study described the abnormal activity characteristics of microbiota and the mechanism of host-microbiota interaction in CSD. IMPORTANCE Cesarean section scar diverticulum (CSD) has become a formidable obstacle preventing women receiving CS from reproducing. In this study, we revealed that potentially harmful microbes do have adverse effects on the host endometrium. The mechanism of these adverse effects includes the inhibition of the activity of beneficial bacteria such as lactobacilli, consumption of protective metabolites of the endometrium, and also the production of harmful metabolites. In the present study, we elucidated the mechanism from the perspectives of microbial, metabolic, and host responses, providing an important rationale to design preventive and therapeutic strategies for CSD.
To compare the ocular surface and meibum microbial communities of humans with Demodex Blepharitis (DB) and healthy controls.
Conjunctival sac and meibum samples from 25 DB patients and 11 healthy controls were analyzed using metagenomic next-generation sequencing (mNGS).
The alpha-diversity of the conjunctival sac microbiome of the DB group (observed, Chao1, ACE) was lower than that of the control group, whereas all meibum diversity indicators were similar. In conjunctival samples, the relative abundance (RA) of the phylum Proteobacteria was significantly higher (p=0.023), and the RA of both phyla Actinobacteria and Firmicutes was significantly lower (p=0.002, 0.025, respectively) in the DB group than that in the control group. In meibum samples, the RA of the phyla Proteobacteria and Actinobacteria were similar, whereas that of the phylum Firmicutes was significantly lower in the DB group (p=0.019) than that in the control group. Linear discriminant analysis with effect size measurement of the conjunctival and meibum microbiomes showed that Sphingobium sp. YG1 and Acinetobacter guillouiae were enriched in the DB group. Sphingobium sp. YG1, Acinetobacter guillouiae and Pseudomonas putida in the DB group were related to more severe ocular surface clinical parameters. Discriminative genera's principal coordinate analysis separated all control and DB microbiomes into two distinct clusters.
Proteobacteria's increased prevalence may indicate ocular microbial community instability. The species Sphingobium sp. YG1 and Acinetobacter guillouiae are potentially pathogenic bacterial biomarkers in DB. Demodex infection mainly affects the ocular surface microbiome rather than penetrating deeper into the meibomian gland.
Evidence supports an association between cholestatic liver disease and changes in microbiome composition. Nevertheless, the identification of this special type of biliary atresia from non-biliary atresia cholestasis is still a major clinical difficulty. The purpose of this study is to compare the differences in the composition of gut microbiome between infants with biliary atresia and infant with non-biliary atrestic cholestasis, to find new ways to identify and diagnose these two diseases early, to understand the influence of the presence or absence of bile on the composition of the gut microbiome in infants with cholestasis.
Using 16S rDNA gene sequencing technology to analyze the intestinal flora of the participants.
In terms of diversity, there is an obvious structural separation in the intestinal microbiota of the BA group and the CD group, and this structural separation also exists in the comparison between the two groups before surgery. Taxonomic analysis demonstrated that the two groups showed an increase in Proteobacteria and Firmicutes before surgery, and the relative abundance of potential pathogens such as Shigella, Streptococcus, Klebsiella, etc. increased, potential probiotics such as Bifidobacteria and Lactobacillus decreased, but the relative abundance of each genus was different between groups. It was found that Enterococcus, Ralstonia, Nitriliruptoraceae, etc. were differentially enriched in the BA group, the CD group are mainly enriched in Veillonella, Clostridium_sensu_stricto_1 and Lactobacillus. Functional analysis of the groups showed that the BA group mainly focused on the processes of energy release processes, and the CD group mainly focused on the biosynthesis of amino-acids to consume energy.
The composition of intestinal flora is different between biliary atresia and non-biliary atretic cholestasis. Enterococcus, Ralstonia, etc. may become biomarkers for the identification and diagnosis of both.
HIV-exposed uninfected infants (HEU) have abnormal immunologic functions and increased infectious morbidity in the first 6 months of life, which gradually decreases thereafter. The mechanisms underlying HEU immune dysfunctions are unknown. We hypothesized that unique characteristics of the HEU gut microbiota associated with maternal HIV status may underlie the HEU immunologic dysfunctions. We characterized the infant gut, maternal gut, and breast milk microbiomes of mother-infant pairs, including 123 with HEU and 117 with HIV-uninfected infants (HUU), from South Africa. Pan-bacterial 16S rRNA gene sequencing was performed on (i) infant stool at 6, 28, and 62 weeks; (ii) maternal stool at delivery and 62 weeks; and (iii) breast milk at 6 weeks. Infant gut alpha and beta diversities were similar between groups. Microbial composition significantly differed, including 12 genera, 5 families and 1 phylum at 6 weeks; 12 genera and 2 families at 28 weeks; and 2 genera and 2 families at 62 weeks of life. Maternal gut microbiomes significantly differed in beta diversity and microbial composition, and breast milk microbiomes differed in microbial composition only. Infant gut microbiotas extensively overlapped with maternal gut and minimally with breast milk microbiotas. Nevertheless, exclusively breastfed HEU and HUU had less divergent microbiomes than nonexclusively breastfed infants. Feeding pattern and maternal gut microbiome imprint the HEU gut microbiome. Compared to HUU, the HEU gut microbiome prominently differs in early infancy, including increased abundance of taxa previously observed to be present in excess in adults with HIV. The HEU and HUU gut microbiome compositions converge over time, mirroring the kinetics of HEU infectious morbidity risk. IMPORTANCE HIV-exposed uninfected infants (HEU) are highly vulnerable to infections in the first 6 months of life, and this vulnerability decreases to the age of 24 months. Because the microbiome plays a critical role in the education of the infant immune system, which protects them against infections, we characterized the gut microbiomes of HEU and HIV-unexposed infants (HUU) in the first year of life. The HEU and HUU gut microbiomes showed prominent differences at 6 and 28 weeks of life but converged at 62 weeks of life, mirroring the time course of the HEU excess infectious morbidity and suggesting a potential association between the infant gut microbiome structure and susceptibility to infections. Infant gut microbiotas extensively overlapped with maternal gut and minimally with breast milk microbiotas. Moreover, exclusively breastfed HEU and HUU had less divergent microbiomes at 6 and 28 weeks than nonexclusively breastfed HEU and HUU. The factors that affect the HEU gut microbiome, maternal gut microbiome and exclusive breastfeeding, may be targeted by interventions.
This study examined the early-life gut microbiota of term small for gestational age (SGA) infants compared with appropriate for gestational age (AGA) infants. Fecal samples were collected on days 1, 3, 5, and 7 of life and analyzed using 16S ribosomal DNA amplicon sequencing. The researchers then followed the SGA infants for 6 months to assess whether early gut microbiota characteristics related to neurodevelopmental outcomes. The work was motivated by prior evidence that gut microbiota in early life can influence later neurodevelopment, a relationship that had been little studied in SGA populations specifically.
A total of 162 term neonates born at Peking University First Hospital between June 2020 and June 2021 were enrolled. Of these, 41 infants (25.3%) were classified as SGA and made up the study group, while 121 infants (74.7%) were classified as AGA and served as the control group. Neurodevelopmental outcomes at 6 months were assessed among the SGA infants using the Ages and Stages Questionnaires-3 (ASQ-3).
Gut microbial diversity was consistently lower in the SGA group than in the AGA group on days 1, 3, 5, and 7 after birth. Non-metric multidimensional scaling and analysis of similarities showed significant differences in the overall composition of the gut microbiota between the two groups. These findings indicate that being born small for gestational age is associated with a distinct and less diverse early gut microbial community from the first days of life.
The findings support the idea that SGA status shapes the gut microbiota from the earliest days of life, in a pattern distinguishable from AGA infants. Because the study also tracked neurodevelopment at 6 months using the ASQ-3, it points toward the gut microbiota as a possible early biological marker linked to the neurodevelopmental risks already known to affect SGA infants. This underscores the value of monitoring gut microbiota composition in SGA newborns as a potential avenue for identifying infants who may benefit from closer developmental follow-up.
Gestation is linked to changes in gut microbiota composition and function. Since gestational diabetes mellitus (GDM) can develop at any time of the pregnancy, we stratified the women into four groups according to the time and test used for the diagnosis. We focused on the gut microbiota pattern in early pregnancy to detect changes which could be linked to later GDM development.
We collected stool samples from 104 pregnant women including obese individuals (first trimester body mass index median was 26.73). We divided the women into four groups according to routine screening of fasting plasma glucose (FPG) levels and oral glucose tolerance test (oGTT) in the first and third trimesters, respectively. We processed the stool samples for bacterial 16S rRNA and fungal ITS1 genes sequencing by Illumina MiSeq approach and correlated the gut microbiota composition with plasma short-chain fatty acid levels (SCFA).
We found that gut bacterial microbiota in the first trimester significantly differs among groups with different GDM onset based on unweighted UniFrac distances (p=0.003). Normoglycemic women had gut microbiota associated with higher abundance of family Prevotellaceae, and order Fusobacteriales, and genus Sutterella. Women diagnosed later during pregnancy either by FGP levels or by oGTT had higher abundances of genera Enterococcus, or Erysipelotrichaceae UCG-003, respectively. We observed significant enrichment of fungal genus Mucor in healthy pregnant women whereas Candida was more abundant in the group of pregnant women with impaired oGTT. Using correlation analysis, we found that Holdemanella negatively correlated with Blautia and Candida abundances and that Escherichia/Shigella abundance positively correlated and Subdoligranulum negatively correlated with plasma lipid levels. Coprococcus, Akkermansia, Methanobrevibacter, Phascolarctobacterium and Alistipes positively correlated with acetate, valerate, 2-hydroxybutyrate and 2-methylbutyrate levels, respectively, in women with GDM.
We conclude that there are significant differences in the gut microbiota composition between pregnant women with and without GDM already at the early stage of pregnancy in our cohort that included also overweight and obese individuals. Specific microbial pattern associated with GDM development during early pregnancy and its correlation to plasma lipid or SCFA levels could help to identify women in higher risk of GDM development.
We aim to evaluate the differences in the microbiome of responders and non-responders, as well as predict the response to probiotic therapy, based on fecal microbiome data in patients with diarrhea-predominant irritable bowel syndrome (IBS-D).
A multi-strain probiotics that contains Lactobacillus acidophilus (KCTC 11906BP), Lactobacillus plantarum (KCTC11867BP), Lactobacillus rhamnosus (KCTC 11868BP), Bifidobacterium breve (KCTC 11858BP), Bifidobacterium lactis (KCTC 11903BP), Bifidobacterium longum (KCTC 11860BP), and Streptococcus thermophilus (KCTC 11870BP) were used. Patients were categorized into probiotic and placebo groups, and fecal samples were collected from all patients before and at the end of 8 weeks of treatment. The probiotic group was further divided into responders and non-responders. Responders were defined as patients who experienced adequate relief of overall irritable bowel syndrome symptoms after probiotic therapy. Fecal microbiota were investigated using Illumina MiSeq and analyzed using the EzBioCloud 16S database and microbiome pipeline (https://www.EZbiocloud.net).
There was no significant difference in the alpha and beta diversity between the responder and non-responder groups. The abundances of the phylum Proteobacteria and genus Bacteroides significantly decreased after probiotic treatment. Bifidobacterium bifidum, Pediococcus acidilactici, and Enterococcus faecium showed a significantly higher abundance in the probiotic group after treatment compared to the placebo group. Enterococcus faecalis and Lactococcus lactis were identified as biomarkers of non-response to probiotics. The abundance of Fusicatenibacter saccharivorans significantly increased in the responders after treatment.
Probiotic treatment changes some composition of fecal bacteria in patients with IBS-D. E. faecalis and L. lactis may be prediction biomarkers for non-response to probiotics. Increased abundance of F. sccharivorans is correlated to symptom improvement by probiotics in patients with IBS-D.
The gut microbiome plays an important role in autoimmunity including multiple sclerosis and its mouse model called experimental autoimmune encephalomyelitis (EAE). Prior studies have demonstrated that the multiple sclerosis gut microbiota can contribute to disease, hence making it a potential therapeutic target. In addition, antibiotic treatment has been shown to ameliorate disease in the EAE mouse model of multiple sclerosis. Yet, to this date, the mechanisms mediating these antibiotic effects are not understood. Furthermore, there is no consensus on the gut-derived bacterial strains that drive neuroinflammation in multiple sclerosis.
Here, we characterized the gut microbiome of untreated and vancomycin-treated EAE mice over time to identify bacteria with neuroimmunomodulatory potential. We observed alterations in the gut microbiota composition following EAE induction. We found that vancomycin treatment ameliorates EAE, and that this protective effect is mediated via the microbiota. Notably, we observed increased abundance of bacteria known to be strong inducers of regulatory T cells, including members of Clostridium clusters XIVa and XVIII in vancomycin-treated mice during the presymptomatic phase of EAE, as well as at disease peak. We identified 50 bacterial taxa that correlate with EAE severity. Interestingly, several of these taxa exist in the human gut, and some of them have been implicated in multiple sclerosis including Anaerotruncus colihominis, a butyrate producer, which had a positive correlation with disease severity. We found that Anaerotruncus colihominis ameliorates EAE, and this is associated with induction of RORγt+ regulatory T cells in the mesenteric lymph nodes.
We identified vancomycin as a potent modulator of the gut-brain axis by promoting the proliferation of bacterial species that induce regulatory T cells. In addition, our findings reveal 50 gut commensals as regulator of the gut-brain axis that can be used to further characterize pathogenic and beneficial host-microbiota interactions in multiple sclerosis patients. Our findings suggest that elevated Anaerotruncus colihominis in multiple sclerosis patients may represent a protective mechanism associated with recovery from the disease. Video Abstract.
This study investigated specific alterations in the gut microbiome and serum metabolome in polycystic ovary syndrome (PCOS) and how the two systems interact. Researchers used shotgun metagenomic sequencing on stool samples and ultrahigh performance liquid chromatography quadrupole time-of-flight mass spectrometry on serum to profile microbial and metabolite changes. They then built an integrative network combining the metagenomics and metabolomics datasets to map possible interactions between gut bacteria and circulating metabolites. This network-derived hypothesis was further tested using fecal microbiota transplantation (FMT) in a rat trial.
The human portion of the study involved stool and serum samples from 32 patients with PCOS and 18 healthy controls. The abstract does not provide further demographic details such as age range or geographic location. The mechanistic findings were additionally tested in a rat model via fecal microbiota transplantation, not in additional human subjects.
Fecal metagenomics identified 64 microbial strains that differed significantly between PCOS patients and healthy controls, with about half of these enriched in the PCOS group. These altered species were associated with disruption of host metabolic homeostasis, including insulin resistance and fatty acid metabolism, and with heightened inflammatory signaling such as the PI3K/Akt/mTOR pathway. The bacteria appeared linked to these effects partly through expression of sterol regulatory element-binding transcription factor-1, serine/threonine-protein kinase mTOR, and 3-oxoacyl-[acyl-carrier-protein] synthase III. The abstract does not mention Faecalibacterium prausnitzii, butyrate, or other anti-inflammatory commensals specifically.
The findings suggest that specific gut microbial strains may causally contribute to the metabolic and inflammatory disturbances seen in PCOS, rather than merely correlating with the condition. The use of an integrative metagenome-metabolome network, validated through fecal microbiota transplantation in rats, strengthens the case for a functional gut microbiome to host metabolism link. This points to the gut microbiome and its metabolic outputs as potential targets for future diagnostic or therapeutic strategies in PCOS. Further human studies would be needed to confirm causality and clinical relevance.
Numerous studies have reported dysbiosis in the naso- and/or oro-pharyngeal microbiota of COVID-19 patients compared with healthy individuals; however, only a few small-scale studies have also included a disease control group. In this study, we characterized and compared the bacterial communities of pooled nasopharyngeal and throat swabs from hospitalized COVID-19 patients (n = 76), hospitalized non-COVID-19 patients with respiratory symptoms or related illnesses (n = 69), and local community controls (n = 76) using 16S rRNA gene V3-V4 amplicon sequencing. None of the subjects received antimicrobial therapy within 2 weeks prior to sample collection. Both COVID-19 and non-COVID-19 hospitalized patients differed in the composition, alpha and beta diversity, and metabolic potential of the naso-oropharyngeal microbiota compared with local controls. However, the microbial communities in the two hospitalized patient groups did not differ significantly from each other. Differential abundance analysis revealed the enrichment of nine bacterial genera in the COVID-19 patients compared with local controls; however, six of them were also enriched in the non-COVID-19 patients. Bacterial genera uniquely enriched in the COVID-19 patients included Alloprevotella and Solobacterium. In contrast, Mogibacterium and Lactococcus were dramatically decreased in COVID-19 patients only. Association analysis revealed that Alloprevotella in COVID-19 patients was positively correlated with the level of the inflammation biomarker C-reactive protein. Our findings reveal a limited impact of SARS-CoV-2 on the naso-oropharyngeal microbiota in hospitalized patients and suggest that Alloprevotella and Solobacterium are more specific biomarkers for COVID-19 detection. IMPORTANCE Our results showed that while both COVID-19 and non-COVID-19 hospitalized patients differed in the composition, alpha and beta diversity, and metabolic potential of the naso-oropharyngeal microbiota compared with local controls, the microbial communities in the two hospitalized patient groups did not differ significantly from each other, indicating a limited impact of SARS-CoV-2 on the naso-oropharyngeal microbiota in hospitalized patients. Besides, we identified Alloprevotella and Solobacterium as bacterial genera uniquely enriched in COVID-19 patients, which may serve as more specific biomarkers for COVID-19 detection.
This study examined the gut microbiome in Parkinson's disease (PD) using large-scale, high-resolution shotgun metagenomic sequencing of fecal DNA. The researchers applied uniform, standardized methods throughout, followed by metagenome-wide association studies requiring agreement between two independent statistical methods (ANCOM-BC and MaAsLin2) before declaring a disease association. They also conducted network analysis to identify clusters of co-occurring microbial species and functional profiling to characterize microbial genes and pathways.
The study enrolled 490 individuals with Parkinson's disease and 234 control individuals. Fecal samples from this cohort underwent deep shotgun sequencing to generate the metagenomic data analyzed in the study. The abstract does not provide further demographic detail on the participants.
Over 30 percent of the species, genes, and pathways tested showed altered abundances in Parkinson's disease, indicating widespread dysbiosis. PD-associated species organized into polymicrobial clusters that grew, shrank, or competed together rather than acting independently. The PD microbiome was disease permissive: it showed overabundance of pathogens and immunogenic components, dysregulated neuroactive signaling, an excess of molecules that induce alpha-synuclein pathology, and overproduction of toxicants, alongside a reduction in anti-inflammatory and neuroprotective factors that would otherwise support recovery.
By validating in human PD patients findings previously seen only in experimental models, this study strengthens the case that the gut microbiome contributes to multiple disease mechanisms in Parkinson's disease. The reconciliation of prior human PD microbiome literature helps resolve inconsistencies across earlier studies and establishes a more standardized foundation for future research. The reduction in anti-inflammatory and neuroprotective microbial factors points to a loss of protective capacity that may limit the body's ability to counteract disease processes, suggesting the microbiome as a potential target for future mechanistic and therapeutic investigation.
Increasing evidence connects the gut microbiome to Parkinson's disease (PD) etiology, but little is known about microbial contributions to PD progression and its clinical features. We aim to explore the association between the gut microbiome with PD, and the microbial association with PD-specific clinical features.
In a community-based case-control study of 96 PD patients and 74 controls, microbiome data were obtained from 16S rRNA gene sequencing of fecal samples, and analyzed for microbial diversity, taxa abundance, and predicted functional pathways that differed in PD patients and controls, and their association with PD-specific features (disease duration, motor subtypes, L-DOPA daily dose, and motor function).
PD patients' gut microbiome showed lower species diversity (p = 0.04) and were compositionally different (p = 0.002) compared to controls but had a higher abundance of three phyla (Proteobacteria, Verrucomicrobiota, Actinobacteria) and five genera (Akkermansia, Enterococcus, Hungatella, and two Ruminococcaceae) controlling for sex, race, age, and sequencing platform. Also, 35 Metacyc pathways were predicted to be differentially expressed in PD patients including biosynthesis, compound degradation/utilization/assimilation, generation of metabolites and energy, and glycan pathways. Additionally, the postural instability gait dysfunction subtype was associated with three phyla and the NAD biosynthesis pathway. PD duration was associated with the Synergistota phylum, six genera, and the aromatic compound degradation pathways. Two genera were associated with motor function.
PD patients differed from controls in gut microbiome composition and its predicted metagenome. Clinical features were also associated with bacterial taxa and altered metabolic pathways of interest for PD progression.
Understanding the violence behaviors in schizophrenia patients has always been the focus of forensic psychiatry. Although many studies show gut microbiota could regulate behavior, to our knowledge, no studies have profiled the gut microbiota structure in schizophrenia patients with violence. We profiled the characteristics of gut microbiota structure in 26 schizophrenia patients with violence (V.SCZ) by comparing with that of 16 schizophrenia patients without violence (NV.SCZ) under the control of confounders, and found the differences of gut microbiota structure between the two groups. Violence was assessed by the MacArthur Community Violence Instrument. Psychiatric symptoms were assessed by the Positive and Negative Syndrome Scale. The 16S rRNA gene sequencing was used to identify and relatively quantify gut microbial composition. Bioinformatics analysis was used to find differential gut microbial composition between the V.SCZ and NV.SCZ groups. Fifty-nine differential microbial taxonomic compositions were found between the two groups. Fifteen gut microbial compositions were the key microbial taxonomic compositions responsible for the differences between the V.SCZ and NV.SCZ groups, including five enriched microbial taxonomic compositions (p_Bacteroidetes, c_Bacteroidia, o_Bacteroidales, f_Prevotellaceae, s_Bacteroides_uniformis), and ten impoverished microbial taxonomic compositions (p_Actinobacteria, c_unidentified_Actinobacteria, o_Bifidobacteriales, f_ Enterococcaceae, f_Veillonellaceae, f_Bifidobacteriaceae, g_Enterococcus, g_Candidatus_Saccharimonas, g_Bifidobacterium, and s_Bifidobacterium_pseudocatenulatum). This study profiled the differences of gut microbiota between schizophrenia patients with violence and without violence. These results could enrich the etiological understanding of violence in schizophrenia and might be helpful to violence management in the future.
This study examined the effect of antiparkinsonian medication, specifically levodopa (LD) and levodopa-carbidopa intestinal gel (LCIG), on the gut microbiota and fecal metabolome in Parkinson disease (PD). Fecal DNA was analyzed using next-generation sequencing of the V3 and V4 regions of the 16S rRNA gene. Fecal metabolic extracts were also evaluated using gas chromatography mass spectrometry to characterize metabolome differences across treatment groups.
The study included 107 patients with a clinical diagnosis of Parkinson disease. Patients were divided into three groups: an LCIG group (n = 38) receiving levodopa-carbidopa intrajejunal gel, an LD group (n = 46) receiving oral levodopa, and a Naive group (n = 23) not taking any antiparkinsonian medications. This design allowed comparison of gut microbiota composition across different treatment exposures within a PD population.
Multivariate analysis showed that the LCIG group had a significantly higher abundance of Enterobacteriaceae, Escherichia, and Serratia compared to the LD group. Compared to the Naive group, the LD group showed a reduction of Blautia and Lachnospirae. The LCIG group additionally showed an increase in Proteobacteria and Enterobacteriaceae alongside a reduction in Firmicutes, Lachnospiraceae, and Blautia relative to the Naive group.
The findings suggest that the route and form of levodopa therapy, oral versus intrajejunal gel, are associated with distinct gut microbiota profiles in Parkinson disease. The reduction of Blautia and Lachnospiraceae, taxa associated with short-chain fatty acid production, alongside enrichment of Enterobacteriaceae in LCIG-treated patients points to a treatment-related shift toward a less favorable microbial composition. These distinctive features may warrant further investigation into how PD medication choice shapes gut microbial and metabolic health over the course of treatment.
This study examined whether gut bacterial microbiome dysbiosis, already reported in type 2 diabetes mellitus (T2DM), also links to diabetic retinopathy (DR). Fecal samples were analyzed using 16S rRNA gene sequencing, with community composition assessed using QIIME and R software. The researchers compared gut bacterial diversity and abundance at the phyla and genera level across groups.
The study compared healthy controls (HC) with people who had T2DM without DR and people who had T2DM with DR. Exact sample sizes are not given in the abstract, but the design involved three human fecal-sample groups defined by diabetes and retinopathy status. This is described as the first report of its kind comparing gut microbiome dysbiosis specifically in people with DR against healthy controls.
Gut microbiome dysbiosis at the phyla and genera level was observed in both T2DM and T2DM-with-DR groups compared to healthy controls. People with DR showed greater discrimination from healthy controls than people with T2DM alone, and the microbiomes of the T2DM and DR groups were also significantly different from each other. Both diabetes and DR were associated with a decrease in anti-inflammatory, probiotic, and other beneficial bacteria relative to healthy controls, alongside an increase in potentially pathogenic bacteria, with this shift being more pronounced in people with DR.
This is the first report demonstrating gut microbiome dysbiosis specifically associated with diabetic retinopathy, distinct from T2DM alone. The findings suggest the gut microbiome could serve as a marker to distinguish DR from T2DM without retinal complications. The authors note this work could help inform the development of novel, targeted therapies aimed at improving treatment of diabetic retinopathy.
This study examined the gut microbiota of patients with COVID-19 pneumonia using 16S rRNA gene sequencing performed on rectal swabs. Researchers compared microbial composition and diversity between patients treated in the intensive care unit (i-COVID19), patients treated in infectious disease wards (w-COVID19), and healthy controls (CTRL). The goal was to characterize how gut microbial communities differ across varying levels of COVID-19 disease severity.
The study population consisted of patients hospitalized with COVID-19 pneumonia, divided into two groups by care setting: those admitted to the intensive care unit and those managed in infectious disease wards. These two patient groups were compared against a control group without COVID-19. The abstract does not report exact sample sizes, ages, or other demographic details for these cohorts.
Patients in the ICU showed a decrease in the Chao1 index compared to both controls and ward patients, indicating lower microbial richness in the most severely ill patients, while the Shannon index showed no significant change. At the phylum level, ward patients showed an increase in Proteobacteria compared to controls. Fusobacteria and Spirochetes were both decreased relative to controls, with Spirochetes showing the greatest decrease in ICU patients specifically.
The findings indicate that gut microbial communities shift in composition and richness according to COVID-19 disease severity, with the most pronounced changes occurring in critically ill ICU patients. These preliminary results suggest the gut microbiota may hold promising biomarkers for diagnosing COVID-19 and gauging disease severity. The authors note that validation in larger cohorts could support using microbiota profiles to help stratify patients by severity.
This study examined whether the gut microbiome carries a detectable signature of prediabetes, a stage preceding type 2 diabetes mellitus (T2D). Researchers sequenced the V1-V5 variable regions of the 16S rRNA gene to profile gut microbiota composition. They also measured fasting serum inflammatory biomarkers in the same participants. The goal was to identify robust microbial signatures that could aid early diagnosis and prevention of T2D.
The study analyzed two cohorts, one from India and one from Denmark, combining prediabetic and normoglycemic individuals. In total, 262 prediabetic subjects were compared against 275 normoglycemic subjects. This trans-ethnic design allowed the researchers to correct for a strong country-specific cohort effect and look for microbial patterns shared across both populations.
After correcting for cohort effects, 16 operational taxonomic units (OTUs) were enriched in normoglycemic subjects relative to those with prediabetes, including members of Prevotella9, Phascolarctobacterium, Barnesiella, Flavonifractor, Tyzzerella_4, Bacteroides, Faecalibacterium, and Agathobacter. Faecalibacterium, a genus that includes the anti-inflammatory, butyrate-producing species Faecalibacterium prausnitzii, was among the taxa depleted in prediabetic subjects. Conversely, 144 OTUs were found enriched in the prediabetic subjects, indicating a broader shift in community composition alongside the loss of these beneficial commensals.
The depletion of Faecalibacterium and other short-chain-fatty-acid-associated genera in prediabetes, observed consistently across two ethnically distinct cohorts, supports gut microbiota as a candidate early marker of metabolic disease risk. Because these signatures held after correcting for country-specific effects, they suggest a trans-ethnic microbial pattern rather than a population-specific artifact. This strengthens the rationale for using microbiome profiling in early prediabetes screening and for exploring interventions that restore anti-inflammatory, butyrate-producing commensals before progression to overt T2D.
We previously discovered that gut microbiota can serve as universal microbial biomarkers for diagnosis, disease activity assessment, and predicting the response to infliximab treatment for inflammatory bowel diseases (IBD). Much still remains unknown about the relationship between alterations in gut microbiota and IBD affected bowel region, in particular in the case of ulcerative colitis (UC) and colonic Crohn's disease (cCD) without endoscopic and biopsy data. In the current study gut microbiota from a population in China was found to be distinct from that of the Western world [Human Microbiome Project (HMP) data]. Furthermore, both gut microbiota greatly differed from microbiota of other anatomical locations (oral, skin, airway, and vagina), with higher alpha-diversity (Chinese gut > HMP gut > oral microbiome > airway microbiome > skin microbiome > vaginal microbiome), and marked differences in microbiome composition. In patients with IBD in China, UC was characterized by the presence of Gardnerella, while cCD was characterized by the presence of Fusobacterium. Moreover, gut microbiota, such as Gardnerella and Fusobacterium, may be potential biomarkers for identifying UC from cCD. Together, this study revealed crucial differences in microbial communities across anatomical locations, and demonstrated that there was an important association between IBD affected bowel region and gut microbiota.
Alternations in gut microbiota and a number of genes have been implicated as risk factors for the development of Alzheimer disease (AD). However, the interactions between the altered bacteria and risk genetic variants remain unclear. We aimed to explore associations of the risk genetic variants with altered gut bacteria in the onset of AD.
We collected baseline data and stool and blood samples from 30 AD patients and 47 healthy controls in a case-control study. The rs42358/rs4512 (ApoE), rs3851179 (PICALM), rs744373 (BIN1), rs9331888 (CLU), rs670139 (MS4A4E), rs3764650 (ABCA7), rs3865444 (CD33), rs9349407 (CD2AP), rs11771145 (EPHA1), and rs3818361/rs6656401 (CR1) were sequenced, and microbiota composition was characterized using 16S rRNA gene sequencing. The associations of the altered gut bacteria with the risk genetics were analyzed.
Apolipoprotein ε4 allele and rs744373 were risk loci for the AD among 12 genetic variants. Phylum Proteobacteria; orders Enterobacteriales, Deltaproteobacteria, and Desulfovibrionales; families Enterobacteriaceae and Desulfovibrionaceae; and genera Escherichia-Shigella, Ruminococcaceae_UCG_002, Shuttleworthia, Anaerofustis, Morganelia, Finegoldia, and Anaerotruncus were increased in AD subjects, whereas family Enterococcaceae and genera Megamonas, Enterococcus, and Anaerostipes were more abundant in controls (P < 0.05). Among the altered microbiota, APOE ε4 allele was positively associated with pathogens: Proteobacteria.
The interaction of APOE ε4 gene and the AD-promoting pathogens might be an important factor requiring for the promotion of AD. Targeting to microbiota might be an effective therapeutic strategy for AD susceptible to APOE ε4 allele. This needs further investigation.
Limited studies have reported the relationship between intestinal flora dysbiosis and clinical characteristics in polycystic ovary syndrome (PCOS). However, the structure and characteristics of gut microbiota in PCOS have not been fully elucidated. To analyze the composition of the Intestinal flora population in normal-weight women with PCOS and insulin resistance(IR) compared to PCOS alone and healthy women.
A total of 14 PCOS patients with insulin resistant(PCOS-IR) and 12 PCOS alone (PCOS-NIR), and 10 age- and body mass index-matched healthy control women (HC).
No significant difference in diversity was observed between PCOA and sample cluster analysis among the three groups (Beta-diversity) and Alpha-diversity. The relative abundance of Rothia, Ruminococcus, and Enterococcus was significantly higher in the PCOS-IR group than in the other two groups (P < 0.05), while that of Prevotella was dramatically decreased (P < 0.05). The abundance of Enterococcus was positively correlated with waist circumference, hip circumference, diastolic blood pressure, and insulin resistance index. Meanwhile, Rothia abundance is positively associated with waist circumference and free fatty acids.
The gut microbial composition of PCOS patients with insulin resistance is different from that of PCOS alone and healthy women. The difference is correlated with the clinical characteristics of PCOS, with regards to insulin resistance, abdominal obesity, free fatty acids, and other indicators. PCOS-IR patients have an increased abundance of Enterococcus which potentially the intestinal environment of the host by enriching the metabolic pathways related to insulin resistance, causing the occurrence and development of PCOS.
To characterise the oral microbiome, gut microbiome and serum lipid profiles in patients with active COVID-19 and recovered patients; evaluate the potential of the microbiome as a non-invasive biomarker for COVID-19; and explore correlations between the microbiome and lipid profile.
We collected and sequenced 392 tongue-coating samples, 172 faecal samples and 155 serum samples from Central China and East China. We characterised microbiome and lipid molecules, constructed microbial classifiers in discovery cohort and verified their diagnostic potential in 74 confirmed patients (CPs) from East China and 37 suspected patients (SPs) with IgG positivity.
Oral and faecal microbial diversity was significantly decreased in CPs versus healthy controls (HCs). Compared with HCs, butyric acid-producing bacteria were decreased and lipopolysaccharide-producing bacteria were increased in CPs in oral cavity. The classifiers based on 8 optimal oral microbial markers (7 faecal microbial markers) achieved good diagnostic efficiency in different cohorts. Importantly, diagnostic efficacy reached 87.24% in the cross-regional cohort. Moreover, the classifiers successfully diagnosed SPs with IgG antibody positivity as CPs, and diagnostic efficacy reached 92.11% (98.01% of faecal microbiome). Compared with CPs, 47 lipid molecules, including sphingomyelin (SM)(d40:4), SM(d38:5) and monoglyceride(33:5), were depleted, and 122 lipid molecules, including phosphatidylcholine(36:4p), phosphatidylethanolamine (PE)(16:0p/20:5) and diglyceride(20:1/18:2), were enriched in confirmed patients recovery.
This study is the first to characterise the oral microbiome in COVID-19, and oral microbiomes and lipid alterations in recovered patients, to explore their correlations and to report the successful establishment and validation of a diagnostic model for COVID-19.
Antibiotics have improved survival from previously deadly infectious diseases. Antibiotics alter the microbial composition of the gut microbiota, and these changes are associated with diminished innate immunity and decline in cognitive function in older adults. The composition of the human microbiota changes with age over the human lifespan. In this pilot study, we sought to identify if age is associated with differential recovery of the microbiota after antibiotic exposure. Using 16S rRNA gene sequencing, we compared recovery of the gut microbiota after the 10-day broad-spectrum antibiotic treatment in wild-type C57BL/six young and older mice. Immediately after antibiotic cessation, as expected, the number of ASVs, representing taxonomic richness, in both young and older mice significantly declined from the baseline. Mice were followed up to 6 months after cessation of the single 10-day antibiotic regimen. The Bray-Curtis index recovered within 20 days after antibiotic cessation in young mice, whereas in older mice the microbiota did not fully recover during the 6-months of follow-up. Bifidobacterium, Dubosiella, Lachnospiraceae_NK4A136_group became dominant in older mice, whereas in young mice, the bacteria were more evenly distributed, with only one dominant genus of Anaeroplasma. From 45 genera that became extinct after antibiotic treatment in young mice, 31 (68.9%) did not recover by the end of the study. In older mice, from 36 extinct genera, 27 (75%) did not recover. The majority of the genera that became extinct and never recovered belonged to Firmicutes phylum and Clostridiales family. In our study, age was a factor associated with the long-term recovery of the gut microbiota after the 10-day antibiotic treatment.
Endometriosis (EM) in reproductive females has an incidence of 6-10% and greatly affects female fertility, quality of life, and long-term health. The gut microbiota can affect the physiological and pathological processes of humans through various pathways, such as those involving the nervous and endocrine systems and immunity, and it plays important roles in endocrine and inflammatory diseases. Whether the gut microbiota plays a role in EM has gradually attracted researchers' attention. In the present study, fecal and blood samples were collected from 12 patients with stage 3/4 EM and 12 healthy controls. We performed 16S rRNA high-throughput sequencing to compare the gut microbiota between the EM and control groups. Serum levels of hormones and inflammatory cytokines were measured. We found that compared with the control group, the EM group had a lower α diversity of gut microbiota and a higher Firmicutes/Bacteroidetes ratio. The abundances of various taxa (such as Actinobacteria, Tenericutes, Blautia, Bifidobacterium, Dorea, and Streptococcus) were significantly different between the two groups. The taxon with the highest abundance in the EM group was Prevotella_7, and that in the control group was Coprococcus_2. The serum levels of E2 and IL-8 were significantly higher in the EM group than in the control group (E2: EM group 74.7 ± 22.5 pg/L vs CON group 47.9 ± 12.5 pg/L; IL-8: EM group 6.39 ± 1.59 pg/mL vs CON group 4.14 ± 0.73 pg/mL). Additionally, the gut microbiota of the EM group was enriched for the microbial function categories environmental information processing, endocrine system, and immune system. Correlations were detected between each of Blautia and Dorea abundance and estradiol level and between Subdoligranulum abundance and IL-8 level. This study elucidated the associations between the gut microbiota and both serum hormones and inflammatory factors in EM. However, the findings need to be verified in future studies.
The aim of this study was to investigate the composition of the intestinal microbiota and its association with fecal short chain fatty acids (SCFAs) in children with drug refractory epilepsy (DRE) before and after treatment with a ketogenic diet (KD).
Herein, we conducted a cross-sectional study of 12 children with DRE and 12 matched healthy controls to compare the changes in fecal microbiomes and SCFAs. Disease cohort also underwent analysis before and after 6 months of KD treatment.
A higher microbial alpha diversity and a significant increase in Actinobacteria at the phylum level and Enterococcus, Anaerostipes, Bifidobacterium, Bacteroides, and Blautia at the genus level were observed in the children with DRE. The abundance of the eight epileptic-associated genera was reversed after six months of KD treatment with decreases in Bifidobacterium, Akkermansia, Enterococcaceae and Actinomyces and increases in Subdoligranulum, Dialister, Alloprevotella (p < 0.05). In particular, we identified some taxa that were more prevalent in patients with an inadequate response to KD than in those with an adequate response. Further, a significant correlation was observed between the change in the microbiome genera after KD treatment. The SCFA content in the fecal after 6 months of KD treatment increased and was highly correlated with the gut bacteria.
Dysbiosis of the microbiome could be involved in the pathogenesis of DRE in children, which can be relieved by a KD to a large extent. Gut microbiota and microbial metabolism could contribute to the antiseizure effect of KD.
This study examined the composition of the gut microbiota in diffuse large B cell lymphoma (DLBCL), a hematological malignancy whose intestinal microecology had not previously been characterized. Fecal samples were analyzed using 16S rRNA gene sequencing to compare bacterial community composition and diversity. The researchers also used PICRUSt functional prediction to estimate differences in metabolic pathway activity between groups.
The study included 25 untreated patients with diffuse large B cell lymphoma and 26 healthy volunteers who served as controls. Fecal samples from these 51 total participants were the basis for the 16S rRNA sequencing analysis. The abstract does not provide further demographic details such as age or sex distribution.
Alpha-diversity (species diversity and abundance) did not differ significantly between DLBCL patients and healthy controls, but beta-diversity did differ significantly, indicating a distinct overall community structure. The DLBCL microbiota showed a continuous evolutionary relationship progressing from the phylum proteobacteria to the genus Escherichia-Shigella, both significantly more abundant than in controls. Allisonella, Lachnospira, and Roseburia were also more abundant at the genus level in DLBCL patients, while PICRUSt functional prediction showed significantly lower thiamine metabolism and phenylalanine, tyrosine, and tryptophan biosynthesis pathways in the DLBCL group.
The findings demonstrate that gut microbiota composition is significantly altered in untreated DLBCL, establishing a baseline microbial signature associated with this malignancy. This work lays groundwork for future prospective studies to determine whether these microbial differences contribute to disease development or progression. It also opens the door to microbiome-directed interventional trials aimed at improving outcomes for patients with DLBCL.
The characteristics of polycystic ovary syndrome (PCOS), a common reproductive endocrinal disorder, are high incidence, complicated aetiology and poor therapeutic effects. PCOS patients frequently exhibit gut dysbiosis; however, its roles in the regulation of metabolic and endocrinal balances in PCOS pathophysiology are not clear.
In this study, gut dysbiosis was reproduced in dehydroepiandrosterone (DHEA)-induced PCOS-like rats. An antibiotic cocktail was used to eliminate gut microbiota during DHEA treatment; however, depletion of the gut microbiota did not prevent the occurrence of PCOS phenotypes in DHEA-treated rats. DHEA-shaped gut microbiota transplanted to pseudo germ-free recipients trigged disturbances in hepatic glucolipid metabolism and reproductive hormone imbalance. The clinical features of PCOS may be correlated with the relative abundance of gut microbes and the levels of faecal metabolites in faecal microbiota transplantation (FMT) recipient rats.
These findings indicate that androgen-induced gut microbiota dysbiosis may aggravate metabolic and endocrinal malfunction in PCOS. Video Abstract.
This study examined how gepotidacin, a first-in-class triazaacenaphthylene antibiotic with a novel mechanism of action, affects the human microbiome during treatment for uncomplicated urinary tract infections. It was conducted as part of a randomised Phase 2a clinical trial evaluating repeated oral doses of gepotidacin (GSK2140944). Researchers tracked microbiota composition across three body sites, the gastrointestinal tract, the pharyngeal cavity, and the vagina, using 16S rRNA gene sequencing. Samples were collected at three time points relative to dosing to capture both immediate effects and later recovery.
The study population consisted of 22 adult female patients with uncomplicated urinary tract infections who were enrolled in the gepotidacin Phase 2a trial (ClinicalTrials.gov NCT03568942). Each participant contributed microbiome samples from the gut, throat, and vagina. Samples were collected pre-dose on Day 1, at the end of dosing on Day 5, and at a Follow-up visit around Day 28. This design allowed within-subject comparison of microbiome changes over the course of treatment and recovery.
By Day 5, at the end of the gepotidacin dosing regimen, significant changes in microbiome diversity were observed relative to pre-dose baseline across all three tested body sites. These shifts indicate that gepotidacin measurably disrupted the gut, pharyngeal, and vaginal microbiota during active treatment. By the Follow-up visit approximately three weeks later, microbiome diversity had reverted to compositions comparable to Day 1 baseline. This pattern points to disruption during dosing followed by recovery after treatment ended, though the abstract does not specify which body site showed the greatest change.
The findings suggest that gepotidacin's effects on the microbiome are transient rather than persistent, with diversity returning to baseline within about a month of treatment completion. This supports the value of characterizing microbiome impacts early in antibiotic drug development, especially for agents with novel mechanisms of action. Demonstrating recovery across multiple body sites, not just the gut, offers reassurance about the drug's broader ecological footprint. The approach also illustrates a model for how future antibiotic trials might systematically monitor microbiome perturbation and recovery as part of safety evaluation.
This study examined whether gut microbiota composition is associated with fever in patients with moderate COVID-19. Researchers compared clinical features and laboratory results between patients with and without fever, and identified inflammatory markers linked to fever. They then conducted a gut metagenome-wide association study to characterize the microbes and microbial epitopes potentially involved in fever and hyperinflammation.
The cohort included 187 patients with moderate COVID-19, of whom 127 (67.9 percent) presented with fever and the remainder did not. A subset of 31 individuals from this group underwent gut metagenome-wide association analysis to identify microbial features linked to fever and hyperinflammation. The abstract does not provide further demographic details such as age or sex distribution.
Patients with fever showed significantly reduced lymphocytes, CD3+ T cells, CD4+ T cells, and CD4+ to CD8+ T cell ratios, alongside significantly elevated AST, LDH, CRP, IL-6, and IL-10. Gut microbiome composition differed significantly between patients with fever and those without. Opportunistic pathogens, including Enterococcus faecalis and Saccharomyces cerevisiae, were enriched in patients with fever, and E. faecalis abundance was positively correlated with LDH and D-dimer levels.
These findings suggest that gut microbiota dysbiosis, particularly enrichment of opportunistic pathogens such as Enterococcus faecalis, may be linked to the abnormal immune responses and inflammation seen in febrile moderate COVID-19 patients. This raises the possibility that gut microbes or their components contribute to fever and hyperinflammation in this population. The results point to gut microbiota as a potential area of interest for understanding COVID-19 severity and prognosis in moderate cases.
The disease severity, ranging from being asymptomatic to having acute illness, and associated inflammatory responses has suggested that alterations in the gut microbiota may play a crucial role in the development of chronic disorders due to COVID-19 infection. This study describes gut microbiota dysbiosis in COVID-19 patients and its implications relating to the disease.
A cross sectional prospective study was performed on thirty RT-PCR-confirmed COVID-19 patients admitted to the All India Institute of Medical Sciences, Bhopal, India, between September 10 and 20, 2020. Ten healthy volunteers were recruited as the control group. IFN, TNF, and IL-21 profiling was conducted using plasma samples, and gut bacterial analysis was performed after obtaining the metagenomics data of stool samples.
Patients with a variable COVID-19 severity showed distinct gut microflora and peripheral interleukin-21 levels. A low Firmicute/Bacteroidetes ratio, caused by the depletion of the fibre-utilizing bacteria, F. prausnitzii, B. Plebius, and Prevotella, and an increase in Bacteroidetes has associated gut microbiota dysbiosis with COVID-19 disease severity.
The loss of the functional attributes of signature commensals in the gut, due to dysbiosis, is a predisposing factor of COVID-19 pathophysiology.
Patients with COVID-19 have been reported to experience gastrointestinal symptoms as well as respiratory symptoms, but the effects of COVID-19 on the gut microbiota are poorly understood. We explored gut microbiome profiles associated with the respiratory infection of SARS-CoV-2 during the recovery phase in patients with asymptomatic or mild COVID-19. A longitudinal analysis was performed using the same patients to determine whether the gut microbiota changed after recovery from COVID-19. We applied 16S rRNA amplicon sequencing to analyze two paired fecal samples from 12 patients with asymptomatic or mild COVID-19. Fecal samples were selected at two time points: during SARS-CoV-2 infection (infected state) and after negative conversion of the viral RNA (recovered state). We also compared the microbiome data with those from 36 healthy controls. Microbial evenness of the recovered state was significantly increased compared with the infected state. SARS-CoV-2 infection induced the depletion of Bacteroidetes, while an abundance was observed with a tendency to rapidly reverse in the recovered state. The Firmicutes/Bacteroidetes ratio in the infected state was markedly higher than that in the recovered state. Gut dysbiosis was observed after infection even in patients with asymptomatic or mild COVID-19, while the composition of the gut microbiota was recovered after negative conversion of SARS-CoV-2 RNA. Modifying intestinal microbes in response to COVID-19 might be a useful therapeutic alternative.
Acute graft-versus-host disease (aGVHD) is one of the major causes of death after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Recently, aGVHD onset was linked to intestinal microbiota (IM) dysbiosis. However, other bacterial-rich gastrointestinal sites, such as the mouth, which hosts several distinctive microbiotas, may also impact the risk of GVHD. The dental biofilm microbiota (DBM) is highly diverse and, like the IM, interacts with host cells and modulates immune homeostasis. We characterized changes in the DBM of patients during allo-HSCT and evaluated whether the DBM could be associated with the risk of aGVHD. DBM dysbiosis during allo-HSCT was marked by a gradual loss of bacterial diversity and changes in DBM genera composition, with commensal genera reductions and potentially pathogenic bacteria overgrowths. High Streptococcus and high Corynebacterium relative abundance at preconditioning were associated with a higher risk of aGVHD (67% vs. 33%; HR = 2.89, P = 0.04 and 73% vs. 37%; HR = 2.74, P = 0.04, respectively), while high Veillonella relative abundance was associated with a lower risk of aGVHD (27% vs. 73%; HR = 0.24, P < 0.01). Enterococcus faecalis bloom during allo-HSCT was observed in 17% of allo-HSCT recipients and was associated with a higher risk of aGVHD (100% vs. 40%; HR = 4.07, P < 0.001) and severe aGVHD (60% vs. 12%; HR = 6.82, P = 0.01). To the best of our knowledge, this is the first study demonstrating that DBM dysbiosis is associated with the aGVHD risk after allo-HSCT.
The human oral and gut commensal microbes play vital roles in the development and maintenance of immune homeostasis, while its association with susceptibility and severity of SARS-CoV-2 infection is barely understood. In this study, we investigated the dynamics of the oral and intestinal flora before and after the clearance of SARS-CoV-2 in 53 COVID-19 patients, and then examined their microbiome alterations in comparison to 76 healthy individuals. A total of 140 throat swab samples and 81 fecal samples from these COVID-19 patients during hospitalization, and 44 throat swab samples and 32 fecal samples from sex and age-matched healthy individuals were collected and then subjected to 16S rRNA sequencing and viral load inspection. We found that SARS-CoV-2 infection was associated with alterations of the microbiome community in patients as indicated by both alpha and beta diversity indexes. Several bacterial taxa were identified related to SARS-CoV-2 infection, wherein elevated Granulicatella and Rothia mucilaginosa were found in both oral and gut microbiome. The SARS-CoV-2 viral load in those samples was also calculated to identify potential dynamics between COVID-19 and the microbiome. These findings provide a meaningful baseline for microbes in the digestive tract of COVID-19 patients and will shed light on new dimensions for disease pathophysiology, potential microbial biomarkers, and treatment strategies for COVID-19.
The lack of tools for the precise manipulation of the tick microbiome is currently a major limitation to achieve mechanistic insights into the tick microbiome. Anti-tick microbiota vaccines targeting keystone bacteria of the tick microbiota alter tick feeding, but their impact on the taxonomic and functional profiles of the tick microbiome has not been tested. In this study, we immunized a vertebrate host model (Mus musculus) with live bacteria vaccines targeting keystone (i.e., Escherichia-Shigella) or non-keystone (i.e., Leuconostoc) taxa of tick microbiota and tested the impact of bacterial-specific antibodies (Abs) on the structure and function of tick microbiota. We also investigated the effect of these anti-microbiota vaccines on mice gut microbiota composition. Our results showed that the tick microbiota of ticks fed on Escherichia coli-immunized mice had reduced Escherichia-Shigella abundance and lower species diversity compared to ticks fed on control mice immunized with a mock vaccine. Immunization against keystone bacteria restructured the hierarchy of nodes in co-occurrence networks and reduced the resistance of the bacterial network to taxa removal. High levels of E. coli-specific IgM and IgG were negatively correlated with the abundance of Escherichia-Shigella in tick microbiota. These effects were not observed when Leuconostoc was targeted with vaccination against Leuconostoc mesenteroides. Prediction of functional pathways in the tick microbiome using PICRUSt2 revealed that E. coli vaccination reduced the abundance of lysine degradation pathway in tick microbiome, a result validated by qPCR. In contrast, the gut microbiome of immunized mice showed no significant alterations in the diversity, composition and abundance of bacterial taxa. Our results demonstrated that anti-tick microbiota vaccines are a safe, specific and an easy-to-use tool for manipulation of vector microbiome. These results guide interventions for the control of tick infestations and pathogen infection/transmission.
Preclinical studies have shown that the gut microbiota can play a role in schizophrenia (SCH) pathogenesis via the gut-brain axis. However, its role in the antipsychotic treatment response is unclear. Here, we present a 24-week follow-up study to identify gut microbial biomarkers for SCH diagnosis and treatment response, using a sample of 107 first-episode, drug-naïve SCH patients, and 107 healthy controls (HCs). We collected biological samples at baseline (all participants) and follow-up time points after risperidone treatment (SCH patients). Treatment response was assessed using the Positive and Negative Symptoms Scale total (PANSS-T) score. False discovery rate was used to correct for multiple testing. We found that SCH patients showed lower α-diversity (the Shannon and Simpson's indices) compared to HCs at baseline (p = 1.21 × 10-9, 1.23 × 10-8, respectively). We also found a significant difference in β-diversity between SCH patients and HCs (p = 0.001). At baseline, using microbes that showed different abundance between patients and controls as predictors, a prediction model can distinguish patients from HCs with an area under the curve (AUC) of 0.867. In SCH patients, after 24 weeks of risperidone treatment, we observed an increase of α-diversity toward the basal level of HCs. At the genus level, we observed decreased abundance of Lachnoclostridium (p = 0.019) and increased abundance Romboutsia (p = 0.067). Moreover, the treatment response in SCH patients was significantly associated with the basal levels of Lachnoclostridium and Romboutsia (p = 0.005 and 0.006, respectively). Our results suggest that SCH patients may present characteristic microbiota, and certain microbiota biomarkers may predict treatment response in this patient population.
This study examined whether the gut microbiome, and specifically its short-chain fatty acid (SCFA) byproducts, are needed for a normal sympathoadrenal stress response to hypoglycemia. Researchers depleted the gut microbiota of adult mice with broad-spectrum, non-absorbable antibiotics and then tested their epinephrine response to insulin-induced low blood sugar. They also tested whether simply recolonizing the gut with bacteria, without restoring SCFA production, could reverse any deficits.
The subjects were male C57Bl6 mice, divided into groups given either regular drinking water (controls) or a cocktail of non-absorbable broad-spectrum antibiotics (Abx) in their drinking water for two weeks. Mice from each group were then injected with either insulin, to induce hypoglycemia, or saline. A separate recolonization group (Abx plus R) was also included to assess reversal of antibiotic effects.
Antibiotic treatment sharply reduced microbial diversity and depleted Bacteroidetes and Firmicutes, enlarged the caecum, and eliminated detectable short-chain fatty acids such as acetate, propionate, and butyrate. These Abx mice showed blunted tonic and stress-induced epinephrine levels. Recolonization restored bacterial diversity but did not restore sympathoadrenal responsiveness or caecal SCFA levels, indicating that bacterial presence alone is insufficient.
The findings suggest that bacterial metabolites, particularly SCFAs, rather than the mere presence of gut bacteria, are what drive normal adrenal catecholamine responses to hypoglycemia. This points to SCFA restoration, not just microbial recolonization, as the relevant target for repairing stress-response deficits after antibiotic-induced dysbiosis. It also implies that antibiotic courses could carry a previously underappreciated risk of disrupting glucose counter-regulatory physiology.
This prospective observational study evaluated whether gut microbiome composition is associated with stroke-associated pneumonia (SAP) in patients with acute ischemic stroke. Researchers collected fecal and serum samples at admission and used 16S rRNA V4 tag sequencing, analyzed with QIIME and LEfSe, to characterize gut microbiota. They also measured fecal short-chain fatty acids and serum markers of gut barrier integrity, including D-lactate, intestinal fatty acid-binding protein, and lipopolysaccharide binding protein.
The training cohort included 188 patients with acute ischemic stroke, of whom 52 (27.7%) developed stroke-associated pneumonia. Findings were validated in an independent cohort of 144 patients, 28 of whom (19.4%) developed SAP. Disease severity scores were recorded by specialized physicians alongside the microbiome and biomarker data.
Gut microbiome composition differed significantly between patients who developed SAP and those who did not. Patients with SAP showed depletion of Roseburia along with enrichment of opportunistic pathogens, a pattern confirmed in the independent validation cohort. Multivariate analysis identified Roseburia as a protective factor against SAP in both the training and validation cohorts, supporting gut dysbiosis as an independent risk factor for this complication.
These findings suggest gut microbiota, particularly Roseburia abundance, could serve as an early biomarker to identify stroke patients at higher risk of pneumonia. Because Roseburia acted as a protective factor across two independent cohorts, restoring or supporting this taxon may represent a potential avenue for reducing SAP risk. The results also point toward gut-lung axis mechanisms as a relevant target for future preventive strategies in acute ischemic stroke care.
Despite advances in the characterization of colorectal cancer (CRC), it still faces a poor prognosis. There is growing evidence that gut microbiota and their metabolites potentially contribute to the development of CRC. Thus, microbial dysbiosis and their metabolites associated with CRC, based on stool samples, may be used to advantage to provide an excellent opportunity to find possible biomarkers for the screening, early detection, prevention, and treatment of CRC. Using 16S rRNA amplicon sequencing coupled with statistical analysis, this study analyzed the cause-effect shift of the microbial taxa and their metabolites that was associated with the fecal gut microbiota of 17 healthy controls, 21 polyps patients, and 21 cancer patients. The microbial taxonomic shift analysis revealed striking differences among the healthy control, polyps and cancer groups. At the phylum level, Synergistetes was reduced significantly in the polyps group compared to the healthy control and cancer group. Additionally, at the genus level and in association with the cancer group, a total of 12 genera were highly enriched in abundance. In contrast, only Oscillosprira was significantly higher in abundance in the healthy control group. Comparisons of the polyps and cancer groups showed a total of 18 significantly enriched genera. Among them, 78% of the genera associated with the cancer group were in higher abundance, whereas the remaining genera showed a higher abundance in the polyps group. Additionally, the comparison of healthy control and polyp groups showed six significantly abundant genera. More than 66% of these genera showed a reduced abundance in the polyps group than in healthy controls, whereas the remaining genera were highly abundant in the polyps group. Based on tumor presence and absence, the abundance of Olsenella and Lactobacillus at the genus level was significantly reduced in the patient group compared to healthy controls. The significant microbial function prediction revealed an increase in the abundance of metabolites in the polyps and cancer groups compared to healthy controls. A correlation analysis revealed a higher contribution of Dorea in the predicted functions. This study showed dysbiosis of gut microbiota at the taxonomic level and their metabolic functions among healthy subjects and in two stages of colorectal cancer, including adenoma and adenocarcinoma, which might serve as potential biomarkers for the early diagnosis and treatment of CRC.
Cancer cachexia is characterized by a negative energy balance, muscle and adipose tissue wasting, insulin resistance, and systemic inflammation. Because of its strong negative impact on prognosis and its multifactorial nature that is still not fully understood, cachexia remains an important challenge in the field of cancer treatment. Recent animal studies indicate that the gut microbiota is involved in the pathogenesis and manifestation of cancer cachexia, but human data are lacking. The present study investigates gut microbiota composition, short-chain fatty acids (SCFA), and inflammatory parameters in human cancer cachexia.
Faecal samples were prospectively collected in patients (N = 107) with pancreatic cancer, lung cancer, breast cancer, or ovarian cancer. Household partners (N = 76) of the patients were included as healthy controls with similar diet and environmental conditions. Patients were classified as cachectic if they lost >5% body weight in the last 6 months. Gut microbiota composition was analysed by sequencing of the 16S rRNA V4 gene region. Faecal SCFA levels were quantified by gas chromatography. Faecal calprotectin was assessed with enzyme-linked immunosorbent assay. Serum C-reactive protein and leucocyte counts were retrieved from medical records.
Cachexia prevalence was highest in pancreatic cancer (66.7%), followed by ovarian cancer (25%), lung cancer (20.8%), and breast cancer (17.3%). Microbial α-diversity was not significantly different between cachectic cancer patients (N = 33), non-cachectic cancer patients (N = 74), or healthy controls (N = 76) (species richness P = 0.31; Shannon effective index P = 0.46). Community structure (β-diversity) tended to differ between these groups (P = 0.053), although overall differences were subtle and no clear clustering of samples was observed. Proteobacteria (P < 0.001), an unknown genus from the Enterobacteriaceae family (P < 0.01), and Veillonella (P < 0.001) were more abundant among cachectic cancer patients. Megamonas (P < 0.05) and Peptococcus (P < 0.001) also showed differential abundance. Faecal levels of all SCFA tended to be lower in cachectic cancer patients, but only acetate concentrations were significantly reduced (P < 0.05). Faecal calprotectin levels were positively correlated with the abundance of Peptococcus, unknown Enterobacteriaceae, and Veillonella. We also identified several correlations and interactions between clinical and microbial parameters.
This clinical study provided the first insights into the alterations of gut microbiota composition and SCFA levels that occur in cachectic cancer patients and how they are related to inflammatory parameters. These results pave the way for further research examining the role of the gut microbiota in cancer cachexia and its potential use as therapeutic target.
This study examined how the gut microbial community changes along different regions of the gastrointestinal tract, comparing the small intestine, cecum, colon, and rectum. It also compared these gut regions across three closely related, co-occurring wild rodent species. The goal was to determine how much of the variation in gut microbiota is explained by gut region versus host species.
The study sampled three sympatric species of wild rodents: Apodemus speciosus, Apodemus argenteus, and Myodes rufocanus. These animals were presumably collected from the wild and sampled at multiple gastrointestinal sites (small intestine, cecum, colon, and rectum) per individual. The abstract does not give an exact number of animals sampled.
The small intestine harbored a microbial community that was distinct from that of the lower gastrointestinal tract (cecum, colon, and rectum) in all three rodent species. The genus Lactobacillus was notably more abundant in the small intestine than in lower gut regions across all three species. This pattern held consistently regardless of host species, suggesting gut region has a strong and generalizable effect on microbiome composition.
The findings indicate that gut region is an important driver of microbiome variation, meaning fecal or colon samples alone may not represent the full gastrointestinal microbial community. This has implications for how wild animal microbiome studies are designed, since relying only on fecal samples could miss important small-intestinal features like Lactobacillus enrichment. Comparative host-microbiome research may need to sample multiple gut regions to draw accurate conclusions about host-microbe interactions.
The gut microbiota can affect human metabolism, immunity, and other biologic pathways through the complex gut-kidney axis (GKA), and in turn participate in the occurrence and development of kidney disease. In this study, 39 patients with stage 4-5 chronic kidney disease (CKD) and 40 healthy individuals were recruited and 16S rDNA sequencing was performed to analyze the V3-V4 conserved regions of their microbiota. A total of 795 operational taxonomic units (OTUs) shared between groups or specific to each group were obtained, among which 255 OTUs with significant differences between the two groups were identified (P<0.05). Adonis differential analysis showed that the diversity of gut microbiota was highly correlated with CKD stages 4-5. Additionally, 61 genera with differences in the two groups were identified (P<0.05) and 111 species with significant differences in the phyla, classes, orders, families, and genera between the two groups were identified (P<0.05). The differential bacterial genera with the greatest contribution were, in descending order: c_Bacteroidia, o_Bacteroidales, p_Bacteroidetes, c_Clostridia, o_Clostridiales, etc. Those with the greatest contribution in stages 4-5 CKD were, in descending order: p_Proteobacteria, f_Enterobacteriaceae, o_Enterobacteriales, c_Gammaproteobacteria, c_Bacilli, etc. The results suggest that the diversity of the microbiota may affect the occurrence, development, and outcome of the terminal stages of CKD.
This study examined the gut microbiota of breast cancer patients according to menopausal status, focusing specifically on premenopausal breast cancer, which has been understudied compared to postmenopausal disease. The researchers assessed overall microbial diversity, community composition, and functional pathways. They also evaluated whether specific gut microbial markers could distinguish breast cancer patients by menopausal status and whether these markers had diagnostic value.
The study analyzed 267 breast cancer patients with different menopausal statuses (premenopausal and postmenopausal) along with age-matched female controls. The abstract notes that premenopausal breast cancer is a growing concern in Asian countries, where younger patients make up an increasing share of cases, in contrast to Western countries where breast cancer more often occurs in older postmenopausal women. Beyond the total cohort size, no further demographic or geographic details are given in the abstract.
Alpha-diversity of the gut microbiota was significantly reduced in premenopausal breast cancer patients, and beta-diversity differed significantly between breast cancer patients and controls. Through multiple analyses and classification approaches, the researchers identified 14 microbial markers that differed according to menopausal status in breast cancer. Notably, Bacteroides fragilis was specifically found in younger, premenopausal patients, while Klebsiella pneumoniae was specifically found in older, postmenopausal patients.
The findings suggest that gut microbial profiles in breast cancer are menopausal-status specific, meaning premenopausal and postmenopausal disease may involve distinct microbial signatures rather than a single uniform pattern. The identification of menopausal-specific microbial markers, such as Bacteroides fragilis in premenopausal patients, points toward potential diagnostic applications tailored to age and menopausal status. This underscores the need for future breast cancer microbiome research to separately account for premenopausal patients rather than focusing predominantly on postmenopausal disease.
This study assessed whether the gut microbiota composition differs between children with autism spectrum disorder (ASD) and healthy children. Researchers used high-throughput sequencing of the V3-V4 region of the 16S rRNA gene to characterize fecal bacterial communities. They evaluated alpha diversity using the Shannon, Chao, and ACE indexes, and beta diversity using unweighted UniFrac analysis and PCA plots. LDA and LEfSe were applied to identify bacterial taxa that differed in abundance between groups.
The study included 25 children diagnosed with ASD and 20 healthy children serving as controls. Autistic symptoms were diagnosed using the Diagnostic and Statistical Manual for Mental Disorders and assessed for severity with the Autism Treatment Evaluation Checklist (ATEC). Gastrointestinal symptoms in the ASD group were further evaluated with a GI Severity Index (GSI) questionnaire.
Children with higher GSI scores had markedly higher ATEC Total scores than those with lower GSI scores, indicating that gastrointestinal symptoms were strongly associated with the severity of autism symptoms. There was no significant difference in overall bacterial diversity, as measured by the Chao, ACE, and Shannon indexes, between children with ASD and healthy controls. Despite similar diversity levels, both groups showed differences in the composition of specific bacterial taxa, based on the abstract provided.
The findings suggest that gastrointestinal symptoms in children with ASD are closely tied to the severity of their behavioral symptoms, reinforcing the relevance of the gut-brain axis in autism. The lack of difference in overall diversity but presence of compositional shifts implies that specific taxonomic imbalances, rather than overall community richness, may be more informative for understanding ASD-related gut disruption. These results support further investigation into targeted microbiota-based markers or interventions tied to GI symptom severity in ASD.
This study examined how gut microbiota composition changes after stroke and whether those changes relate to functional recovery. Researchers compared fecal microbial diversity, composition, and species cooccurrence between stroke patients and healthy controls. They used 16S rRNA gene sequencing (V3-V4 regions) on the Illumina MiSeq platform to characterize the bacterial communities. Random forest and receiver operating characteristic analyses were then applied to identify bacterial genera that might serve as diagnostic biomarkers linked to poststroke outcomes.
The cohort consisted of thirty-eight patients who had experienced a stroke and thirty-five healthy controls matched to the patients by demographics. Fecal DNA was extracted from all participants for microbial sequencing. This was a prospective cohort study comparing a clinical stroke population against a demographically similar healthy comparison group.
Poststroke patients showed significantly higher alpha diversity of gut microbiota than healthy controls. Beta diversity analysis confirmed that overall microbiota composition differed significantly between the two groups. At the genus level, nine genera increased significantly in abundance in poststroke patients, while eighty-two genera decreased significantly, indicating a broad and pronounced shift in the gut microbial community following stroke.
The findings support the existence of a distinct poststroke gut microbiota signature linked to the gut-microbiota-brain axis. Because specific bacterial genera were identified as potential discriminant markers with ties to functional outcomes, gut microbiota profiling may eventually help predict or monitor functional recovery after stroke. This adds to evidence that stroke does not just affect the brain but is accompanied by substantial, measurable disruption of the gut microbial ecosystem.
The aim of this study was to determine the diversity of intestinal microflora and its correlation with clinical parameters in diabetic patients and healthy subjects and to assess the importance of intestinal flora in patients with diabetes. Forty-four patients with diabetes were included. The control group included 47 healthy people. Their data, biochemical indicators and results from 16S rRNA sequencing of their fecal samples were collected. Compared with the healthy population, the intestinal flora of the diabetic patients was obviously abnormal. Within the diabetes group, the abundances of the genera Faecalibacterium, Prevotella, and Roseburia were higher, and the abundances of the genera Shigella and Bifidobacterium were lower. In the correlation analysis between bacteria and clinical indicators, it was found that the genera Veillonella and unclassified_Enterobacteriaceae were negatively related to blood glucose, while the genera Phascolarctobacterium, unidentified_Bacteroidales and Prevotella were significantly positively correlated with fasting blood glucose. Twelve microbial markers were detected in the random forest model, and the area under the curve (AUC) was 84.1%. This index was greater than the diagnostic effect of fasting blood glucose. This was also supported by the joint diagnostic model of microorganisms and clinical indicators. In addition, the intestinal flora significantly improved the diagnosis of diabetes. In conclusion, it can be concluded from these results that intestinal flora is essential for the occurrence and development of diabetes, which seems to be as important as blood glucose itself.Abbreviations: PCoA: principal coordinate analysis; NMDS: non econometric multidimensional scaling analysis; LEfSe: linear discriminant analysis effect size; LDA: linear discriminant analysis; POD: probability of disease; BMI: body mass index; DCA: decision curve analysis.
Next-generation sequencing has revolutionized our perspective on the gut microbiome composition, revealing the true extent of the adverse effects of antibiotics. The impact of antibiotic treatment on gut microbiota must be considered and researched to provide grounds for establishing new treatment strategies that are less devastating on commensal bacteria. This study investigates the impact on gut microbiome when a commonly used antibiotic, azithromycin is administered, as well as uncovers the benefits induced when it is used in combination with lactulose, a prebiotic known to enhance the proliferation of commensal microbes.
16S rRNA gene sequencing analysis of stool samples obtained from 87 children treated with azithromycin in combination with or without lactulose have been determined. Children's gut microbial profile was established at the pre- and post-treatment stage.
Azithromycin caused an increase in the relative abundance of opportunistic pathogens such as Streptococcus that was evident 60 days after treatment. While few days after treatment, children who also received lactulose started to show a higher relative abundance of saccharolytic bacteria such as Lactobacillus, Enterococcus, Anaerostipes, Blautia and Roseburia, providing a protective role against opportunistic pathogens. In addition, azithromycin-prebiotic combination was able to provide a phylogenetic profile more similar to the pre-treatment stage.
It is suggested that during azithromycin treatment, lactulose is able to reinstate the microbiome equilibrium much faster as it promotes saccharolytic microbes and provides a homeostatic effect that minimizes the opportunistic pathogen colonization.
Small intestinal bacterial overgrowth (SIBO) has been proposed as an etiologic factor in irritable bowel syndrome, particularly the diarrhea-predominant subtype (IBS-D). We aimed to identify potential intestinal microbial pattern in IBS-D patients with SIBO.
Diarrhea-predominant irritable bowel syndrome patients fulfilling Rome III criteria were recruited and randomly divided into an exploratory cohort (57 cases) and a validation cohort (20 cases). SIBO was identified according to standard glucose hydrogen breath test. For 16S rRNA gene sequencing, samples of duodenal mucosa, duodenal fluid, rectal mucosa, and fresh feces were collected and performed. The α and β diversity, as well as differences in microbial composition and function, in SIBO+ and SIBO- IBS-D subjects were evaluated.
The microbial diversity and composition obviously differed between SIBO+ and SIBO- IBS-D in duodenal and rectal mucosa but not in duodenal fluid and fresh feces. For rectal mucosal microbiota, it displayed markedly reduced aerobe and Gram-negative bacteria and increased facultative anaerobe and Gram-positive bacteria, moreover, altered functions of microbial metabolism in SIBO+ IBS-D. Significantly higher rectal mucosa-related microbial dysbiosis index was observed in SIBO+ IBS-D, and a cut-off value at -0.37 had a sensitivity of 56.55% and specificity of 90.91% to identify the SIBO in IBS-D subjects.
Mucosal microbiota, rather than luminal bacteria, has a more apparent dysbiosis in SIBO+ IBS-D patients relative to those without SIBO. Rectal mucosa-associated microbiota may act as a potential predictor of SIBO in IBS-D patients.
This study examined whether travel undertaken by elite athletes in the build-up to the 2016 Cricket World Cup altered the composition of the gut microbiome. Researchers collected faecal samples at baseline and after travel and analyzed them using 16S rRNA amplicon sequencing. A subset of samples was also examined with shotgun metagenomic sequencing to look at antibiotic resistance and virulence genes in more detail. The work was motivated by concern that travel-related stress and antibiotic resistance gene spread could affect gut microbiome stability and, potentially, athletic performance.
The cohort consisted of Irish cricket players preparing for the 2016 Cricket World Cup, including 14 male and 7 female athletes. Faecal samples were collected from all 21 participants at baseline and after travel. A smaller subset of four participants had their samples additionally analyzed by shotgun metagenomic sequencing.
One particular travel time point was identified as having the potential to disrupt the gut microbiome, unlike other travel periods examined. Following this travel, alpha diversity of the gut microbiome decreased, accompanied by shifts in the taxonomic profile of the microbial community. Shotgun metagenomic analysis also revealed changes in antibiotic resistance genes and virulence genes after travel. These changes appeared to be linked, in particular, to episodes of gastrointestinal distress during travel.
The findings suggest that travel, especially when accompanied by gastrointestinal distress, can disrupt the gut microbiome of elite athletes, including reductions in diversity and changes in resistance and virulence gene content. Because this analysis was conducted in athletes, the authors note the findings may have broader relevance beyond sport. The results raise concern that travel-associated microbiome disruption could carry implications for health and, potentially, performance in populations that travel frequently. This underscores the value of monitoring gut microbiome stability during periods of travel.
The meconium microbiome may provide insight into intrauterine and peripartum exposures and the very earliest intestinal pioneering microbes. Prenatal antibiotics have been associated with later obesity in children, which is thought to be driven by microbiome dependent mechanisms. However, there is little data regarding associations of prenatal or peripartum antibiotic exposure, with or without cesarean section (CS), with the features of the meconium microbiome. In this study, 16S ribosomal RNA gene sequencing was performed on bacterial DNA of meconium samples from 105 infants in a birth cohort study. After multivariable adjustment, delivery mode (p = 0.044), prenatal antibiotic use (p = 0.005) and peripartum antibiotic use (p < 0.001) were associated with beta diversity of the infant meconium microbiome. CS (vs. vaginal delivery) and peripartum antibiotics were also associated with greater alpha diversity of the meconium microbiome (Shannon and Simpson, p < 0.05). Meconium from infants born by CS (vs. vaginal delivery) had lower relative abundance of the genus Escherichia (p < 0.001). Prenatal antibiotic use and peripartum antibiotic use (both in the overall analytic sample and when restricting to vaginally delivered infants) were associated with differential abundance of several bacterial taxa in the meconium. Bacterial taxa in the meconium microbiome were also differentially associated with infant excess weight at 12 months of age, however, sample size was limited for this comparison. In conclusion, prenatal and peripartum antibiotic use along with CS delivery were associated with differences in the diversity and composition of the meconium microbiome. Whether or not these differences in the meconium microbiome portend risk for long-term health outcomes warrants further exploration.
This study examined whether the gut microbiome is altered in schizophrenia (SCZ) and whether such alterations relate to brain structure. Researchers used 16S rRNA gene sequencing of faecal samples to profile gut microbial composition. They also acquired T1-weighted structural MRI brain imaging data to test for correlations between microbial composition and structural brain signatures. The goal was to determine whether microbiome changes were linked to SCZ itself or to antipsychotic treatment.
The study included 40 first-episode drug-naive schizophrenia (FSCZ) patients, 85 chronically antipsychotic-treated schizophrenia (TSCZ) patients, and 69 healthy controls (HCs). Faecal samples were collected from all participants for microbiome analysis. A subset also underwent structural brain MRI to allow correlation with microbial composition.
TSCZ patients showed lower microbiome alpha-diversity compared to healthy controls, but this reduction was not seen in FSCZ patients. Both FSCZ and TSCZ patients had distinct changes in gut microbial composition compared to healthy controls, including alterations in Christensenellaceae, Enterobacteriaceae, Pasteurellaceae, and Turicibacteraceae at the family level, and Escherichia at the genus level. The abstract also indicates significant disturbances in gut microbial composition when comparing TSCZ to FSCZ patients directly.
The findings suggest gut microbiome alterations, including in Christensenellaceae, are present from the earliest, treatment-naive stage of schizophrenia and are further altered with chronic antipsychotic treatment. Linking microbial composition to regional brain volumes supports a potential gut-brain connection in the pathogenesis of schizophrenia. This distinguishes disease-associated microbial changes from those attributable to medication, informing future work on the gut microbiome as a biomarker or target in psychiatric illness.
It has been largely accepted that dietary changes have an effect on gut microbial composition. In this pilot study we hypothesised that Ramadan fasting, which can be considered as a type of time-restricted feeding may lead to changes in gut microbial composition and diversity. A total of 9 adult subjects were included in the study. Stool samples were collected before (baseline) and at the end of the Ramadan fasting (after 29 days). Following the construction of an 16S rRNA amplicon library, the V4 region was sequenced using the Illumina Miseq platform. Microbial community analysis was performed using the QIIME program. A total of 27,521 operational taxonomic units (OTUs) with a 97% similarity were determined in all of the samples. Microbial richness was significantly increased after Ramadan according to observed OTU results (P=0.016). No significant difference was found in terms of Shannon index or phylogenetic diversity metrics of alpha diversity. Microbial community structure was significantly different between baseline and after Ramadan samples according to unweighted UniFrac analysis (P=0.025). LEfSe analysis revealed that Butyricicoccus, Bacteroides, Faecalibacterium, Roseburia, Allobaculum, Eubacterium, Dialister and Erysipelotrichi were significantly enriched genera after the end of Ramadan fasting. According to random forest analysis, the bacterial species most affected by the Ramadan fasting was Butyricicoccus pullicaecorum. Despite this is a pilot study with a limited sample size; our results clearly revealed that Ramadan fasting, which represents an intermittent fasting regime, leads to compositional changes in the gut microbiota.
This work aimed to identify and compare the bacterial patterns present in endometriotic lesions, eutopic endometrium and vaginal fluid from endometriosis patients with those found in the vaginal fluid and eutopic endometrium of control patients. Vaginal fluid, eutopic endometrium and endometriotic lesions were collected. DNA was extracted and the samples were analyzed to identify microbiome by high-throughput DNA sequencing of the 16S rRNA marker gene. Amplicon sequencing from vaginal fluid, eutopic endometrium and endometriotic lesion resulted in similar profiles of microorganisms, composed most abundantly by the genus Lactobacillus, Gardnerella, Streptococcus and Prevotella. No significant differences were found in the diversity analysis of microbiome profiles between control and endometriotic patients; however deep endometriotic lesions seems to present different bacterial composition, less predominant of Lactobacillus and with more abundant Alishewanella, Enterococcus and Pseudomonas.
Discriminating depressive episodes of bipolar disorder (BD) from major depressive disorder (MDD) is a major clinical challenge. Recently, gut microbiome alterations are implicated in these two mood disorders; however, little is known about the shared and distinct microbial characteristics in MDD versus BD. Here, using 16S ribosomal RNA (rRNA) gene sequencing, the microbial compositions of 165 subjects with MDD are compared with 217 BD, and 217 healthy controls (HCs). It is found that the microbial compositions are different between the three groups. Compared to HCs, MDD is characterized by altered covarying operational taxonomic units (OTUs) assigned to the Bacteroidaceae family, and BD shows disturbed covarying OTUs belonging to Lachnospiraceae, Prevotellaceae, and Ruminococcaceae families. Furthermore, a signature of 26 OTUs is identified that can distinguish patients with MDD from those with BD or HCs, with area under the curve (AUC) values ranging from 0.961 to 0.986 in discovery sets, and 0.702 to 0.741 in validation sets. Moreover, 4 of 26 microbial markers correlate with disease severity in MDD or BD. Together, distinct gut microbial compositions are identified in MDD compared to BD and HCs, and a novel marker panel is provided for distinguishing MDD from BD based on gut microbiome signatures.
Endometriosis (EMS) is a multifactorial disease that affects 10%-15% women of reproductive age and is associated with chronic pelvic pain and infertility. The pathogenesis of EMS has not been consistently explained until now. In this study, we involved 36 endometriosis patients and 14 control subjects who performed laparoscopic surgery due to gynecological benign tumor. The samples from lower third of vagina (CL), posterior vaginal fornix (CU), cervical mucus (CV), endometrium (ET) and peritoneal fluid (PF), were collected and sequenced by 16S rRNA amplicon. The continuous change of the microbiota distribution was identified along the reproductive tract. The flora in lower reproductive tract (CL, CU) were dominated by Lactobacillus. Significant difference of the community diversity began showing in the CV of EMS patients and gradually increased upward the reproductive tract. It indicates the microbiota in cervical samples is expected to be an indicator for the risk of EMS. This study also highlights the decreasing of Lactobacillus in vaginal flora and the increasing of signature Operational Taxonomic Units (OTUs) in transaction zone (CV) and upper reproductive tract (ET, PF) of EMS patients, which reflect the alteration of microbial community associated with EMS, participation of specific colonized bacteria in the EMS pathogenesis and relationship between microbiota and development of disease.
It is important to understand the consequences of pre-emptive antibiotic treatment in neonates, as disturbances in microbiota development during this key developmental time window might affect early and later life health outcomes. Despite increasing knowledge regarding the detrimental effect of antibiotics on the gut microbiota, limited research focussed on antibiotic treatment duration. We determined the effect of short and long amoxicillin/ceftazidime administration on gut microbiota development during the immediate postnatal life of preterm and term infants.
Faeces was collected from 63 (pre) term infants at postnatal weeks one, two, three, four and six. Infants received either no (control), short-term (ST) or long-term (LT) postpartum amoxicillin/ceftazidime treatment.
Compared to control infants, ST and LT infants' microbiota contained significantly higher abundance of Enterococcus during the first two postnatal weeks at the expense of Bifidobacterium and Streptococcus. Short and long antibiotic treatment both allowed for microbiota restoration within the first six postnatal weeks. However, Enterococcus and Bifidobacterium abundances were affected in fewer ST than LT infants.
Intravenous amoxicillin/ceftazidime administration affects intestinal microbiota composition by decreasing the relative abundance of Escherichia-Shigella and Streptococcus, while increasing the relative abundance of Enterococcus and Lactobacillus species during the first two postnatal weeks. Thriving of enterococci at the expense of bifidobacteria and streptococci should be considered as aspect of the cost-benefit determination for antibiotic prescription.
Very low-carbohydrate, high-fat ketogenic diets (KDs) induce a pronounced shift in metabolic fuel utilization that elevates circulating ketone bodies; however, the consequences of these compounds for host-microbiome interactions remain unknown. Here, we show that KDs alter the human and mouse gut microbiota in a manner distinct from high-fat diets (HFDs). Metagenomic and metabolomic analyses of stool samples from an 8-week inpatient study revealed marked shifts in gut microbial community structure and function during the KD. Gradient diet experiments in mice confirmed the unique impact of KDs relative to HFDs with a reproducible depletion of bifidobacteria. In vitro and in vivo experiments showed that ketone bodies selectively inhibited bifidobacterial growth. Finally, mono-colonizations and human microbiome transplantations into germ-free mice revealed that the KD-associated gut microbiota reduces the levels of intestinal pro-inflammatory Th17 cells. Together, these results highlight the importance of trans-kingdom chemical dialogs for mediating the host response to dietary interventions.
The mother's vaginal microbiota represents the first microbes to which a child is exposed when delivered vaginally. However, little is known about the composition and development of the vaginal microbiota during pregnancy and birth. Here, we analyzed the vaginal microbiota of 57 women in pregnancy week 24, 36 and at birth after rupture of membranes but before delivery, and further compared the composition with that of the gut and airways of the 1-week-old child. The vaginal community structure had dramatic changes in bacterial diversity and taxonomic distribution, yet carried an individual-specific signature. The relative abundance of most bacterial taxa increased stepwise from week 24 of pregnancy until birth, with a gradual decline of Lactobacillus. Mother-to-child vertical transfer, as suggested by sharing, was modest, with the strongest transfer being for Clostridiales followed by Lactobacillales and Enterobacteriales. In conclusion, late gestation is associated with an increase in maternal vaginal microbiota diversity, and vaginal bacteria at birth only modestly predict the composition of the neonatal microbiota.
Coronavirus disease 2019 (COVID-19) is an emerging serious global health problem. Gastrointestinal symptoms are common in COVID-19 patients, and severe acute respiratory syndrome coronavirus 2 RNA has been detected in stool specimens. However, the relationship between the gut microbiome and disease remains to be established.
We conducted a cross-sectional study of 30 patients with COVID-19, 24 patients with influenza A(H1N1), and 30 matched healthy controls (HCs) to identify differences in the gut microbiota by 16S ribosomal RNA gene V3-V4 region sequencing.
Compared with HCs, COVID-19 patients had significantly reduced bacterial diversity; a significantly higher relative abundance of opportunistic pathogens, such as Streptococcus, Rothia, Veillonella, and Actinomyces; and a lower relative abundance of beneficial symbionts. Five biomarkers showed high accuracy for distinguishing COVID-19 patients from HCs with an area under the curve (AUC) up to 0.89. Patients with H1N1 displayed lower diversity and different overall microbial composition compared with COVID-19 patients. Seven biomarkers were selected to distinguish the 2 cohorts (AUC = 0.94).
The gut microbial signature of patients with COVID-19 was different from that of H1N1 patients and HCs. Our study suggests the potential value of the gut microbiota as a diagnostic biomarker and therapeutic target for COVID-19, but further validation is needed.
General chronic periodontitis (GCP) is a bacterial inflammatory disease with complex pathology. Despite extensive studies published on the variation in the oral microbiota and metabolic profiles of GCP patients, information is lacking regarding the correlation between host-bacterial interactions and biochemical metabolism. This study aimed to analyze the oral microbiome, the oral metabolome, and the link between them and to identify potential molecules as useful biomarkers for predictive, preventive, and personalized medicine (PPPM) in GCP.
In this study, gingival crevicular fluid (GCF) samples were collected from patients with GCP (n = 30) and healthy controls (n = 28). The abundance of oral microbiota constituents was obtained by Illumina sequencing, and the relative level of metabolites was measured by gas chromatography-mass spectrometry. Full-mouth probing depth, clinical attachment loss, and bleeding on probing were recorded as indices of periodontal disease.
The relative abundances of 7 phyla and 82 genera differed significantly between the GCP and healthy groups. Seventeen differential metabolites involved in different metabolism pathways were selected based on variable influence on projection values (VIP > 1) and P values (P < 0.05). Through Spearman's correlation analysis, microorganisms, metabolites in GCF, and clinical data together showed a clear trend, and clinical data regarding periodontitis can be reflected in the shift of the oral microbial community and the change in metabolites in GCF. A combination of citramalic acid and N-carbamylglutamate yielded satisfactory accuracy (AUC = 0.876) for the predictive diagnosis of GCP.
Dysbiosis in the polymicrobial community structure and changes in metabolism could be mechanisms underlying periodontitis. The differential microorganisms and metabolites in GCF between periodontitis patients and healthy individuals are possibly biomarkers, pointing to a potential strategy for the prediction, diagnosis, prognosis, and management of personalized periodontal therapy.
Perturbation of vaginal microbiome of reproductive-age women influences all the phases of a woman's reproductive life. Although studies have shown that dynamic changes in vaginal microbiome can affect pregnancy, its role in secondary infertility (i.e., inability to become pregnant or to carry a pregnancy successfully after previous success in delivering a child) and in vitro fertilization (IVF) remains to be unraveled. To determine the vaginal microbiome in women undergoing in vitro fertilization and embryo transfer (IVF-ET) and investigate its potential correlations with hormone stimulation, we recruited 30 patients with secondary infertility and receiving IVF and 92 matched healthy women and analyzed their vaginal microbiome composition using 16S rRNA gene sequencing. Our results show that women suffering from infertility (infertile women) exhibit a significant decrease in microbiome diversity and richness compared with healthy women during the nonovulation period (follicular phase) (P < 0.01), whereas vaginal microbiome of healthy women reveals dramatic fluctuations during ovulation (P < 0.05). Interestingly, infertility patients show no change of the vaginal microbiome under conditions of gonadotropin-releasing hormone (GnRH) agonist and recombinant human chorionic gonadotropin (r-hCG) induction (P > 0.05). Moreover, our results indicate that infertile women show characteristic variations in vaginal microbiome, such as increased abundance of Atopobium, Aerococcus, and Bifidobacterium and decreased abundance of Lactobacillus and Leuconostoc IMPORTANCE The microbiome had been hypothesized to be involved in the physiology and pathophysiology of assisted reproduction before the first success in IVF, while the data supporting or refuting this hypothesis were less than conclusive. Thanks to sequencing data from the 16S rRNA subunit, we characterized the microbiome in the reproductive tract of infertile women, and we found that changes in the vaginal microbiome are related to female infertility. We also found that the characteristic microbiome bacteria are mainly members of several genera and that the vaginal microbiome of infertile women is not sensitive to hormonal changes during IVF. In conclusion, our report provides data that can be used for discovering the role of the vaginal microbiome in patients suffering from secondary infertility.
The study used shotgun metagenomic sequencing to compare the microbial communities of three ocular surface sites (meibum, eyelid skin, and conjunctiva) between patients with meibomian gland dysfunction (MGD) and healthy controls. The goal was to characterize taxonomic composition, resident pathogens, and functional and virulence features associated with MGD.
The cohort was 76 Chinese Han volunteers recruited at the Dry Eye Center of the Eye Hospital of Wenzhou Medical University, comprising 61 treatment-naive MGD patients and 15 healthy controls, sampled between April and September 2017. After quality control, 117 metagenome datasets were analyzed (58 meibum, 44 eyelid skin, and 15 conjunctiva), generated by whole-genome amplification and paired-end Illumina HiSeq shotgun sequencing (2 x 150 bp).
The MGD meibum microbiome had lower community richness (chao1) than controls while diversity indices (Shannon, Simpson) were similar, and its significant taxonomic changes were largely shared with eyelid skin but not conjunctiva. MGD meibum carried fewer pathogens on average than controls (mean 13 vs 36, p = 0.0014), yet Campylobacter coli, Campylobacter jejuni, and Enterococcus faecium were strongly enriched in MGD meibum (positive rates of about 57%, 51%, and 47% versus 0% in controls, with abundance more than 16-fold higher). Functional profiling showed increased carbohydrate and lipid metabolism enzymes, a microbial capacity to degrade benzoate, and an approximately fivefold increase in the type IV secretion system virulence factor (p = 0.017).
The authors conclude that MGD meibum contains distinct microbiota with stronger immune-evasive virulence, characterizing microbial community changes associated with MGD disease status. Because this is an observational case-control comparison, the results indicate association rather than causation, and the authors call for validation in larger and more geographically diverse populations.
Primary ovarian failure (POF) is defined as follicular failure in women of reproductive age. Although many factors are speculated to contribute to the occurrence of POF, the exact aetiology remains unclear. Moreover, alterations in the microbiome of patients with POF are poorly studied.
This study investigated the vaginal microbiota of 22 patients with POF and 29 healthy individuals. High-throughput Illumina MiSeq sequencing targeting the V3-V4 region of the 16S ribosomal RNA (rRNA) gene was used to evaluate the relationships between the vaginal flora and clinical characteristics of POF. Different from results of previous studies, we found that the diversity and richness of the vaginal flora of patients with POF was significantly different from those of healthy controls. Comparison of the vaginal flora of patients with POF with that of menopausal women revealed that the relative abundance of Lactobacillus was significantly reduced in the latter. A reduced abundance of Lactobacillus was furthermore associated with a lower pregnancy success rate. Of particular interest is that L. gallinarum especially appeared to be beneficially associated with reproductive-related indicators (FSH, E2, AMH, PRL) whilst L. iners appeared to have a detrimental effect. The result of the present study may enable the identification of microbiota associated with POF, however, further investigations of differences in the microbiota in the context of POF will enable a deeper understanding of the disease pathogenesis that involves modification of the vaginal microbiota.
The present study identified the microbiota associated with POF. Further investigations on the differences in the microbiota in the context of POF will improve our understanding of the pathogenesis of the disease which involves modification of the vaginal microbiota.
The characterization of the microbial population of many niches of the organism, as the gastrointestinal tract, is now possible thanks to the use of high-throughput DNA sequencing technique. Several studies in the companion animals field already investigated faecal microbiome in healthy or affected subjects, although the methodologies used in the different laboratories and the limited number of animals recruited in each experiment does not allow a straight comparison among published results. In the present study, we report data collected from several in house researches carried out in healthy dogs, with the aim to seek for a variability of microbial taxa in the faeces, caused by factors such as diet and sex. The database contains 340 samples from 132 dogs, collected serially during dietary intervention studies. The procedure of samples collection, storage, DNA extraction and sequencing, bioinformatic and statistical analysis followed a standardized pipeline. Microbial profiles of faecal samples have been analyzed applying dimensional reduction discriminant analysis followed by random forest analysis to the relative abundances of genera in the feces as variables. The results supported the responsiveness of microbiota at a genera taxonomic level to dietary factor and allowed to cluster dogs according this factor with high accuracy. Also sex factor clustered dogs, with castrated males and spayed females forming a separated group in comparison to intact dogs, strengthening the hypothesis of a bidirectional interaction between microbiota and endocrine status of the host. The findings of the present analysis are promising for a better comprehension of the mechanisms that regulate the connection of the microorganisms living the gastrointestinal tract with the diet and the host. This preliminary study deserves further investigation for the identification of the factors affecting faecal microbiome in dogs.
Increasing researches have confirmed the relationship between slow-transit constipation and gut microbiota dysbiosis. Many population and animal experiments have identified probiotics as effectors for the relief of constipation symptoms, but the specific mechanism remains unclear. In this intervention study, Lactobacillus rhamnosus strains isolated from five different sources were administered to mice with loperamide-induced constipation, and the impacts of these strains on constipation-related indicators were evaluated. All five strains of L. rhamnosus were found to improve constipation to various degrees. However, contrary to previous studies, the abilities of L. rhamnosus strains to improve constipation symptoms were not associated with the levels of short-chain fatty acids (SCFAs) in the colon. The effects of different strains of L. rhamnosus on constipation relief were associated with different aspects of the GI tract, including gastrointestinal regulatory peptides, neurotransmitters, neurotrophic factors, and gut microbiota. The findings of this study demonstrate that L. rhamnosus strains can alleviate constipation-related symptoms via different pathways independent of SCFAs regulation. This study yields a new perspective for clinical use of probiotics to better improve constipation symptoms, by combining strains with different mechanisms for alleviation of constipation.
This pilot study examined whether the gut microbiota is linked to unintentional weight loss in Parkinson's disease (PD). Researchers profiled gut microbiota composition using 16S rRNA gene sequencing and applied KEGG functional predictions to infer the metabolic pathways associated with the bacterial communities present. The aim was to compare microbiota profiles and predicted functions between PD patients who had experienced weight loss and those who had not.
The study compared three groups: PD patients with unintended weight loss (WL), PD patients with steady weight (non-WL, or NWL), and matched normal (non-PD) subjects. The abstract does not report specific sample sizes for any of the three groups. It is described as a pilot study, indicating a small, exploratory cohort rather than a large-scale trial.
Gut microbiota profiles differed between the weight-loss (WL) and steady-weight (NWL) PD patients. Predicted functional pathways also diverged: the WL group's microbiota was characterized by fatty acid biosynthesis pathways, while the NWL group's microbiota was characterized by inflammation-related pathways. These findings suggest that distinct microbial functional signatures accompany different weight trajectories in PD.
The findings suggest the gut microbiota may actively participate in the weight changes observed in Parkinson's disease. This could occur through bacteria associated with weight gain and inflammation on one hand, or through bacteria linked to energy expenditure on the other. If confirmed in larger studies, gut microbiota profiling could help identify PD patients at risk of unintentional weight loss and point toward microbiome-targeted strategies to address it.
This study characterized alterations in the gut microbiome associated with chronic kidney disease (CKD). The researchers analyzed fecal samples to compare microbial diversity, community composition, and predicted microbial functions between CKD patients and healthy controls. They also constructed and validated diagnostic classifiers for CKD based on microbial markers using a random forest model, and examined relationships between specific taxa, disease progression, and clinical indicators.
A total of 520 fecal samples were collected from different regions of China. The discovery and comparison cohort included 110 patients with CKD and 210 healthy controls (HC). The classifier was further tested in a validation cohort of 49 CKD cases versus 63 HC, and in an extra diagnosis cohort from Hangzhou.
Gut microbial diversity was significantly decreased in CKD patients compared with healthy controls, and the overall microbial community composition was distinctly different between groups. The genera Klebsiella and Enterobacteriaceae were enriched in CKD, while Blautia and Roseburia were reduced. Fifty predicted microbial functions, including tryptophan and phenylalanine metabolism, increased in CKD, while 36 functions, including arginine and proline metabolism, decreased. A five-marker microbial classifier achieved an area under the curve (AUC) of 0.9887 in the discovery cohort, 0.9512 in the validation cohort, and 0.8986 in the extra Hangzhou diagnosis cohort, and Thalassospira and Akkermansia increased with CKD progression.
These findings indicate that CKD is associated with a distinct, less diverse gut microbial community and altered amino acid metabolism pathways. The high diagnostic accuracy of the identified microbial markers across discovery, validation, and independent cohorts suggests gut microbiome signatures could serve as a non-invasive tool for CKD detection. The correlation between specific taxa and clinical indicators, along with taxa that shift with disease progression, points to the gut microbiome as a potential avenue for monitoring CKD severity.
This study examined how HIV infection and men who have sex with men (MSM) status are each associated with changes in the gut microbiome. The researchers conducted a meta-analysis of 16S rRNA gene amplicon sequencing data related to HIV/AIDS. They evaluated alpha diversity, beta diversity, differentially enriched bacterial genera and species, and KEGG functional pathways to identify consistent patterns across studies.
The meta-analysis screened 12 published studies from the NCBI and EBI databases, six of which contained data relevant to MSM status. The HIV analysis included 1,288 gut microbiome samples, comprising 744 HIV-positive individuals and 544 HIV-negative individuals. The MSM analysis included 632 samples, comprising 328 MSM and 304 non-MSM individuals.
HIV-positive status was associated with decreased alpha diversity of the gut microbiome compared to HIV-negative status. MSM status was identified as an important factor affecting the gut microbiome independent of HIV infection status. The abstract does not provide the specific differentially enriched genera, species, or KEGG pathway results before being cut off, so those details cannot be reported here.
By pooling multiple studies, this meta-analysis helps clarify a consistent pattern of gut microbiome change associated with HIV infection, namely reduced alpha diversity. Recognizing MSM status as an independent influencing factor suggests that future gut microbiome research on HIV must account for sexual orientation as a confounding variable rather than attributing all differences to HIV infection itself. This distinction could improve the design and interpretation of future microbiome studies in HIV populations.
The intestinal bacterial flora of febrile neutropenic patients has been found to be significantly diverse. However, there are few reports of alterations of in adult acute myeloid leukemia (AML) patients. Stool samples of each treatment-naïve AML patient were collected the day before initiation of induction chemotherapy (pretreatment), on the first date of neutropenic fever and first date of bone marrow recovery. Bacterial DNA was extracted from stool samples and bacterial 16s ribosomal RNA genes were sequenced by next-generation sequencing. Relative abundance, overall richness, Shannon's diversity index and Simpson's diversity index were calculated. No antimicrobial prophylaxis was in placed in all participants. Ten cases of AML patients (4 male and 6 female) were included with a median age of 39 years (range: 19-49) and all of patients developed febrile neutropenia. Firmicutes dominated during the period of neutropenic fever, subsequently declining after bone marrow recovery a pattern in contrast to that shown by Bacteroidetes and Proteobacteria. Enterococcus was more abundant in the febrile neutropenia period compared to pretreatment (mean difference +20.2; p < 0.0001) while Escherichia notably declined during the same period (mean difference -11.2; p = 0.0064). At the operational taxonomic unit (OTU) level, there was a significantly higher level of overall richness in the pretreatment period than in the febrile neutropenic episode (mean OTU of 203.1 vs. 131.7; p = 0.012). Both of the diversity indexes of Shannon and Simpson showed a significant decrease during the febrile neutropenic period. Adult AML patients with a first episode of febrile neutropenia after initial intensive chemotherapy demonstrated a significant decrease in gut microbiota diversity and the level of diversity remained constant despite recovery of bone marrow.
Postpartum depressive disorder (PPD) is a unique subtype of major depressive disorder and a substantial contributor to maternal morbidity and mortality. However, the pathogenesis of PPD has still remained elusive, and it may associate with genetic and environmental factors. Gut microbiota has already been proved to be associated with depression; however, a limited number of studies have concentrated on PPD. The present study aimed to explore the potential correlations between gut microbiota and PPD. In this study, 57 participants were enrolled, in which fecal samples of 28 patients with PPD and 16 healthy controls (HCs) were collected and then analyzed by high-throughput sequencing of the 16S ribosomal RNA (rRNA) gene. The results showed that diversity and composition of gut microbial communities were partly different between PPD patients and HCs. The relative abundance of Firmicutes phyla was lower in PPD patients. The levels of several predominant genera were significantly different between PPD patients and HCs. More importantly, the PPD patients experienced reduced levels of Faecalibacterium, Phascolarctobacterium, Butyricicoccus, and Lachnospiraceae, as well as increased levels of Enterobacteriaceae family. In addition, a correlation was observed between levels of Phascolarctobacterium, Lachnospiraceae, Faecalibacterium, and Tyzzerella.3 and the severity of depressive symptoms. Various kinds of bacteria, such as Lachnospiraceae and Faecalibacterium, were found to be associated with levels of sex hormones. This study indicated the correlation between gut microbiota and PPD, and gut microbiota-based biomarkers may be helpful for the diagnosis and treatment of PPD patients. However, further studies need to be conducted to clarify the cause-effect relationship between PPD patients and gut microbiota and to highlight the suitability of gut microbiome as a biomarker.
This study characterized the gut and genital microbial ecosystems of wild vervet monkeys naturally infected with simian immunodeficiency virus (SIV). Researchers profiled fecal, rectal, vaginal, and penile microbiomes to examine shifts in microbial diversity, composition, and functionality during natural SIV infection. Unlike HIV-infected humans, SIV-infected vervet monkeys do not experience gut dysfunction, microbial translocation, or chronic immune activation, so the study aimed to describe this nonprogressing host-pathogen relationship at the microbiome level for the first time.
The subjects were wild vervet monkeys from populations across diverse locations in South Africa that were heavily infected with SIV. Fecal, rectal, vaginal, and penile samples were collected from these free-ranging animals rather than from a laboratory cohort. The abstract indicates the population varied by geographic site, age, and sex, all of which were examined as factors affecting the microbiome.
Geographic site, age, and sex all affected the vervet microbiome across different body sites. The fecal microbiome showed marked stratification into three enterotypes, and the vaginal microbiome stratified into two vagitypes, each predicted to be functionally distinct within its respective body site. External bioclimatic factors, biome type, and environmental temperature also influenced the microbiome locally, indicating that environment plays a substantial role alongside host factors in shaping microbial community structure.
By characterizing the gut and genital microbiome of a natural, nonprogressing SIV host, this study provides a comparative framework for understanding why vervet monkeys avoid the gut dysfunction, microbial translocation, and immune activation seen in HIV-infected humans. The identification of distinct, functionally stratified enterotypes and vagitypes suggests that microbiome composition and function, not just viral dynamics, may contribute to disease outcome in lentivirus infection. These findings support further investigation into host, environmental, and microbial factors that distinguish nonpathogenic SIV infection from progressive HIV disease in humans.
Background: Offspring of mothers with gestational diabetes mellitus (GDM) have increased risk of developing metabolic disorders as they grow up. Microbial colonization of the newborn gut and environmental exposures affecting the configuration of the gut microbiota during infancy have been linked to increased risk of developing disease during childhood and adulthood. In a convenience sample, we examined whether the intestinal tract of children born to mothers with GDM is differentially colonized in early life compared to offspring of mothers with normal gestational glucose regulation. Secondly, we examined whether any such difference persists during infancy, thus potentially conferring increased risk of developing metabolic disease later in life. Methods: Fecal samples were collected from children of mothers with (n = 43) and without GDM (n = 82) during the first week of life and again at an average age of 9 months. The gut microbiota was characterized by 16S rRNA gene amplicon sequencing (V1-V2). Differences in diversity and composition according to maternal GDM status were assessed, addressing potential confounding by mode of delivery, perinatal antibiotics treatment, feeding and infant sex. Results: Children of mothers with GDM were featured by a differential composition of the gut microbiota, both during the first week of life and at 9 months, at higher taxonomic and OTU levels. Sixteen and 15 OTUs were differentially abundant after correction for multiple testing during the first week of life and at 9 months, respectively. Two OTUs remained differentially abundant after adjustment for potential confounders both during the first week of life and at 9 months. Richness (OTU) was decreased in neonates born to mothers with GDM; however, at 9 months no difference in richness was observed. There was no difference in Shannon's diversity or Pielou's evenness at any timepoint. Longitudinally, we detected differential changes in the gut microbiota composition from birth to infancy according to GDM status. Conclusion: Differences in glycaemic regulation in late pregnancy is linked with relatively modest variation in the gut microbiota composition of the offspring during the first week of life and 9 months after birth.
Background: Diabetes mellitus (DM) has become one of the most common chronic metabolic diseases worldwide. Due to the increasing prevalence and various complications, diabetes brings about a huge financial burden to DM patients. Nowadays, more and more studies reveal the relationship between diseases and gut microbial community. We aimed to explore the alteration in composition and function of the gut microbiome in T2DM patients. Methods: A total of 137 patients with diabetes and 179 age- and gender-matched healthy controls selected from the healthy people sample center in the First Affiliated Hospital of Zhengzhou University were divided into the DM group and the Con group, respectively. We collected their venous blood for laboratory tests and stool samples for 16S rRNA sequencing. The comparison between the two groups including both composition and function of the gut microbiome is presented. Results: We found that the α-diversity of bacterial taxa in the DM group had an evident decrease compared to that in the Con group. At the phylum level, the DM group had an obvious decrease of Bacteroidetes and a marked increase of Proteobacteria, Actinobacteria, and Verrucomicrobia. At the genus level, Bacteroides and Prevotella decreased the most while Escherichia-Shigella, Lachnospiraceae_incertae_sedis, Subdoligranulum, Enterococcus, and Klebsiella had different degrees of expansion in the DM group. The ROC based on 246 optimum OTUs had very high test efficiency with an AUC of 92.25% in the training set and 90.48% in the test set. As for prediction of metabolic function, the gut microbiome of DM patients was predicted to be more active in environmental information processing and human diseases but less in metabolism. Conclusion: We observed alteration of composition and function of the gut microbiome in the DM group. These changes may provide a new treatment strategy for DM patients and new research targets.
Background: Cervical cancer is reportedly caused by the synergistic effects of persistent high-risk human papillomavirus (HPV) infection. Cervical microbiota represent a unique and dynamically changing microecological system that is directly exposed to the vagina. The relationship between HPV and the composition of the cervical microbiome has long been a primary focus of research. Methods: To determine the specific differential florae throughout the process of cervical cancer development, in the present study, 16S rRNA sequencing was combined with KEGG pathway enrichment analysis to analyse five groups of cervical scraping samples with increasing durations of HPV infection and cervical intraepithelial neoplasia pathological classification. Results: The findings revealed that decreasing levels of probiotics, including Shuttleworthia, Prevotella, Lactobacillus, and Sneathia, and increasing levels of pathogenic bacteria, including Dispar, Streptococcus, and Faecalibacterium prausnitzii, could be the direct result of early HPV infection. Other pathogenic bacteria, such as Bifidobacteriaceae, might represent key factors in cancer progression. Additionally, KEGG pathway enrichment analysis indicated that HPV infection directly inhibits multiple pathways, including those of sporulation, porphyrin and chlorophyll metabolism, arginine and proline metabolism, isoquinoline alkaloid biosynthesis, and ansamycin biosynthesis, which may lead to the development of early symptoms of cervical cancer. Biomarkers were predicted based on operational taxonomic unit (OTU) abundance data, and OTU851726 and OTU715913 were undoubtedly the best potential indicators of cervical cancer. Conclusions: The findings of the present study could assist with the development of a guideline for screening new clinical drugs for cervical cancer.
Gut tryptophan (Trp) metabolites are produced by microbiota and/or host metabolism. Some of them have been proven to promote or inhibit colorectal cancer (CRC) in vitro and animal models. We hypothesized that there is an alteration of gut Trp metabolism mediated by microbiota and that it might be involved in the pathogenesis of cancer in patients with CRC. To investigate the features of Trp metabolism in CRC and the correlation between fecal Trp metabolites and gut microbiota.
Seventy-nine patients with colorectal neoplastic lesions (33 with colon adenoma and 46 with sporadic CRC) and 38 healthy controls (HCs) meeting the inclusion and exclusion criteria were included in the study. Their demographic and clinical features were collected. Fecal Trp, kynurenine (KYN), and indoles (metabolites of Trp metabolized by gut microbiota) were examined by ultraperformance liquid chromatography coupled to tandem mass spectrometry. Gut barrier marker and indoleamine 2,3-dioxygenase 1 (IDO1) mRNA were analyzed by quantitative real-time polymerase chain reaction. Zonula occludens-1 (ZO-1) protein expression was analyzed by immunohistochemistry. The gut microbiota was detected by 16S ribosomal RNA gene sequencing. Correlations between fecal metabolites and other parameters were examined in all patients.
The absolute concentration of KYN [1.51 (0.70, 3.46) nmol/g vs 0.81 (0.64, 1.57) nmol/g, P = 0.036] and the ratio of KYN to Trp [7.39 (4.12, 11.72) × 10-3 vs 5.23 (1.86, 7.99) × 10-3, P = 0.032] were increased in the feces of patients with CRC compared to HCs, while the indoles to Trp ratio was decreased [1.34 (0.70, 2.63) vs 2.46 (1.25, 4.10), P = 0.029]. The relative ZO-1 mRNA levels in patients with CRC (0.27 ± 0.24) were significantly lower than those in HCs (1.00 ± 0.31) (P < 0.001), and the relative IDO1 mRNA levels in patients with CRC [1.65 (0.47-2.46)] were increased (P = 0.035). IDO1 mRNA levels were positively associated with the KYN/Trp ratio (r = 0.327, P = 0.003). ZO-1 mRNA and protein levels were positively correlated with the indoles/Trp ratio (P = 0.035 and P = 0.009, respectively). In addition, the genera Asaccharobacter (Actinobacteria) and Parabacteroides (Bacteroidetes), and members of the phylum Firmicutes (Clostridium XlVb, Fusicatenibacter, Anaerofilum, and Anaerostipes) decreased in CRC and exhibited a positive correlation with indoles in all subjects.
Alteration of fecal Trp metabolism mediated by microbiota is associated with intestinal barrier function and tissue Trp metabolism, and may be involved in the pathogenesis of CRC.
Increasing evidence suggests that gut dysbiosis plays vital roles in a variety of gut-brain disorders, such as Alzheimer's disease (AD). However, alterations of the gut microbiota as well as their correlations with cognitive scores and host immunity have remained unclear in well-controlled trials on Chinese AD patients. In this study, samples from 100 AD patients, and 71 age- and gender-matched, cognitively normal controls were obtained to explore the structural and functional alterations of the fecal microbiota targeting the V3-V4 region of the 16S rRNA gene by MiSeq sequencing, and to analyze their associations with clinical characteristics. Our data demonstrated a remarkably reduction in the bacterial diversity and alterations in the taxonomic composition of the fecal microbiota of the AD patients. Interestingly, the abundant butyrate-producing genera such as Faecalibacterium decreased significantly, where this was positively correlated with such clinical indicators as the MMSE, WAIS, and Barthel scores in the AD patients. On the contrary, abundant lactate-producing genera, such as Bifidobacterium, increased prominently, and were inversely correlated with these indicators. This shift in the gut dysbiosis of the microbiota, from being butyrate producers to lactate producers, contributed to immune disturbances in the host that could be used as non-invasive biomarkers to distinguish the controls from the AD patients. Moreover, several predicted functional modules, including the biosynthesis and the metabolism of fatty acids, that were altered in the microbiota of the AD patients could be utilized by the bacteria to produce immunomodulatory metabolites. Our study established the structural and functional dysbiosis of fecal microbiota in AD patients, and the results suggest the potential for use of gut bacteria for the early, non-invasive diagnosis of AD, personalized treatment, and the development of tailor-made probiotics designed for Chinese AD patients.
The ongoing global pandemic of COVID-19 disease, which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), mainly infect lung epithelial cells, and spread mainly through respiratory droplets. However, recent studies showed potential intestinal infection of SARS-CoV-2, implicated the possibility that the intestinal infection of SARS-CoV-2 may correlate with the dysbiosis of gut microbiota, as well as the severity of COVID-19 symptoms. Here, we investigated the alteration of the gut microbiota in COVID-19 patients, as well as analyzed the correlation between the altered microbes and the levels of intestinal inflammatory cytokine IL-18, which was reported to be elevated in the serum of in COVID-19 patients. Comparing with healthy controls or seasonal flu patients, the gut microbiota showed significantly reduced diversity, with increased opportunistic pathogens in COVID-19 patients. Also, IL-18 level was higher in the fecal samples of COVID-19 patients than in those of either healthy controls or seasonal flu patients. Moreover, the IL-18 levels were even higher in the fecal supernatants obtained from COVID-19 patients that tested positive for SARS-CoV-2 RNA than those that tested negative in fecal samples. These results indicate that changes in gut microbiota composition might contribute to SARS-CoV-2-induced production of inflammatory cytokines in the intestine and potentially also to the onset of a cytokine storm.
Posttransplant diarrhea is associated with kidney allograft failure and death, but its etiology remains unknown in the majority of cases. Because altered gut microbial ecology is a potential basis for diarrhea, we investigated whether posttransplant diarrhea is associated with gut dysbiosis. We enrolled 71 kidney allograft recipients for serial fecal specimen collections in the first 3 months of transplantation and profiled the gut microbiota using 16S ribosomal RNA (rRNA) gene V4-V5 deep sequencing. The Shannon diversity index was significantly lower in 28 diarrheal fecal specimens from 25 recipients with posttransplant diarrhea than in 112 fecal specimens from 46 recipients without posttransplant diarrhea. We found a lower relative abundance of 13 commensal genera (Benjamini-Hochberg adjusted P ≤ .15) in the diarrheal fecal specimens including the same 4 genera identified in our prior study. The 28 diarrheal fecal specimens were also evaluated by a multiplexed polymerase chain reaction (PCR) assay for 22 bacterial, viral, and protozoan gastrointestinal pathogens, and 26 specimens were negative for infectious etiologies. Using PICRUSt (Phylogenetic Investigation of Communities by Reconstruction of Unobserved States) to predict metagenomic functions, we found that diarrheal fecal specimens had a lower abundance of metabolic genes. Our findings suggest that posttransplant diarrhea is not associated with common infectious diarrheal pathogens but with a gut dysbiosis.
This study examined how the composition of the human gut microbiota relates to age, sex, and stool consistency in healthy adults. Researchers analyzed fecal samples to characterize the gut microbiome and compared microbial community structure and diversity across demographic groups. They also assessed stool consistency using the Bristol stool scale (BSS) and tested its association with microbial composition. The investigation aimed to fill a gap, since sex-related and stool-consistency-related differences in gut microbiota had not been fully characterized previously.
The study enrolled 277 healthy Japanese subjects ranging in age from 20 to 89 years. Fecal samples were collected from this cohort to profile the gut microbiome. Both sexes were represented, allowing comparisons of microbial structure between males and females and across different age groups.
Overall microbial diversity (alpha-diversity) did not differ significantly by sex or by age group, but the underlying microbial community structure did differ significantly between males and females. Prevotella, Megamonas, Fusobacterium, and Megasphaera were significantly increased in males, while Bifidobacterium, Ruminococcus, and Akkermansia were significantly increased in females. Stool consistency also varied by sex: hard stools (BSS types 1 and 2) were more common in females, loose stools (BSS type 6) were more common in males, and no younger male had hard stool types 1 or 2. Fusobacterium levels in males were significantly higher among those with loose stool consistency.
These findings suggest that sex and stool consistency, rather than age or overall microbial diversity, are meaningfully linked to variation in gut microbial composition in healthy adults. The association between specific genera, such as Fusobacterium, and stool consistency indicates that bowel habit should be considered as a variable in microbiome research. This has implications for study design, since failing to account for sex and stool consistency could confound comparisons of gut microbiota across populations or in disease-association studies.
This study examined whether commensal intestinal bacteria from human infants can regulate allergic responses to food. Researchers colonized germ-free mice with fecal bacteria from either healthy infants or infants with cow's milk allergy (CMA). They then compared the mice's susceptibility to anaphylactic reactions against a cow's milk allergen, along with differences in bacterial composition and ileal gene expression between the two groups.
The human component involved fecal samples from healthy infants and infants diagnosed with cow's milk allergy, used as donor material for colonization. The abstract does not give an exact number of infant donors. The bulk of the experimental work was carried out in germ-free mice colonized with these human-derived bacterial communities.
Mice colonized with bacteria from healthy infants were protected against anaphylactic responses to a cow's milk allergen, while mice colonized with bacteria from CMA infants were not. Bacterial composition clearly separated the healthy and CMA groups in both the original infant donors and the colonized mice. The two groups of colonized mice also showed distinct ileal epithelial transcriptome signatures, and correlating bacterial taxa with these gene expression changes identified the clostridial species Anaerostipes caccae as linked to protection against the allergic response.
The findings show that specific intestinal bacteria, rather than the microbiome in general, are critical for regulating allergic responses to food in early life. Identifying Anaerostipes caccae as a protective species suggests a concrete, testable target for interventions aimed at preventing or treating food allergy. This supports the broader hypothesis that early-life disruptions to gut bacterial communities, from factors such as antibiotic use, diet, Caesarean birth, or formula feeding, may contribute to the rising prevalence of food allergy.
This study examined how daily consumption of orange juice from two Citrus sinensis cv. cultivars, Cara Cara and Bahia, affects the gut microbiota and faecal metabolome. Researchers used a randomized crossover design comparing each juice against an isocaloric control drink. Faecal samples were analyzed with an integrated meta-omics approach, combining 16S rRNA pyrosequencing of microbial operational taxonomic units (OTUs) with untargeted metabolomics based on 1H NMR spectroscopy. Samples were collected at baseline and after one week of each intervention to capture short-term shifts in microbial composition and metabolite output.
The abstract describes healthy subjects who consumed 500 mL per day of either Cara Cara orange juice, Bahia orange juice, or an isocaloric control drink in a crossover design. No specific sample size, age range, or other demographic details are given in the abstract. The population can be described only as healthy adult volunteers participating in a controlled dietary intervention trial.
Orange juice intake increased the abundance of a network of Clostridia OTUs drawn from the Mogibacteriaceae, Tissierellaceae, Veillonellaceae, Odoribacteraceae, and Ruminococcaceae families. The specific members of this network responded differently depending on whether subjects drank Cara Cara or Bahia juice, indicating cultivar-specific microbial effects. Metabolomic analysis also identified a core set of six faecal metabolites, inositol, choline, lysine, arginine, urocanic acid, and formate, that rose significantly more after Cara Cara consumption than after Bahia consumption.
The findings suggest that even closely related citrus cultivars can exert distinct effects on gut microbial communities and their metabolic output, meaning food source and variety may matter for microbiome-targeted dietary strategies. The consistent rise in specific Clostridia taxa points to a reproducible short-term dietary effect on the gut ecosystem worth further mechanistic study. The identified metabolite shifts offer candidate biomarkers for tracking individualized responses to citrus juice intake in future microbiome research.
The aim of the present study was to investigate the effects of prebiotics (containing fructooligosaccharides, xylooligosaccharides, polydextrose, and resistant dextrin) intake on immune function and intestinal microbiota structure in perioperative patients with colorectal cancer (CRC).
A randomized, double-blind, no-treatment parallel control clinical trial involving 140 perioperative patients (90 men and 50 women, aged 40-75 y) with CRC was performed. Patients were randomly divided into two groups: an intervention group (prebiotic group, n = 70) that received prebiotic supplementation of 30 g/d for 7 d, and a control group (non-prebiotic group, n = 70) that received no prebiotic supplementation. The nutritional and immunologic indices were evaluated for both groups before and after operation and analyzed against baseline values. Moreover, fecal samples were collected from 40 patients randomly chosen from the two groups to study intestinal microbiota, which was analyzed by sequencing the V3-V4 region of 16S ribosomal DNA using the Illumina (San Diego, CA) MiSeq (PE 2 × 300 bp) platform.
Oral intake of prebiotics produced significant effects on immunologic indices in both the preoperative and postoperative periods, but the patterns of effects were different. In the preoperative period, prebiotics increased serum levels of immunoglobulin G (IgG; P = 0.02), IgM (P = 0.00), and transferrin (P = 0.027; all P < 0.05). In the postoperative period, enhanced levels of IgG (P = 0.003), IgA (P = 0.007), suppressor/cytotoxic T cells (CD3+CD8+; P = 0.043), and total B lymphocytes (CD19+; P = 0.012) were identified in the prebiotic group (all P < 0.05). The differences in the intestinal microbiota at the phylum level were not statistically significant between the intervention and control groups (P > 0.05). At the genus level, prebiotics increased the abundance of Bifidobacterium (P = 0.017) and Enterococcus (P = 0.02; both P < 0.05) but decreased the abundance of Bacteroides (P = 0.04) in the preoperative period (all P < 0.05). In the postoperative period, the abundance of Bacteroides (P = 0.04) was decreased, but the abundance of Enterococcus (P = 0.00), Bacillus (P = 0.01), Lactococcus (P = 0.00), and Streptococcus (P = 0.037) increased in the non-prebiotic group (all P < 0.05); however, no significant change was identified in the abundance of Enterococcus (P = 0.56), Lactococcus (P = 0.07), and Streptococcus (P = 0.56) as a result of prebiotic intervention in this period (all P > 0.05). The abundance of Escherichia-Shigella was increased after prebiotic intake in the postoperative period (P = 0.014, P < 0.05). There was a notable trend of decline in the abundance of intestinal microbiota from preoperative to postoperative in the non-prebiotic group.
Prebiotic intake is recommended to improve serum immunologic indicators in patients with CRC 7 d before operation. Prebiotics improved the abundance of four commensal microbiota containing opportunistic pathogens in patients with CRC. Surgical stress decreased the abundance of most intestinal microbiota in the intestinal tract but increased the abundance of some opportunistic pathogens and commensal microbiota. Bacteroides is a relevant bacterial species for further research on the mechanism of prebiotics.
New microbiome sequencing technologies provide novel information about the potential interactions among intestinal microorganisms and the host in some neuropathologies as autism spectrum disorders (ASD). The microbiota⁻gut⁻brain axis is an emerging aspect in the generation of autistic behaviors; evidence from animal models suggests that intestinal microbial shifts may produce changes fitting the clinical picture of autism. The aim of the present study was to evaluate the fecal metagenomic profiles in children with ASD and compare them with healthy participants. This comparison allows us to ascertain how mental regression (an important variable in ASD) could influence the intestinal microbiota profile. For this reason, a subclassification in children with ASD by mental regression (AMR) and no mental regression (ANMR) phenotype was performed. The present report was a descriptive observational study. Forty-eight children aged 2⁻6 years with ASD were included: 30 with ANMR and 18 with AMR. In addition, a control group of 57 normally developing children was selected and matched to the ASD group by sex and age. Fecal samples were analyzed with a metagenomic approach using a next-generation sequencing platform. Several differences between children with ASD, compared with the healthy group, were detected. Namely, Actinobacteria and Proteobacteria at phylum level, as well as, Actinobacteria, Bacilli, Erysipelotrichi, and Gammaproteobacteria at class level were found at higher proportions in children with ASD. Additionally, Proteobacteria levels showed to be augmented exclusively in AMR children. Preliminary results, using a principal component analysis, showed differential patterns in children with ASD, ANMR and AMR, compared to healthy group, both for intestinal microbiota and food patterns. In this study, we report, higher levels of Actinobacteria, Proteobacteria and Bacilli, aside from Erysipelotrichi, and Gammaproteobacteria in children with ASD compared to healthy group. Furthermore, AMR children exhibited higher levels of Proteobacteria. Further analysis using these preliminary results and mixing metagenomic and other "omic" technologies are needed in larger cohorts of children with ASD to confirm these intestinal microbiota changes.
Early disruption of the microbial community may influence life-long health. Environmental toxicants can contaminate breast milk and the developing infant gut microbiome is directly exposed. We investigated whether environmental toxicants in breastmilk affect the composition and function of the infant gut microbiome at 1 month. We measured environmental toxicants in breastmilk, fecal short-chain fatty acids (SCFAs), and gut microbial composition from 16S rRNA gene amplicon sequencing using samples from 267 mother-child pairs in the Norwegian Microbiota Cohort (NoMIC). We tested 28 chemical exposures: polychlorinated biphenyls (PCBs), polybrominated flame retardants (PBDEs), per- and polyfluoroalkyl substances (PFASs), and organochlorine pesticides. We assessed chemical exposure and alpha diversity/SCFAs using elastic net regression modeling and generalized linear models, adjusting for confounders, and variation in beta diversity (UniFrac), taxa abundance (ANCOM), and predicted metagenomes (PiCRUSt) in low, medium, and high exposed groups.
PBDE-28 and the surfactant perfluorooctanesulfonic acid (PFOS) were associated with less microbiome diversity. Some sub-OTUs of Lactobacillus, an important genus in early life, were lower in abundance in samples from infants with relative "high" (> 80th percentile) vs. "low" (< 20th percentile) toxicant exposure in this cohort. Moreover, breast milk toxicants were associated with microbiome functionality, explaining up to 34% of variance in acetic and propionic SCFAs, essential signaling molecules. Per one standard deviation of exposure, PBDE-28 was associated with less propionic acid (- 24% [95% CI - 35% to - 14%] relative to the mean), and PCB-209 with less acetic acid (- 15% [95% CI - 29% to - 0.4%]). Conversely, PFOA and dioxin-like PCB-167 were associated with 61% (95% CI 35% to 87%) and 22% (95% CI 8% to 35%) more propionic and acetic acid, respectively.
Environmental toxicant exposure may influence infant gut microbial function during a critical developmental window. Future studies are needed to replicate these novel findings and investigate whether this has any impact on child health.
Substantial evidence indicates that gastric microbiota dysbiosis, immune system dysfunction especially immune escape are critical for gastric cancer (GC) occurrence and progression. As two important elements of tumor microenvironment (TME), the relationship between gastric microbiota and tumor-immune microenvironment is still unclear. Our present study aimed to explore the correlation between gastric mucosal microbiota in different microhabitats and its corresponding gastric immunosuppressive cells such as regulatory T cells (Tregs) and plasmacytoid dendritic cells (pDCs) in the TME. A cohort of 64 GC patients without preoperative chemotherapy was enrolled retrospectively, and 60 normal, 61 peritumoral and 59 tumoral tissues were obtained for gastric mucosal microbiota analysis and immunohistochemistry analysis. From different microhabitats, BDCA2+pDCs and Foxp3+Tregs were observed positively correlated, and increased in tumoral and peritumoral tissues compared to normal ones. The diversity, composition and function of gastric mucosal microbiota also changed more significantly in tumoral tissues than those in normal and peritumoral ones. With pearson's correlation analysis, we found that several non-abundant genera such as Stenotrophomonas and Selenomonas were positively correlated with BDCA2+pDCs and Foxp3+Tregs, respectively, while Comamonas and Gaiella were negatively correlated with BDCA2+pDCs and Foxp3+ Tregs, respectively. The increased BDCA2+pDCs and Foxp3+Tregs might be modulated by gastric mucosal microbiota, both participated in the immunosuppression microenvironment of GC, which might provide evidence to establish new strategies in antitumor therapy targeting on gastric microbiota.
Early establishment of the infant gut microbiome has been attributed to various environmental factors that may influence long-term health. The aim of this study was to determine the single and combined impacts of the delivery mode, feeding pattern and postnatal antibiotic exposure on the initial establishment of infant gut microbiome at 6 weeks postpartum. A cross-sectional study was conducted at a single center in China. Fecal samples were collected from 120 infants at 6 weeks postpartum. The V3-V4 regions of 16S rRNA gene were analyzed by Illumina sequencing, and clinical information was obtained from medical records and questionnaire survey. Compared with vaginally delivered infants, the gut microbial community structure of cesarean delivered infants were significantly different (P = 0.044), in parallel with the decreased relative abundance of Bifidobacterium (P = 0.028), which contrasts with the normal gut microbial establishment. Using the vaginally delivered and exclusively breastfed (VB) infants as a reference, the comparative analysis of cesarean delivered and exclusively breastfed (CB) infants with cesarean delivered and mixed-fed (CM) infants showed that both within- and between-group UniFrac distance were significantly smaller in CB infants (P < 0.001, P < 0.001). LEfSe analysis showed that the relative abundances of Enterococcus, Veillonella, and Faecalibacterium were significantly different between CB and CM infants, whereas the relative abundances of those genera in VB infants were close to those of CB infants, and distinct from those of CM infants. Additionally, no significant difference of microbial composition, alpha diversity, or community structure was observed between postnatal antibiotics exposed infants and unexposed infants. In summary, delivery mode had a significant impact on the infant gut microbial community structure and composition, and the gut microbiota was disturbed in infants delivered by cesarean section. However, our study showed that this disturbance of gut microbiota in cesarean delivered infants was partially restored by exclusive breastfeeding in comparison with mixed feeding. No distinct impact of postnatal antibiotic exposure on infant gut microbiome was found at 6 weeks of age.
Mother's own milk (MOM) is protective against gut microbiota alterations associated with necrotizing enterocolitis (NEC) and feeding intolerance among preterm infants. It is unclear whether this benefit is preserved with donor milk (DM) feeding. We aimed to compare microbiota development, growth, and feeding tolerance in very-low-birth-weight (VLBW) infants fed an exclusively human milk diet of primarily MOM or DM.
One hundred and twenty-five VLBW infants born at Texas Children's Hospital were enrolled and grouped into cohorts based on percentage of MOM and DM in enteral feeds. Feeds were fortified with DM-derived fortifier per unit protocol. Weekly stool samples were collected for 6 wk for microbiota analysis [16S ribosomal RNA (rRNA) sequencing]. A research nurse obtained weekly anthropometrics. Clinical outcomes were compared via Wilcoxon's rank-sum test and Fisher's exact test, as well as multivariate analysis.
The DM cohort (n = 43) received on average 14% mothers' milk compared with 91% for the MOM cohort (n = 74). Diversity of gut microbiota across all time points (n = 546) combined was increased in MOM infants (P < 0.001). By 4 and 6 wk of life, microbiota in MOM infants contained increased abundance of Bifidobacterium (P = 0.02) and Bacteroides (P = 0.04), whereas DM-fed infants had increased abundance of Staphylococcus (P = 0.02). MOM-fed infants experienced a 60% reduction in feeding intolerance (P = 0.03 by multivariate analysis) compared with DM-fed infants. MOM-fed infants had greater weight gain than DM-fed infants.
Compared with DM-fed infants, MOM-fed infants have increased gut microbial community diversity at the phylum and genus levels by 4 and 6 wk of life, as well as better feeding tolerance. MOM-fed infants had superior growth. The incidence of NEC and other gastrointestinal morbidity is low among VLBW infants fed an exclusively human milk diet including DM-derived fortifier. This trial was registered at clinicaltrials.gov as NCT02573779.
Acute leukemia (AL) patients undergoing intensive induction chemotherapy develop severe gut dysbiosis, placing them at heightened risk for infectious complications. Some AL patients will undergo "repeat therapy" (re-induction or salvage) due to persistent or relapsed disease. We hypothesized that prior injury to the microbiome during induction may influence dysbiosis patterns during repeat therapy. To test this hypothesis, we analyzed the bacterial microbiome profiles of thrice-weekly stool samples from 20 intensively treated AL patients (first induction: 13, repeat therapy: 7) by 16S rRNA sequencing. In mixed-effects modeling, repeat therapy was a significant predictor of Enterococcus expansion (P = 0.006), independently of antibiotic exposure, disease type, feeding mode, and week of chemotherapy. Bayesian analysis of longitudinal data demonstrated larger departures of microbial communities from the pre-chemotherapy baseline during repeat therapy compared to induction. This increased ecosystem instability during repeat therapy possibly impairs colonization resistance and increases vulnerability to Enterococcus outgrowth. Microbiota restoration therapies at the end of induction or before starting subsequent therapy warrant investigation.
Lung cancer (LC) is one of the most serious malignant tumors, which has the fastest growing morbidity and mortality worldwide. A role of the lung microbiota in LC pathogenesis has been analyzed, but a comparable role of the gut microbiota has not yet been investigated. In this study, the gut microbiota of 30 LC patients and 30 healthy controls were examined via next-generation sequencing of 16S rRNA and analyzed for diversity and biomarkers. We found that there was no decrease in significant microbial diversity (alpha diversity) in LC patients compared to controls (P observed = 0.1422), while the composition (beta diversity) differed significantly between patients and controls (phylum [stress = 0.153], class [stress = 0.16], order [stress = 0.146], family [stress = 0.153]). Controls had a higher abundance of the bacterial phylum Actinobacteria and genus Bifidobacterium, while patients with LC showed elevated levels of Enterococcus. These bacteria were found as possible biomarkers for LC. A decline of normal function of the gut microbiome in LC patients was also observed. These results provide the basic guidance for a systematic, multilayered assessment of the role of the gut microbiome in LC, which has a promising potential for early prevention and targeted intervention.
Background: Accumulating evidence suggests that the intestinal microbiome may dramatically affect the outcomes of hematopoietic stem cell transplant (HSCT) recipients. Providing 16S ribosomal RNA based microbiome characterization in a clinically actionable time frame is currently problematic. Thus, determination of microbial metabolites as surrogates for microbiome composition could offer practical biomarkers. Methods: Longitudinal fecal specimens (n = 451) were collected from 44 patients before HSCT through 100 days after transplantation, as well as 1-time samples from healthy volunteers (n = 18) as controls. Microbiota composition was determined using 16S ribosomal RNA V4 sequencing. Fecal indole and butyrate levels were determined using liquid chromatography tandem mass spectrometry. Results: Among HSCT recipients, both fecal indole and butyrate levels correlated with the Shannon diversity index at baseline (P = .02 and P = .002, respectively) and directly after transplantation (P = .006 and P < .001, respectively). Samples with high butyrate levels were enriched for Clostridiales, whereas samples containing high indole were also enriched for Bacteroidales. A lower Shannon diversity index at the time of engraftment was associated with increased incidence of acute intestinal graft-vs-host disease (iGVHD) (P = .02) and transplant-related deaths (P = .03). Although fecal metabolites were not associated with acute iGVHD or overall survival, patients contracting bloodstream infections within 30 days after transplantation had significantly lower levels of fecal butyrate (P = .03). Conclusions: Longitudinal analysis of fecal microbiome and metabolites after HSCT identified butyrate and indole as potential surrogate markers for microbial diversity and specific taxa. Further studies are needed to ascertain whether fecal metabolites can be used as biomarkers of acute iGVHD or bacteremia after HSCT.
The intestinal microbiota is a fundamental factor that broadly influences physiology. Thus, studies using transgenic animals should be designed to limit the confounding effects of microbiota variation between strains. Here, we report the impact on intestinal microbiota of co-housed versus F2-generation littermates, two commonly used techniques to standardize microbiota in animal models. Our results establish that while fecal microbiota is partially normalized by extended co-housing, mucosal communities associated with the proximal colon and terminal ileum remain stable and distinct. In contrast, strain inter-crossing to generate F2 littermates allows robust microbiota standardization in fecal, colon, and ileum sampling locations. Using reciprocal inter-crosses of P1 parents, we identify dissymmetry in F2 community structures caused by maternal transmission, in particular of the Verrucomicrobiaceae. Thus, F2 littermate animals from a unidirectional P1 cross should be used as a standard method to minimize the influence of the microbiota in genotype-phenotype studies.
This study investigated dysbiosis of the gut microbiota in Parkinson's disease (PD) patients from Central Italy. The researchers used 16s ribosomal RNA gene amplicon sequencing to characterize fecal microbiota composition. They also examined dietary and lifestyle data alongside clinical variables to identify confounders and predictors that might correlate with clinical phenotypes. The aim was to find potential microbiota-based correlates of PD status and severity.
The study included 152 fecal samples collected from 80 PD patients and 72 healthy controls. Patients were enrolled according to tight inclusion criteria, though the abstract does not specify the exact nature of those criteria. Age, sex, and weight loss were treated as confounding factors in the analysis, while PD status, age, Body Mass Index, cereal consumption, weight gain, and physical activity were treated as predictors.
Fecal levels of Lactobacillaceae, Enterobacteriaceae, and Enterococcaceae were significantly higher in PD patients than in healthy controls. Lachnospiraceae, by contrast, were significantly reduced in PD patients. Lower Lachnospiraceae and higher Enterobacteriaceae levels also correlated with increased disease severity, linking this specific bacterial family shift to clinical progression.
The findings reinforce the hypothesis that gut microbiota dysbiosis is associated with Parkinson's disease, with the Enterobacteriaceae family emerging as a marker that tracks with disease severity. This suggests dysbiosis is not just present in PD but may relate to how advanced the disease is in a given patient. The results support continued investigation of specific bacterial families, particularly Enterobacteriaceae and Lachnospiraceae, as potential biomarkers or targets tied to clinical phenotype in PD.
A comprehensive metabolomics-based approach to address the impact of specific gut microbiota on allergen sensitization for childhood rhinitis and asthma is still lacking.
Eighty-five children with rhinitis (n = 27) and with asthma (n = 34) and healthy controls (n = 24) were enrolled. Fecal metabolomic analysis with 1 H-nuclear magnetic resonance (NMR) spectroscopy and microbiome composition analysis by bacterial 16S rRNA sequencing were performed. An integrative analysis of their associations with allergen-specific IgE levels for allergic rhinitis and asthma was also assessed.
Amino acid, β-alanine, and butanoate were the predominant metabolic pathways in the gut. Among them, amino acid metabolism was negatively correlated with the phylum Firmicutes, which was significantly reduced in children with rhinitis and asthma. Levels of histidine and butyrate metabolites were significantly reduced in children with rhinitis (P = 0.029) and asthma (P = 0.009), respectively. In children with asthma, a reduction in butyrate-producing bacteria, including Faecalibacterium and Roseburia spp., and an increase in Clostridium spp. were negatively correlated with fecal amino acids and butyrate, respectively (P < 0.01). Increased Escherichia spp. accompanied by increased β-alanine and 4-hydroxybutyrate appeared to reduce butyrate production. Low fecal butyrate was significantly associated with increased total serum and mite allergen-specific IgE levels in children with asthma (P < 0.05).
A reduced fecal butyrate is associated with increased mite-specific IgE levels and the risk of asthma in early childhood. Fecal β-alanine could be a specific biomarker connecting the metabolic dysbiosis of gut microbiota, Clostridium and Escherichia spp., in childhood asthma.
Prenatal antibiotic exposure has been associated with an altered infant gut microbiome composition and higher risk of childhood obesity, but no studies have examined if prenatal antibiotics simultaneously alter the gut microbiome and adiposity in infants.
In this prospective study (Nurture: recruitment 2013-2015 in North Carolina, United States), we examined in 454 infants the association of prenatal antibiotic exposure (by any prenatal antibiotic exposure; by trimester of pregnancy; by number of courses; by type of antibiotics) with infant age- and sex-specific weight-for-length z score (WFL-z) and skinfold thicknesses (subscapular, triceps, abdominal) at 12 months of age. In a subsample, we also examined whether prenatal antibiotic exposure was associated with alterations in the infant gut microbiome at ages 3 and 12 months.
Compared to infants not exposed to prenatal antibiotics, infants who were exposed to any prenatal antibiotics had 0.21 (95% confidence interval [CI] 0.02, 0.41) higher WFL-z at 12 months, and 0.28 (95% CI 0.02, 0.55) higher WFL-z if they were exposed to antibiotics in the second trimester, after adjustment for potential confounders, birth weight, and gestational age. We also observed a dose-dependent association (P-value for trend = 0.006) with infants exposed to ≥ 3 courses having 0.41 (95% CI 0.13, 0.68) higher WFL-z at 12 months. After further adjustment for delivery method, only second-trimester antibiotic exposure remained associated with higher infant WFL-z (0.27, 95% CI 0.003, 0.54) and subscapular skinfold thickness (0.49 mm, 95% CI 0.11, 0.88) at 12 months. Infants exposed to second-trimester antibiotics versus not had differential abundance of 13 bacterial amplicon sequence variants (ASVs) at age 3 months and 17 ASVs at 12 months (false discovery rate adjusted P-value < 0.05).
Prenatal antibiotic exposure in the second trimester was associated with an altered infant gut microbiome composition at 3 and 12 months and with higher infant WFL-z and subscapular skinfold thickness at 12 months.
This study examined whether alterations in gut microbiome composition are linked to host cytokine responses in Parkinson's disease (PD). Researchers sequenced the V3-V4 region of the 16S ribosomal RNA gene from fecal samples to characterize gut microbiota communities. They then measured plasma concentrations of nine inflammatory cytokines (IL-1β, IL-2, IL-4, IL-6, IL-13, IL-18, GM-CSF, IFNγ, and TNFα) and analyzed relationships between microbiota composition, clinical characteristics, and cytokine levels.
The primary analysis included 80 Taiwanese patients with Parkinson's disease and 77 age and gender-matched controls. Diet and comorbidities were controlled for in the analyses. Findings on cytokine changes were then examined in a second, independent cohort of 120 PD patients and 120 controls.
Gut microbiota in PD patients differed from controls, with Verrucomicrobia, Mucispirillum, Porphyromonas, Lactobacillus, and Parabacteroides more abundant, while Prevotella was more abundant in controls. Bacteroides abundance was higher in the non-tremor PD subtype than the tremor subtype and correlated with motor symptom severity (UPDRS part III scores). Altered microbiota correlated with plasma IFNγ and TNFα, and the independent cohort confirmed significantly elevated plasma TNFα and IFNγ in PD patients compared to controls.
The findings support a link between gut microbiome alterations and immune activation in Parkinson's disease, suggesting that dysbiosis may contribute to neuroinflammation in the condition's pathogenesis. The correlation between specific bacterial taxa, cytokine levels, and motor symptom severity suggests the gut microbiome could serve as a biomarker of disease phenotype. These results point toward the gut-brain-immune axis as a potential target for future PD research and intervention.
Objectives: To explore the microbiome of the prostatic fluid in high prostate-specific antigen (PSA) patients. Patients and Methods: The microbiome profiles of prostatic fluid samples from 32 prostate cancer (PCa) patients and 27 non-PCa people were assessed. Microbiome analysis was assessed by massive 16S ribosomal RNA gene sequencing. Results: Compared with the NCA group, the microbial diversity was lower in the CA group. There were no specific microbial species in the CA group or NCA group. However, many species, such as those in the genera Alkaliphilus, Enterobacter, Lactococcus, Cronobacter, Carnobacterium, and Streptococcus, showed a significant difference between the CA group and NCA group. Conclusion: The prostate contains reduced bacteria, suggesting a possible pathophysiological correlation between the composition of the microbiome and PCa. Meanwhile, this study uncovered that the microbiome may be beneficial in maintaining the stability of the microenvironment of the prostate and provides interesting perspectives for the identification of novel biomarkers in high-PSA patients.
This study examined how the oral microbiome influences the development of oral squamous cell carcinoma (OSCC), the most common head and neck malignancy worldwide. Using 16S rRNA gene sequencing and metatranscriptomic analysis, researchers tracked longitudinal changes in oral microbiome composition and function in a 4-nitroquinoline-1-oxide (4-NQO)-induced mouse model of OSCC. The work compared gnotobiotic mice colonized with different oral microbiome inocula to mice exposed to 4-NQO without any microbiome present.
The subjects were gnotobiotic (germ-free) mice experimentally colonized with one of two oral microbiome inocula, one sourced from healthy mice and the other from mice bearing a 4-NQO-induced tumor. Controls consisted of mice exposed to 4-NQO but lacking any microbiome colonization. This was an animal model study, not a human cohort, designed to isolate the microbiome's contribution to tumorigenesis.
Mice colonized with an oral microbiome and exposed to 4-NQO developed more tumors and larger tumors than 4-NQO-exposed controls with no microbiome, indicating the microbiome actively promoted tumorigenesis rather than merely accompanying it. Tumorigenic samples showed an overall increase in microbial diversity compared to non-tumor, non-4-NQO-exposed samples. Despite variable community dynamics across groups, consistent patterns emerged during disease progression, including opposite abundance trends for Parabacteroides and Corynebacterium in the two groups inoculated with the OSCC-associated microbiome, with Parabacteroides decreasing in the control group.
The findings suggest the oral microbiome is not a passive bystander in OSCC but an active promoter of tumor initiation and growth, supporting a causal rather than merely correlative role for oral dysbiosis in this cancer. The divergent Parabacteroides and Corynebacterium dynamics point to specific taxa that could serve as markers of tumorigenic risk or as targets for future mechanistic study. Because the model used gnotobiotic mice with defined inocula, it offers a controlled system for further dissecting which microbial functions drive carcinogenesis in the oral cavity.
This study characterized the gut microbiome of the Yanomami, a semi-nomadic hunter-gatherer group in the Amazon rainforest, using shotgun metagenomic sequencing. Researchers compared the taxonomic composition and functional gene content of the Brazilian Yanomami gut microbiome against the Venezuelan Yanomami, other traditional Amazonian groups, and an urban-industrialized population. The goal was to identify taxonomic and functional biomarkers that distinguish these groups and to understand how traditional, non-industrialized lifestyles shape the gut microbiome.
The subjects were members of the Yanomami, the largest semi-nomadic hunter-gatherer group in the Americas, sampled from populations in Brazil and Venezuela. The study also drew on comparison groups consisting of other traditional Amazonian populations and an urban-industrialized group. The abstract does not give specific sample sizes or additional demographic details for these cohorts.
Distinct taxonomic biomarkers were identified for each South American traditional group studied, including separate signatures for the Brazilian and Venezuelan Yanomami. Broad functional categories did not strongly distinguish traditional groups from the urban-industrialized group, but when these categories were stratified into finer detail, clear segregation between groups emerged. The Brazilian Yanomami gut microbiome showed unique functional features, including a higher abundance of gene families related to regulation and cell signaling, motility and chemotaxis, and virulence, setting it apart from the other groups compared.
The findings suggest that even within a single traditional hunter-gatherer group, geography and local ecological niches can shape distinct gut microbiome taxonomic and functional profiles. This indicates that broad category-level functional comparisons may obscure meaningful differences between populations, and that finer-grained analysis is needed to capture true microbiome variation. These results contribute to a baseline understanding of non-industrialized human gut microbiomes that can inform how urbanization and lifestyle change affect microbiome structure and function.
Cigarette smoking is a common risk factor for diseases and cancers. Oral microbiota is also associated with diseases and cancers. However, little is known about the impact of cigarette smoking on the oral microbiota, especially among ethnic minority populations.
We investigated cigarette smoking in relationship with the oral microbiota in a large population of predominately low-income and African-American participants. Mouth rinse samples were collected from 1616 participants within the Southern Community Cohort Study, including 592 current-smokers, 477 former-smokers and 547 never-smokers. Oral microbiota was profiled by 16S ribosomal RNA gene deep sequencing.
Current-smokers showed a different overall microbial composition from former-smokers (p=6.62×10-7) and never-smokers (p=6.00×10-8). The two probiotic genera, Bifidobacterium and Lactobacillus, were enriched among current-smokers when compared with never-smokers, with Bonferroni-corrected p values (PBonferroni ) of 1.28×10-4 and 5.89×10-7, respectively. The phylum Actinobacteria was also enriched in current-smokers when compared with never-smokers, with a median relative abundance of 12.35% versus 9.36%, respectively, and with a PBonferroni =9.11×10-11. In contrast, the phylum Proteobacteria was depleted in current smokers (PBonferroni =5.57×10-13), with the relative abundance being almost three times that of never-smokers (7.22%) when compared with that of current-smokers (2.47%). Multiple taxa within these two phyla showed differences in abundance/prevalence between current-smokers and never-smokers at PBonferroni <0.05. The differences in the overall microbial composition and abundance/prevalence of most taxa were observed among both African-Americans and European-Americans. Meanwhile, such differences were not observed between former-smokers and never-smokers.
Smoking has strong impacts on oral microbial community, which was recovered after smoking cessation.
The Westernized diet has been associated with the pathogenesis of metabolic diseases, whereas a Korean diet has been reported to exert beneficial effects on health in several studies. However, the effects of Western and Korean diets on the gut microbiome and host metabolome are unclear. To examine the diet-specific effects on microbiome and metabolome, we conducted a randomized crossover clinical trial of typical Korean diet (TKD), typical American diet (TAD), and recommended American diet (RAD). The trial involved a 4-week consumption of an experimental diet followed by a 2-week interval before diet crossover. 16S rRNA sequencing analysis identified 16, 10, and 14 differential bacteria genera specific to TKD, RAD, and TAD, respectively. The Firmucutes-Bacteroidetes ratio was increased by TKD. Nuclear magnetic resonance metabolome profiling revealed that TKD enriched branched chain amino acid metabolism, whereas ketone body metabolism was evident in RAD and TAD. Microbiome and metabolome responses to the experimental diets varied with individual enterotypes. These findings provide evidence that the gut microbiome and host metabolome rapidly respond to different cultural diets. The findings will inform clarification of the diet-related communication networks of the gut microbiome and host metabolome in humans.
The aim of this prospective, two center study was to investigate the dynamics of the microbial changes in relation to the development of ulcerative oral mucositis in autologous SCT (autoSCT) recipients. Fifty-one patients were diagnosed with multiple myeloma and treated with high-dose melphalan followed by autoSCT. They were evaluated before, three times weekly during hospitalization, and three months after autoSCT. At each time point an oral rinse was collected and the presence or absence of ulcerative oral mucositis (UOM) was scored (WHO scale). Oral microbiome was determined by using 16S rRNA amplicon sequencing and fungal load by qPCR. Twenty patients (39%) developed UOM. The oral microbiome changed significantly after autoSCT and returned to pre-autoSCT composition after three months. However, changes in microbial diversity and similarity were more pronounced and rapid in patients who developed UOM compared to patients who did not. Already before autoSCT, different taxa discriminated between the 2 groups, suggesting microbially-driven risk factors. Samples with high fungal load (>0.1%) had a significantly different microbial profile from samples without fungi. In conclusion, autoSCT induced significant and reversible changes in the oral microbiome, while patients who did not develop ulcerative oral mucositis had a more resilient microbial ecosystem.
This study examined the composition of gut microbiota in pediatric patients with pulmonary tuberculosis (PTB) compared with healthy controls. Researchers collected fecal samples upon admission and analyzed microbial DNA using 16SrDNA sequencing on the Illumina MiSeq platform. A follow-up assessment was also conducted one month after anti-tuberculosis treatment to track changes in the gut microbiota over the course of therapy.
The study population consisted of pediatric patients diagnosed with pulmonary tuberculosis alongside healthy pediatric controls, using a case-controlled design. Fecal samples were gathered from both groups at admission, with PTB patients reassessed one month later following anti-tuberculosis treatment. The abstract does not specify exact sample sizes or additional demographic details beyond the pediatric PTB and healthy control groups.
Children with pulmonary tuberculosis showed decreased microbial diversity in their gut microbiota compared with healthy controls. PTB patients had increased levels of the pro-inflammatory bacterium Prevotella and the opportunistic pathogen Enterococcus. At the same time, beneficial bacteria including Ruminococcaceae, Bifidobacteriaceae, and Faecalibacterium prausnitzii were reduced. One month after anti-tuberculosis therapy, the richness of the gut microbiota was further depleted.
These findings suggest that pulmonary tuberculosis in children is associated with a disrupted gut microbiota, marked by loss of diversity and depletion of beneficial, anti-inflammatory commensals such as Faecalibacterium prausnitzii, alongside expansion of pro-inflammatory and opportunistic organisms. The further depletion of microbial richness after anti-tuberculosis treatment raises the possibility that therapy itself compounds gut microbial disruption in these children. This points to the gut microbiota as a potentially important, underexplored factor in the physiological response to pulmonary tuberculosis and its treatment in pediatric patients.
The relationship between oral microbiota and IE (infective endocarditis) is well established. Opportunistic pathogens in normal oral flora enter the bloodstream through daily oral cleaning or invasive dental procedures, leading to the occurrence of infective endocarditis. An in vitro iron-deficient condition leads to a drastic community shift in oral microbiota with increasing proportions of taxa related to infective endocarditis. To investigate the relationship among insufficient iron supply, oral microbiota and the risk of IE and to conduct a population amplification study, iron-deficiency anaemia is used as an in vivo model.
This cross-sectional study enrolled 24 primary iron-deficiency anemia (IDA) patients from 2015.6 to 2016.6 from the hematology department of West China Hospital, Sichuan University, and 24 healthy controls. High-throughput sequencing compared the dental plaque microbiota of 24 IDA (iron-deficiency anaemia) patients and 24 healthy controls.
Sequences were classified into 12 phyla, 28 classes, 50 orders, 161 genera and 497 OTUs (the IDA and control groups shared the same 384 OTUs). Iron deficiency leads to lower internal diversity in the oral flora. The abundances of genera Corynebacterium, Neisseria, Cardiobacterium, Capnocytophaga, and Aggregatibacter were significantly higher in healthy controls, while genera Lactococcus, Enterococcus, Lactobacillus, Pseudomonas and Moraxella showed higher proportions in the IDA group (P < 0.05). The relative abundances of genera Lactococcus, Enterococcus, Pseudomonas and Moraxella were significantly negatively correlated with the concentration of serum ferritin (P < 0.05).
Without an increase of oral streptococci, the main pathogen of IE, it is difficult to determine whether IDA can increase the risk of IE. However, the iron-deficient condition did lead to changes in the oral microbiota community structure. The genera that showed higher proportions in the IDA group were frequently reported as antibiotic-resistant. As antibiotics are commonly recommended to prevent IE before dental procedures, this study offers new ideas of personalized prevention of IE.
Female sex workers (FSWs) are key groups in the transmission of sexual transmitted infections (STI), and vaginal microbiome variations play an important role in transmission. We aimed to explore the characteristics of vaginal microbiome among FSWs.
A total of 24 cross-border FSWs were randomly selected from a cross-sectional survey for female sex workers in southwest China. Thirty-seven female non-sex workers (FNSWs) were randomly selected from the gynecology clinic and health examination center. Vaginal swabs were collected, bacterial DNA extracted and 16S rRNA genes were sequenced. Differences in the vaginal microbiome between both groups were compared using bioinformatics analysis.
One DNA sample was excluded due to unqualified concentration, therefore 60 samples were sequenced. FSWs had significantly different vaginal microbiota β diversity, but undifferentiated α diversity when compared with non-sex workers. The average relative abundance of Sneathia, Shigella, Neisseria, Chlamydia, Prevotella, Enterococcus and Ureaplasma among FSWs was higher than FNSWs, and relative abundance of Atopobium in FSWs was lower than FNSWs. The Lactobacillus genus was the major genus in both groups. At the species level, Lactobacllus crispatus, Lactobacllus gasseri and Lactobacllus jensenii, in female sex workers, were lower when compared to FNSWs.
There were distinct differences in vaginal bacteria variety between FSWs and FNSWs. Some disease-related genus were also more abundant in FSWs. Based on these observations, further research is required to identify microbiome communities related to high STI risks and other diseases in these cohorts.
Parkinson's disease (PD) is one of the most common neurodegenerative disorders. PD patients suffer from gastrointestinal dysfunctions and alterations of the autonomous nervous system, especially its part in the gut wall, i.e., the enteric nervous system (ENS). Such alterations and functional gastrointestinal deficits often occur years before the classical clinical symptoms of PD appear. Until now, only little is known about PD-associated changes in gut microbiota composition and their potential implication in PD development. In order to increase knowledge in this field, fecal samples of 34 PD patients and 25 healthy, age-matched control persons were investigated. Here, the V4 and V5 hypervariable region of bacterial 16S rRNA genes was PCR-amplified and sequenced using an Ion Torrent PGM platform. Within the PD group, we observed a relative decrease in bacterial taxa which are linked to health-promoting, anti-inflammatory, neuroprotective or other beneficial effects on the epithelial barrier, such as Faecalibacterium and Fusicatenibacter. Both taxa were lowered in PD patients with elevated levels of the fecal inflammation marker calprotectin. In addition, we observed an increase in shares of the Clostridiales family XI and their affiliated members in these samples. Finally, we found that the relative abundances of the bacterial genera Peptoniphilus, Finegoldia, Faecalibacterium Fusicatenibacter, Anaerococcus, Bifidobacterium, Enterococcus, and Ruminococcus were significantly influenced by medication with L-dopa and entacapone, respectively. Our data confirm previously reported effects of COMT inhibitors on the fecal microbiota of PD patients and suggest a possible effect of L-dopa medication on the relative abundance of several bacterial genera.
The mucosa-associated gut microbiota directly modulates epithelial and mucosal function. In this study, we investigated the mucosa-associated microbial community in patients with inflammatory bowel disease (IBD), using endoscopic brush samples.
A total of 174 mucus samples from 43 patients with ulcerative colitis (UC), 26 with Crohn's disease (CD) and 14 non-IBD controls were obtained by gentle brushing of mucosal surfaces using endoscopic cytology brushes. The gut microbiome was analyzed using 16S rRNA gene sequencing.
There were no significant differences in microbial structure among different anatomical sites (the ileum, cecum and sigmoid colon) within individuals. There was, however, a significant difference in microbial structure between CD, UC and non-IBD controls. The difference between CD and non-IBD controls was more marked than that between UC patients and non-IBD controls. α-Diversity was significantly lower in UC and CD patients than non-IBD controls. When comparing CD patients with non-IBD controls, the phylum Proteobacteria was significantly increased and the phyla Firmicutes and Bacteroidetes were significantly reduced. These included a significant increase in the genera Escherichia, Ruminococcus (R. gnavus), Cetobacterium, Actinobacillus and Enterococcus, and a significant decrease in the genera Faecalibacterium, Coprococcus, Prevotella and Roseburia. Comparisons between CD and UC patients revealed a greater abundance of the genera Escherichia, Ruminococcus (R. gnavus), Clostridium, Cetobacterium, Peptostreptococcus in CD patients, and the genera Faecalibacterium, Blautia, Bifidobacterium, Roseburia and Citrobacter in UC patients.
Mucosa-associated dysbiosis was identified in IBD patients. CD and UC may be distinguishable from the mucosa-associated microbial community structure.
Dietary supplementation with fermentable fiber suppresses adiposity and the associated parameters of metabolic syndrome. Microbiota-generated fiber-derived short-chain fatty acids (SCFAs) and free fatty acid receptors including GPR43 are thought to mediate these effects. We find that while fermentable (inulin), but not insoluble (cellulose), fiber markedly protected mice against high-fat diet (HFD)-induced metabolic syndrome, the effect was not significantly impaired by either inhibiting SCFA production or genetic ablation of GPR43. Rather, HFD decimates gut microbiota, resulting in loss of enterocyte proliferation, leading to microbiota encroachment, low-grade inflammation (LGI), and metabolic syndrome. Enriching HFD with inulin restored microbiota loads, interleukin-22 (IL-22) production, enterocyte proliferation, and antimicrobial gene expression in a microbiota-dependent manner, as assessed by antibiotic and germ-free approaches. Inulin-induced IL-22 expression, which required innate lymphoid cells, prevented microbiota encroachment and protected against LGI and metabolic syndrome. Thus, fermentable fiber protects against metabolic syndrome by nourishing microbiota to restore IL-22-mediated enterocyte function.
This study examined patterns of gut microbiota composition in people living with HIV/AIDS compared to HIV-uninfected healthy individuals. Stool samples were profiled by sequencing bacterial 16S rRNA genes to characterize community structure and abundance of specific taxa. The researchers also compared microbiota differences between treated and untreated HIV patients, and between patients grouped by mode of HIV transmission (homosexual versus heterosexual).
The study enrolled 33 patients with HIV/AIDS from a population in South China, including 14 participants who had received highly active antiretroviral therapy (HAART) for more than 3 months and 19 who had not received treatment. A comparison group of 35 healthy controls was also enrolled. This was a cross-sectional design using stool samples collected from these participants.
Dysbiosis was more common in patients with AIDS than in healthy controls, marked by decreased alpha-diversity. Patients with AIDS had lower mean counts of Bacteroidetes, Faecalibacterium, Prevotella, Bacteroides vulgatus, Dialister, and Roseburia inulnivorans, alongside higher mean counts of Proteobacteria, Enterococcus, Streptococcus, Lactobacillus, Lachnoclostridium, Ruminococcus gnavus, and Streptococcus vestibularis. Bacilli abundance was increased specifically in homosexual patients, while Proteobacteria abundance was higher among heterosexual patients with HIV.
These findings reinforce that HIV/AIDS is associated with a distinct, reproducible gut dysbiosis signature involving both reduced beneficial commensals and increased pro-inflammatory or opportunistic taxa. The differences observed by transmission route and treatment status suggest that host behavioral and clinical factors may shape the gut microbiome in HIV infection beyond the virus itself. Characterizing these shifts could help identify microbial targets relevant to the gastrointestinal disease and systemic immune activation seen in AIDS.
This study examined how the human gut microbiome changes during infection with soil-transmitted helminths (STHs), intestinal parasites that infect roughly 1.5 billion people worldwide. Researchers used a cross-sectional analysis to compare microbial signatures across two countries, Liberia and Indonesia, and also analyzed longitudinal samples from a double-blind randomized deworming trial. The goal was to characterize cross-kingdom interactions between STHs and gut bacteria and to see how the microbiome responds to treatment.
The abstract describes cohorts from two countries, Liberia and Indonesia, that were compared in a cross-sectional design. A subset of participants was also followed longitudinally as part of a double-blind randomized trial of deworming treatment. Exact sample sizes are not given in the abstract, so no specific participant count can be stated.
Conserved microbial signatures were positively or negatively associated with STH infection across both Liberia and Indonesia, including 12 bacterial taxa significant in both countries and one taxon, Lachnospiraceae, negatively associated with infection in both settings. Olsenella, a taxon associated with reduced gut inflammation, was also significantly reduced in abundance after infection clearance. Individuals who self-cleared their infection had more similar microbiome assemblages to one another than those who remained infected, and deworming altered microbial community gene abundances, including functional categories such as arachidonic acid metabolism, without fully shifting the microbiome back to an uninfected-like state.
The findings suggest that STH infection leaves a reproducible, cross-population signature on the gut microbiome rather than a country-specific one, pointing to shared host-parasite-microbe biology. The persistence of an altered microbiome state even after deworming implies that treatment alone may not restore a pre-infection microbial community, which could have consequences for recovery and reinfection risk. Identifying taxa like Olsenella and functional pathways such as arachidonic acid metabolism offers potential leads for understanding inflammation and immune modulation during STH infection and clearance.
This study examined whether alterations in the gut microbiota are associated with Henoch-Schonlein Purpura (HSP), an allergic-type vasculitis in children. The researchers profiled fecal microbial composition using 16S rRNA gene-based pyrosequencing. They compared microbial diversity, richness, and community composition between children with HSP and healthy controls.
The study included 85 children diagnosed with HSP and 70 healthy children as controls, for a total of 155 subjects. Fecal samples from these children were analyzed to characterize their gut bacterial communities. No further demographic details are given in the abstract.
Children with HSP had lower gut microbial diversity and richness than healthy controls, and their overall microbiota composition differed significantly from controls (r = 0.306, P = 0.001). The genera Dialister, Roseburia, and Parasutterella were significantly decreased in HSP children (all P < 0.0001), while Parabacteroides (P < 0.006) and Enterococcus (P < 0.0001) were significantly increased. A Spearman correlation analysis also found a significant negative relationship involving LOS, though the abstract is truncated before fully describing this association.
The findings support a link between gut microbial dysbiosis and HSP in children, adding this condition to the list of allergic-type diseases associated with intestinal microbiota alterations. The depletion of short-chain-fatty-acid-associated genera like Roseburia alongside enrichment of Parabacteroides and Enterococcus suggests a shift toward a less protective, more pro-inflammatory microbial community. These results point to the gut microbiota as a potential factor in HSP pathogenesis and a possible avenue for future diagnostic or therapeutic exploration, though causality cannot be established from this abstract alone.
This study examined how gut microbiota respond to a short-term, self-directed personalized diet intervention. Researchers compared the effects of long-term dietary habits versus a brief two-week dietary change on gut community structure. Stool samples were analyzed using 16S rRNA sequencing before and after the intervention to detect shifts in microbial composition. The work aimed to clarify how the duration of a diet change relates to its impact on the gut microbiome.
The study involved 248 citizen-science volunteers who participated in a self-reported, uncontrolled two-week personalized diet intervention. Participants provided stool samples both before and after the intervention, and their long-term dietary habits and lifestyle information were also collected. This was a citizen-science cohort rather than a tightly controlled clinical trial population.
Long-term dietary habits correlated strongly with overall gut community structure, and higher vegetable and fruit intake was linked to more butyrate-producing Clostridiales and greater community richness. Even the brief, uncontrolled two-week intervention produced substantial changes in community structure, including decreased Bacteroidaceae, Porphyromonadaceae and Rikenellaceae and reduced alpha-diversity. This shift was accompanied by increases in Methanobrevibacter, Bifidobacterium, Clostridium and butyrate-producing Lachnospiraceae, along with a change in the prevalence of a permatype (a bootstrapping-based variant of enterotype). The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, sulfide, or sulfur metabolism.
The findings suggest that gut microbiota can shift meaningfully within just two weeks, even without tightly controlled dietary conditions. This implies that short, self-directed diet changes may be a practical lever for altering microbial composition, including beneficial shifts toward butyrate producers. The results also support the value of citizen-science approaches for studying personalized nutrition at scale. Both long-term dietary patterns and short-term interventions appear to matter for shaping the gut microbiome, suggesting they may act through different or complementary mechanisms.
While high-risk human papillomavirus (HPV) infection is a well-established risk factor for cervical cancer, there are likely other factors within the local microenvironment that contribute to cervical carcinogenesis. Here we investigated relationships between HPV, vaginal pH, vaginal microbiota (VMB) composition, level of genital immune mediators and severity of cervical neoplasm. We enrolled women with low- and high-grade cervical dysplasia (LGD, HGD), invasive cervical carcinoma (ICC), and healthy controls. HPV16, HPV45, HPV58, and HPV31 were the most prevalent in our cohort with HPV16 and HPV31 genotypes more prevalent in Hispanics. Vaginal pH was associated with ethnicity and severity of cervical neoplasm. Lactobacillus dominance decreased with the severity of cervical neoplasm, which correlated with elevated vaginal pH. Hispanic ethnicity was also associated with decreased Lactobacillus dominance. Furthermore, Sneathia was enriched in all precancerous groups, ICC, abnormal pH and Hispanic origin. Patients with ICC, but not LGD and HGD, exhibited increased genital inflammatory scores and elevated specific immune mediators. Notably, IL-36γ was significantly associated with ICC. Our study revealed local, host immune and microbial signatures associated with cervical carcinogenesis and provides an initial step to understanding the complex interplay between mucosal inflammation, HPV persistence and the VMB.
Previous studies on the differences in gut microbiota between exclusively breastfed (EBF) and non-EBF infants have provided highly variable results. Here we perform a meta-analysis of seven microbiome studies (1825 stool samples from 684 infants) to compare the gut microbiota of non-EBF and EBF infants across populations. In the first 6 months of life, gut bacterial diversity, microbiota age, relative abundances of Bacteroidetes and Firmicutes, and predicted microbial pathways related to carbohydrate metabolism are consistently higher in non-EBF than in EBF infants, whereas relative abundances of pathways related to lipid metabolism, vitamin metabolism, and detoxification are lower. Variation in predicted microbial pathways associated with non-EBF infants is larger among infants born by Caesarian section than among those vaginally delivered. Longer duration of exclusive breastfeeding is associated with reduced diarrhea-related gut microbiota dysbiosis. Furthermore, differences in gut microbiota between EBF and non-EBF infants persist after 6 months of age. Our findings elucidate some mechanisms of short and long-term benefits of exclusive breastfeeding across different populations.
Cholestasis is a major hepatic disease in infants, with increasing morbidity in recent years. Accumulating evidence has revealed that the gut microbiota (GM) is associated with liver diseases, such as non-alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. However, GM alterations in cholestatic infants and the correlation between the GM and hepatic functions remain uninvestigated. In this study, 43 cholestatic infants (IC group) and 37 healthy infants (H group) were enrolled to detect GM discrepancies using 16S rDNA analysis. The diversity in the bacterial community was significantly lower in the IC group than that in the H group (P = 0.013). After determining the top 10 abundant genera of microbes in the IC and H groups, we found that 13 of them were differentially enriched, including Bifidobacterium, Bacteroides, Streptococcus, Enterococcus, and Staphylococcus. As compared with the H group, the IC group had a more complex GM co-occurrence network featured by three core nodes: Phyllobacterium, Ruminococcus, and Anaerostipes. In addition, the positive correlation between Faecalibacterium and Erysipelatoclostridium (r = 0.689, P = 0.000, FDR = 0.009) was not observed in the IC patients. Using the GM composition, the cholestatic patients can be distinguished from healthy infants with high accuracy [areas under receiver operating curve (AUC) > 0.97], wherein Rothia, Eggerthella, Phyllobacterium, and Blautia are identified as valuable biomarkers. Using KEGG annotation, we identified 32 functional categories with significant difference in enrichment of the GM of IC patients, including IC-enriched functional categories that were related to lipid metabolism, biodegradation and metabolism of xenobiotics, and various diseases. In contrast, the number of functions associated with amino acid metabolism, nucleotide metabolism, and vitamins metabolism was reduced in the IC patients. We also identified significant correlation between GM composition and indicators of hepatic function. Megasphaera positively correlated with total bilirubin (r = 0.455, P = 0.002) and direct bilirubin (r = 0.441, P = 0.003), whereas γ-glutamyl transpeptidase was positively associated with Parasutterella (r = 0.466, P = 0.002) and negatively related to Streptococcus (r = -0.450, P = 0.003). This study describes the GM characteristics in the cholestatic infants, illustrates the association between the GM components and the hepatic function, and provides a solid theoretical basis for GM intervention for the treatment of infantile cholestasis.
A signature that unifies the colorectal cancer (CRC) microbiota across multiple studies has not been identified. In addition to methodological variance, heterogeneity may be caused by both microbial and host response differences, which was addressed in this study.
We prospectively studied the colonic microbiota and the expression of specific host response genes using faecal and mucosal samples ('ON' and 'OFF' the tumour, proximal and distal) from 59 patients undergoing surgery for CRC, 21 individuals with polyps and 56 healthy controls. Microbiota composition was determined by 16S rRNA amplicon sequencing; expression of host genes involved in CRC progression and immune response was quantified by real-time quantitative PCR.
The microbiota of patients with CRC differed from that of controls, but alterations were not restricted to the cancerous tissue. Differences between distal and proximal cancers were detected and faecal microbiota only partially reflected mucosal microbiota in CRC. Patients with CRC can be stratified based on higher level structures of mucosal-associated bacterial co-abundance groups (CAGs) that resemble the previously formulated concept of enterotypes. Of these, Bacteroidetes Cluster 1 and Firmicutes Cluster 1 were in decreased abundance in CRC mucosa, whereas Bacteroidetes Cluster 2, Firmicutes Cluster 2, Pathogen Cluster and Prevotella Cluster showed increased abundance in CRC mucosa. CRC-associated CAGs were differentially correlated with the expression of host immunoinflammatory response genes.
CRC-associated microbiota profiles differ from those in healthy subjects and are linked with distinct mucosal gene-expression profiles. Compositional alterations in the microbiota are not restricted to cancerous tissue and differ between distal and proximal cancers.
This study examined whether chronic early-life stress in rat pups alters basal corticosterone levels, intestinal permeability, and fecal microbiota composition at weaning. Wistar rat dams and litters were exposed to a limited nesting and bedding stress (LNS) paradigm from postnatal day 2 to postnatal day 10, then returned to normal housing until weaning at postnatal day 21. Researchers measured plasma corticosterone by enzyme immunoassay, in vivo intestinal to colonic permeability using fluorescein isothiocyanate-dextran, and fecal microbiota via 16S rRNA gene sequencing of the V4 region. The design specifically compared outcomes between male and female offspring to assess sex-dependent effects.
The subjects were Wistar rat dams and their litters, with pups randomized to either the limited nesting stress condition or a normal housing control condition. Both male and female pups from these litters were followed from the early postnatal period through weaning at postnatal day 21. The abstract does not report a specific total number of animals, so the exact sample size cannot be stated. This was a controlled animal model study rather than a human cohort.
At weaning, pups exposed to limited nesting stress showed elevated basal corticosterone (hypercorticosteronemia) and increased intestinal permeability compared to controls, with females showing a greater increase in permeability than males. Body weights were similar between stressed and control pups, indicating the effects were not simply due to growth differences. Limited nesting stress also decreased fecal microbial diversity and produced a distinct microbial community composition compared to controls. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism specifically.
These findings suggest that early-life stress can disrupt the hypothalamic-pituitary-adrenal axis, intestinal barrier integrity, and gut microbiota composition well before adulthood, with weaning representing a critical window of vulnerability. The sex-specific difference in permeability, with females affected more than males, points to biological sex as an important variable in how early adversity programs gut physiology. This model may help explain how early-life stress contributes to later-life gastrointestinal and stress-related disorders and underscores the need to consider sex as a factor in future mechanistic and therapeutic research.
Perturbations to the colonization process of the human gastrointestinal tract have been suggested to result in adverse health effects later in life. Although much research has been performed on bacterial colonization and succession, much less is known about the other two domains of life, archaea, and eukaryotes. Here we describe colonization and succession by bacteria, archaea and microeukaryotes during the first year of life (samples collected around days 1, 3, 5, 28, 150, and 365) within the gastrointestinal tract of infants delivered either vaginally or by cesarean section and using a combination of quantitative real-time PCR as well as 16S and 18S rRNA gene amplicon sequencing. Sequences from organisms belonging to all three domains of life were detectable in all of the collected meconium samples. The microeukaryotic community composition fluctuated strongly over time and early diversification was delayed in infants receiving formula milk. Cesarean section-delivered (CSD) infants experienced a delay in colonization and succession, which was observed for all three domains of life. Shifts in prokaryotic succession in CSD infants compared to vaginally delivered (VD) infants were apparent as early as days 3 and 5, which were characterized by increased relative abundances of the genera Streptococcus and Staphylococcus, and a decrease in relative abundance for the genera Bifidobacterium and Bacteroides. Generally, a depletion in Bacteroidetes was detected as early as day 5 postpartum in CSD infants, causing a significantly increased Firmicutes/Bacteroidetes ratio between days 5 and 150 when compared to VD infants. Although the delivery mode appeared to have the strongest influence on differences between the infants, other factors such as a younger gestational age or maternal antibiotics intake likely contributed to the observed patterns as well. Our findings complement previous observations of a delay in colonization and succession of CSD infants, which affects not only bacteria but also archaea and microeukaryotes. This further highlights the need for resolving bacterial, archaeal, and microeukaryotic dynamics in future longitudinal studies of microbial colonization and succession within the neonatal gastrointestinal tract.
The aim of this study was to compare the structure of gut microbiota in Parkinson's disease (PD) patients and healthy controls; and to explore correlations between gut microbiota and PD clinical features. We analyzed fecal bacterial composition of 24 PD patients and 14 healthy volunteers by using 16S rRNA sequencing. There were significant differences between PD and healthy controls, as well as among different PD stages. The putative cellulose degrading bacteria from the genera Blautia (P=0.018), Faecalibacterium (P=0.048) and Ruminococcus (P=0.019) were significantly decreased in PD compared to healthy controls. The putative pathobionts from the genera Escherichia-Shigella (P=0.038), Streptococcus (P=0.01), Proteus (P=0.022), and Enterococcus (P=0.006) were significantly increased in PD subjects. Correlation analysis indicated that disease severity and PD duration negatively correlated with the putative cellulose degraders, and positively correlated with the putative pathobionts. The results suggest that structural changes of gut microbiota in PD are characterized by the decreases of putative cellulose degraders and the increases of putative pathobionts, which may potentially reduce the production of short chain fatty acids, and produce more endotoxins and neurotoxins; and these changes is potentially associated with the development of PD pathology.
This study examined how conventional anti-tuberculosis drug therapy affects the intestinal microbiome. Researchers used 16S rRNA sequencing to longitudinally track microbial diversity and community composition in Mycobacterium tuberculosis-infected mice treated with the standard isoniazid-rifampin-pyrazinamide (HRZ) regimen. They also tested each antibiotic individually and in various combinations to identify which drug or drugs drove any observed changes.
The study population was Mtb-infected mice, not human subjects. The abstract does not give an exact number of animals, but it describes longitudinal sampling across the treatment course and a post-treatment follow-up period of at least three months. Comparisons were made across mice receiving monotherapy, different combination therapies, and the full HRZ regimen.
HRZ treatment caused only a transient dip in microbial diversity, but it triggered an immediate, marked, and reproducible shift in gut community structure that persisted throughout therapy and for at least three months after stopping treatment. Members of the order Clostridiales decreased in relative frequency during treatment, while the family Porphyromonadaceae increased afterward. Experiments isolating individual drugs identified rifampin as the major driver of these compositional alterations.
Because this multi-drug regimen is administered to millions of people annually worldwide, a persistent, rifampin-driven dysbiosis lasting months beyond treatment could have broad public health relevance. The findings suggest that standard TB therapy leaves a durable signature on the gut microbiota rather than a transient one. This raises the question of whether such prolonged dysbiosis contributes to downstream health effects in treated patients, warranting further investigation in humans.
The assessment and characterization of the gut microbiome has become a focus of research in the area of human autoimmune diseases. Ankylosing spondylitis is an inflammatory autoimmune disease and evidence showed that ankylosing spondylitis may be a microbiome-driven disease.
To investigate the relationship between the gut microbiome and ankylosing spondylitis, a quantitative metagenomics study based on deep shotgun sequencing was performed, using gut microbial DNA from 211 Chinese individuals. A total of 23,709 genes and 12 metagenomic species were shown to be differentially abundant between ankylosing spondylitis patients and healthy controls. Patients were characterized by a form of gut microbial dysbiosis that is more prominent than previously reported cases with inflammatory bowel disease. Specifically, the ankylosing spondylitis patients demonstrated increases in the abundance of Prevotella melaninogenica, Prevotella copri, and Prevotella sp. C561 and decreases in Bacteroides spp. It is noteworthy that the Bifidobacterium genus, which is commonly used in probiotics, accumulated in the ankylosing spondylitis patients. Diagnostic algorithms were established using a subset of these gut microbial biomarkers.
Alterations of the gut microbiome are associated with development of ankylosing spondylitis. Our data suggest biomarkers identified in this study might participate in the pathogenesis or development process of ankylosing spondylitis, providing new leads for the development of new diagnostic tools and potential treatments.
Human schistosomiasis is a highly prevalent neglected tropical disease (NTD) caused by Schistosoma species. Research on the molecular mechanisms influencing the outcomes of bladder infection by Schistosoma haematobium is urgently needed to develop new diagnostics, therapeutics and infection prevention strategies. The objective of the research study was to determine the microbiome features and changes in urine during urogenital schistosomiasis and induced bladder pathologies.
Seventy participants from Eggua, southwestern Nigeria provided morning urine samples and were screened for urogenital schistosomiasis infection and bladder pathologies in a cross-sectional study. Highthroughput NGS sequencing was carried out, targeting the 16S V3 region. Filtered reads were processed and analyzed in a bioinformatics pipeline.
The study participants (36 males and 34 females, between ages 15 and 65) were categorized into four groups according to status of schistosomiasis infection and bladder pathology. Data analytics of the next-generation sequencing reads revealed that Proteobacteria and Firmicutes dominated and had influence on microbiome structure of both non-infected persons and persons with urogenital schistosomiasis. Furthermore, gender and age influenced taxa abundance independent of infection or bladder pathology. Several taxa distinguished urogenital schistosomiasis induced bladder pathologies from urogenital schistosomiasis infection alone and from healthy persons, including known immune-stimulatory taxa such as Fusobacterium, Sphingobacterium and Enterococcus. Some of these significant taxa, especially Sphingobacterium were projected as markers of infection, while several genera including potentially beneficial taxa such as Trabulsiella and Weissella, were markers of the non-infected. Finally, expected changes in protein functional categories were observed to relate to cellular maintenance and lipid metabolism.
The urinary microbiome is a factor to be considered in developing biomarkers, diagnostic tools, and new treatment for urogenital schistosomiasis and induced bladder pathologies.
The early postnatal period is the most dynamic and vulnerable stage in the assembly of intestinal microbiota. Antibiotics are commonly prescribed to newborn preterm babies and are frequently used for a prolonged duration in China. We hypothesized that the prolonged antibiotic therapy would affect the early development of intestinal microbiota and their metabolites. To test this hypothesis, we analyzed the stool microbiota and metabolites in 36 preterm babies with or without antibiotic treatment. These babies were divided into three groups, including two groups treated with the combination of penicillin and moxalactam or piperacillin-tazobactam for 7 days, and the other group was free of antibiotics. Compared to the antibiotic-free group, both antibiotic-treated groups had distinct gut microbial communities and metabolites, including a reduction of bacterial diversity and an enrichment of harmful bacteria such as Streptococcus and Pseudomonas. In addition, there was a significant difference in the composition of gut microbiota and their metabolites between the two antibiotic-treated groups, where the piperacillin-tazobactam treatment group showed an overgrowth of Enterococcus. These findings suggest that prolonged antibiotic therapy affects the early development of gut microbiota in preterm infants, which should be considered when prescribing antibiotics for this population.
The human gut microbiome plays a crucial role in the compositional development of gut microbiota. Though well documented in western pediatrics population, little is known about how various host conditions affect populations in different geographic locations such as the Indian subcontinent. Given the impact of distinct environmental conditions, our study assess the gut bacterial diversity of a small cohort of Indian and Finnish children and investigated the influence of FUT2 secretor status and birth mode on the gut microbiome of these populations. Using multiple profiling techniques, we show that the gut bacterial community structure in 13-14-year-old Indian (n = 47) and Finnish (n = 52) children differs significantly. Specifically, Finnish children possessed higher Blautia and Bifidobacterium, while genera Prevotella and Megasphaera were predominant in Indian children. Our study also demonstrates a strong influence of FUT2 and birth mode variants on specific gut bacterial taxa, influence of which was noticed to differ between the two populations under study.
To investigate whether patients with refractory epilepsy and healthy infants differ in gut microbiota (GM), and how ketogenic diet (KD) alters GM.
A total of 14 epileptic and 30 healthy infants were recruited and seizure frequencies were recorded. Stool samples were collected for 16S rDNA sequencing using the Illumina Miseq platform. The composition of GM in each sample was analyzed with MOTHUR, and inter-group comparison was conducted by R software.
After being on KD treatment for a week, 64% of epileptic infants showed an obvious improvement, with a 50% decrease in seizure frequency. GM structure in epileptic infants (P1 group) differed dramatically from that in healthy infants (Health group). Proteobacteria, which had accumulated significantly in the P1 group, decreased dramatically after KD treatment (P2 group). Cronobacter predominated in the P1 group and remained at a low level both in the Health and P2 groups. Bacteroides increased significantly in the P2 group, in which Prevotella and Bifidobacterium also grew in numbers and kept increasing.
GM pattern in healthy infants differed dramatically from that of the epileptic group. KD could significantly modify symptoms of epilepsy and reshape the GM of epileptic infants.
This study examined whether gut dysbiosis correlates with clinical progression of Parkinson's disease (PD) over a two-year period. Researchers tracked changes in gut microbiota composition alongside demographic and clinical features across that follow-up window. The work builds on a prior report from the same group describing gut dysbiosis in PD patients. The aim was to link baseline microbial counts to later changes in motor and non-motor symptom severity.
The cohort consisted of 36 patients with Parkinson's disease who were followed for two years. Patients were later divided evenly into a deteriorated group and a stable group based on how much their total UPDRS scores worsened over that period. The abstract does not provide further demographic details such as age, sex distribution, or disease duration at enrollment.
Change in total UPDRS score over two years was predicted by baseline counts of Bifidobacterium and the Atopobium cluster, with a correlation coefficient of 0.52. Low baseline counts of Bifidobacterium and Bacteroides fragilis were associated with worsening of UPDRS I scores over two years. Low baseline Bifidobacterium was specifically linked to worsening hallucinations and delusions, while low baseline B. fragilis was linked to worsening motivation and initiative. The deteriorated group had lower baseline counts of Bifidobacterium, B. fragilis, and Clostridium leptum than the stable group at year zero, though not at year two, suggesting an accelerated decline in these bacteria preceded clinical worsening.
These findings suggest that baseline levels of specific gut bacteria, including Bifidobacterium and Bacteroides fragilis, may serve as early indicators of which PD patients are likely to experience faster clinical deterioration. The distinct associations between particular taxa and specific symptom domains (psychiatric versus motivational) point toward possible microbiota-linked pathways influencing different aspects of PD progression. This raises the possibility that monitoring or modulating these bacterial populations could eventually inform prognostic assessment or intervention strategies in PD, though the abstract does not describe any mechanistic or interventional testing.
Cesarean (C-section) delivery, recently shown to cause excess weight gain in mice, perturbs human neonatal gut microbiota development due to the lack of natural mother-to-newborn transfer of microbes. Neonates excrete first the in-utero intestinal content (referred to as meconium) hours after birth, followed by intestinal contents reflective of extra-uterine exposure (referred to as transition stool) 2 to 3 days after birth. It is not clear when the effect of C-section on the neonatal gut microbiota emerges. We examined bacterial DNA in carefully-collected meconium, and the subsequent transitional stool, from 59 neonates [13 born by scheduled C-section and 46 born by vaginal delivery] in a private hospital in Brazil. Bacterial DNA was extracted, and the V4 region of the 16S rRNA gene was sequenced using the Illumina MiSeq (San Diego, CA, USA) platform. We found evidence of bacterial DNA in the majority of meconium samples in our study. The bacterial DNA structure (i.e., beta diversity) of meconium differed significantly from that of the transitional stool microbiota. There was a significant reduction in bacterial alpha diversity (e.g., number of observed bacterial species) and change in bacterial composition (e.g., reduced Proteobacteria) in the transition from meconium to stool. However, changes in predicted microbiota metabolic function from meconium to transitional stool were only observed in vaginally-delivered neonates. Within sample comparisons showed that delivery mode was significantly associated with bacterial structure, composition and predicted microbiota metabolic function in transitional-stool samples, but not in meconium samples. Specifically, compared to vaginally delivered neonates, the transitional stool of C-section delivered neonates had lower proportions of the genera Bacteroides, Parabacteroides and Clostridium. These differences led to C-section neonates having lower predicted abundance of microbial genes related to metabolism of amino and nucleotide sugars, and higher abundance of genes related to fatty-acid metabolism, amino-acid degradation and xenobiotics biodegradation. In summary, microbiota diversity was reduced in the transition from meconium to stool, and the association of delivery mode with microbiota structure, composition and predicted metabolic function was not observed until the passing of the transitional stool after meconium.
Objectives: Emerging evidence indicates that alterations to the urinary microbiome are related to lower urinary tract symptoms. Overactive bladder (OAB) is a common disorder with complex etiologies and usually accompanied by psychological diseases. More information concerning the urinary microbiome and psychological factors in OAB is required. The aim of this study was to characterize the female urinary microbiome associated with OAB and investigate the relationships between urinary microbiome and psychological factors. Methods: Thirty women with OAB and 25 asymptomatic controls were recruited and asked to finish the Overactive Bladder Symptom Score, Self-Rating Anxiety Scale and Self-Rating Depression Scale. Urine specimens were collected by transurethral catheterization and processed for 16S rRNA gene sequencing using Illumina MiSeq. Sequencing reads were processed using QIIME. LEfSe revealed significant differences in bacterial genera between controls and OAB patients. The relationships between the diversity of the urinary microbiome and psychological scores were identified by Pearson's correlation coefficient. Results: We found that bacterial diversity (Simpson index) and richness (Chao1) were lower in OAB samples compared to controls (P both = 0.038). OAB and control bacterial communities were significantly different (based on weighted UniFrac distance metric, R = 0.064, P = 0.037). LEfSe demonstrated that 7 genera were increased (e.g., Proteus and Aerococcus) and 13 were reduced (e.g., Lactobacillus and Prevotella) in OAB group compared to controls. There were negative correlations between scores on Self-Rating Depression Scale and both richness (Chao1, r = -0.458, P = 0.011) and diversity (Shannon index, r = -0.516, P = 0.003) of urinary microbiome in OAB group. Some bacterial genera of OAB women with anxiety or depression were significantly different from those without. Conclusions: The aberrant urinary microbiome with decreased diversity and richness may have strong implications in pathogenesis and treatment of OAB. Psychological conditions were correlated with characteristics of urinary microbiome in women with OAB. Further research is needed to understand the connection between central nervous system and urinary microbiome.
We hypothesized that food sensitization (FS) in children could be linked to specific gut microbiota. The aim of our study is to quantify and evaluate differences in gut microbiota composition between children with FS and healthy controls.
A case-control study of 23 children with FS and 22 healthy children was performed. Individual microbial diversity and composition were analyzed via parallel barcoded 454 pyrosequencing targeting the 16S rRNA gene hypervariable V3-V5 regions.
The children with FS exhibited lower diversity of both the total microbiota (p = 0.01) and the bacterial phylum Bacteroidetes (p = 0.02). In these children, the number of Bacteroidetes bacteria was significantly decreased and that of Firmicutes were significantly increased compared with the healthy children. At the genus level, we observed significant increases in the numbers of Sphingomonas, Sutterella, Bifidobacterium, Collinsella, Clostridium sensu stricto, Clostridium IV, Enterococcus, Lactobacillus, Roseburia, Faecalibacterium, Ruminococcus, Subdoligranulum, and Akkermansia in the FS group. We also found significant decreases in the numbers of Bacteroides, Parabacteroides, Prevotella, Alistipes, Streptococcus, and Veillonella in this group. Furthermore, linear discriminant analysis (LDA) coupled with effect size measurements revealed the most differentially abundant taxa (increased abundances of Clostridium IV and Subdoligranulum and decreased abundances of Bacteroides and Veillonella), which could be used to identify FS.
Our results showed that FS is associated with compositional changes in the gut microbiota. These findings could be useful for developing strategies to control the development of FS or atopy by modifying the gut microbiota.
This study examined whether the enteric virome, alongside the bacterial microbiome, contributes to HIV-associated immunodeficiency and gut disease. Researchers characterized viral and bacterial communities in stool to see how they relate to HIV infection, antiretroviral therapy (ART) status, and CD4 T cell counts. The goal was to determine whether virome alterations track with immune decline independent of treatment.
The cohort consisted of Ugandan patients, including individuals without HIV infection and individuals with HIV infection who were either on ART or untreated. The abstract does not give an exact sample size or additional demographic detail. Findings are grouped by HIV status, treatment status, and peripheral CD4 T cell count level.
Low peripheral CD4 T cell counts were associated with an expansion of enteric adenovirus sequences, and this pattern held regardless of ART treatment. Patients with lower CD4 counts also had a bacterial microbiome with reduced phylogenetic diversity and richness. Specific bacterial taxa showed differential abundance, notably an increase in Enterobacteriaceae, a group linked to inflammation.
The findings suggest that immunodeficiency in progressive HIV infection is accompanied by coordinated shifts in both the enteric virome and bacterial microbiome, not bacterial changes alone. Because the adenovirus expansion occurred regardless of ART status, viral alterations may persist even in treated patients and could still contribute to gut dysfunction. These combined viral and bacterial changes may help drive AIDS-associated enteropathy and disease progression, pointing to the virome as an underexplored factor in HIV-related gut pathology.
TB is a worldwide pandemic. India has the highest burden of TB, with WHO statistics for 2013 giving an estimated incidence figure of 2.1 million cases for India out of a global incidence of 9 million. Microbiota have been shown to be associated with many disease conditions; however, only few studies have been reported for microbiota associated with TB infection. For the first time, we characterized the composition of microbiota of TB patients of India, using high-throughput 16S rRNA gene sequencing and compared it with healthy controls. Phylum-level analysis showed that the relative abundance of Firmicutes and Actinobacteria was significantly higher in TB samples and Neisseria and Veillonella were two dominant genera after Streptococcus. In our study, significantly different core genera in TB and normal population were found as compared with the reported studies. Also, the presence of diverse opportunistic pathogenic microbiota in TB patients increases the complexity and diversity of sputum microbiota. Characterization of the sputum microbiome is likely to provide important pathogenic insights into pulmonary tuberculosis.
This study examined how the infant gut microbiota develops during the first six months of life. Researchers measured 33 bacterial taxa and 8 bacterial metabolites in fecal samples using qPCR and RT qPCR. They then used regression analysis to look for associations between microbiota composition and early-life factors over time.
The study followed 108 healthy neonates who were sampled repeatedly during their first half year of life. Alongside the fecal samples, questionnaires collected information on each infant's gender, place and mode of birth, presence of siblings or pets, feeding pattern, and antibiotic use. This allowed the researchers to relate microbiota measurements directly to these early-life exposures within the same cohort.
Bacterial DNA was detected in most meconium samples, suggesting that bacterial exposure may begin in utero, before birth itself. After birth, colonization by Bifidobacterium, Lactobacillus, and Bacteroides species was shaped by mode of delivery, type of feeding, and the presence of siblings. These effects were evident at the species level and changed over the first six months of life. Infant-type bifidobacterial species such as B. breve and B. longum subsp. infantis showed distinct patterns tied to these early-life factors.
The findings support the idea that mode of delivery, feeding type, siblings, and gender are meaningful, modifiable or identifiable factors shaping early gut colonization. Because altered early colonization has been linked to higher disease risk later in life, understanding these influences could inform strategies to support healthy infant microbiota development. The detection of bacterial DNA in meconium also raises the possibility that microbial exposure begins earlier than birth, a question worth further investigation.
The available evidence suggests that alterations in gut microbiota may be tightly linked to the increase in microbial translocation and systemic inflammation in patients with human immunodeficiency virus 1 (HIV-1) infection. We profiled the fecal microbiota as a proxy of gut microbiota by parallel barcoded 454-pyrosequencing in 67 HIV-1-infected patients (32 receiving highly active antiretroviral therapy [HAART] and 35 HAART naïve) and 16 healthy controls from a Chinese population. We showed that α-diversity indices did not differ significantly between the healthy control and HIV-1-infected patients. The ratio of Firmicutes/Bacteroidetes increased significantly in HIV-1-infected patients. Several key bacterial phylotypes, including Prevotella, were prevalent in HIV-1-infected patients; whereas Phascolarctobacterium, Clostridium XIVb, Dialister and Megamonas were significantly correlated with systemic inflammatory cytokines. After short-term, effective HAART, the viral loads of HIV-1 were reduced; however, the diversity and composition of the fecal microbiota were not completely restored. and the dysbiosis remained among HIV-1-infected subjects undergoing HAART. Our detailed analysis demonstrated that dysbiosis of fecal microbiota might play an active role in HIV-1 infection. Thus, new insights may be provided into therapeutics that target the microbiota to attenuate the progression of HIV disease and to reduce the risk of gut-linked disease in HIV-1-infected patients.
This study examined whether the gut microbiome influences the development and severity of arthritis in a mouse model. The researchers used 16S rRNA sequencing to characterize gut bacterial communities in DBA1 mice before and after collagen-induced arthritis (CIA) induction. They compared mice that went on to develop arthritis with those that remained resistant, then tested whether transferring this microbiota into germ-free mice could transmit disease susceptibility.
The subjects were DBA1 mice, a strain commonly used to model collagen-induced arthritis, divided into groups that did or did not develop arthritis after collagen induction. A separate set of germ-free mice was also used as recipients in microbiota transfer (conventionalization) experiments. No human cohort was involved; this was an entirely animal-model study.
Gut microbiota composition diverged significantly between CIA-susceptible and CIA-resistant mice after induction. Lactobacillus was the dominant enriched genus in susceptible mice before arthritis onset, while Bacteroidaceae, Lachnospiraceae, and S24-7 increased significantly as disease developed. Germ-free mice conventionalized with microbiota from CIA-susceptible mice developed arthritis more frequently than those given microbiota from resistant mice, and they also showed higher serum interleukin-17, more CD8+ T cells, and more Th17 lymphocytes in the spleen.
The findings suggest that the gut microbiome is not just a bystander but can actively drive arthritis susceptibility through immune modulation, particularly by promoting Th17-skewed inflammatory responses. Because microbiota transfer alone was sufficient to raise arthritis incidence, the gut microbial community may represent a modifiable environmental factor in rheumatoid arthritis risk. This strengthens the case for investigating microbiome-targeted strategies, such as modulating specific bacterial taxa, as potential approaches to arthritis prevention or management.
Emerging evidence suggests that the in utero environment is not sterile as once presumed. Work in the mouse demonstrated transmission of commensal bacteria from mother to fetus during gestation, though it is unclear what modulates this process. We have previously shown in the nonhuman primate that, independent of obesity, a maternal high-fat diet during gestation and lactation persistently shapes the juvenile gut microbiome. We therefore sought to interrogate in a population-based human longitudinal cohort whether a maternal high-fat diet similarly alters the neonatal and infant gut microbiome in early life.
A representative cohort was prospectively enrolled either in the early third trimester or intrapartum (n = 163), with a subset consented to longitudinal sampling through the postpartum interval (n = 81). Multiple body site samples, including stool and meconium, were collected from neonates at delivery and by 6 weeks of age. A rapid dietary questionnaire was administered to estimate intake of fat, added sugars, and fiber over the past month (National Health and Examination Survey). DNA was extracted from each infant meconium/stool sample (MoBio) and subjected to 16S rRNA gene sequencing and analysis.
On average, the maternal dietary intake of fat ranged from 14.0 to 55.2 %, with an average intake of 33.1 % (σ = 6.1 %). Mothers whose diets significantly differed from the mean (±1 standard deviation) were separated into two distinct groups, a control group (n = 13, μ = 24.4 %) and a high-fat group (n = 13, μ = 43.1 %). Principal coordinate analysis revealed that the microbiome of the neonatal stool at birth (meconium) clustered differently by virtue of maternal gestational diet (PERMANOVA p = 0.001). LEfSe feature selection identified several taxa that discriminated the groups, with a notable relative depletion of Bacteroides in the neonates exposed to a maternal high-fat gestational diet (Student's t-test, p < 0.05) that persisted to 6 weeks of age.
Similar to the primate, independent of maternal body mass index, a maternal high-fat diet is associated with distinct changes in the neonatal gut microbiome at birth which persist through 4-6 weeks of age. Our findings underscore the importance of counseling pregnant mothers on macronutrient consumption during pregnancy and lactation.
The joint impact of pregnancy, environmental, and sociocultural exposures on early life gut microbiome is not yet well-characterized, especially in racially and socioeconomically diverse populations. Gut microbiota of 298 children from a Detroit-based birth cohort were profiled using 16S rRNA sequencing: 130 neonates (median age = 1.2 months) and 168 infants (median age = 6.6 months). Multiple factors were associated with neonatal gut microbiome composition in both single- and multi-factor models, with independent contributions of maternal race-ethnicity, breastfeeding, mode of delivery, marital status, exposure to environmental tobacco smoke, and indoor pets. These findings were consistent in the infants, and networks demonstrating the shared impact of factors on gut microbial composition also showed notable topological similarity between neonates and infants. Further, latent groups defined by these factors explained additional variation, highlighting the importance of combinatorial effects. Our findings also have implications for studies investigating the impact of the early life gut microbiota on disease.
This study examined whether short chain fatty acid (SCFA) concentrations and gut microbiota composition differ between people with Parkinson's disease (PD) and matched controls. Researchers measured fecal SCFA levels by gas chromatography and quantified bacterial groups by quantitative PCR. The work was motivated by PD's frequent gastrointestinal symptoms, such as constipation, and by PD-typical pathological changes in the enteric nervous system that can precede motor symptoms. It builds on prior reports linking altered gut microbiota composition to PD.
The study included 34 patients with Parkinson's disease and 34 age-matched controls. Fecal samples were collected from each participant for SCFA and microbiota analysis. The abstract does not provide further demographic, geographic, or disease-severity details about the cohort.
Fecal SCFA concentrations were significantly reduced in PD patients compared to controls. Within the microbiota, the phylum Bacteroidetes and the family Prevotellaceae were reduced in PD patients, while the family Enterobacteriaceae was more abundant. These findings confirm previously reported associations between PD and specific shifts in gut microbiota composition.
The findings support a link between altered gut bacterial composition and reduced SCFA production in Parkinson's disease, connecting a metabolic deficit to the compositional shifts seen in prior microbiome studies. Because SCFA are a main metabolic product of gut bacteria, this reduction may be relevant to the gastrointestinal and enteric nervous system changes seen early in PD. These results strengthen the rationale for further investigating gut microbiota and its metabolic output as a factor in PD pathophysiology.
The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein α-synuclein (αSyn), often resulting in motor dysfunction as exemplified by Parkinson's disease (PD). Using mice that overexpress αSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and αSyn pathology. Antibiotic treatment ameliorates, while microbial re-colonization promotes, pathophysiology in adult animals, suggesting that postnatal signaling between the gut and the brain modulates disease. Indeed, oral administration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symptoms. Remarkably, colonization of αSyn-overexpressing mice with microbiota from PD-affected patients enhances physical impairments compared to microbiota transplants from healthy human donors. These findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations in the human microbiome represent a risk factor for PD.
This study examined how the gut microbiota relates to the two major precursor lesions of colorectal cancer: conventional adenomas and serrated polyps. Colorectal cancer is a heterogeneous disease, and the authors tested for the first time whether the gut microbiota's relationship to colorectal cancer differs by the specific type of precursor polyp. Gut microbiota were assessed using 16S rRNA gene sequencing of stool samples, allowing comparison of diversity, overall composition, and taxon abundance across groups.
The study included 540 adults who underwent colonoscopy screening. Participants were categorized as conventional adenoma cases (n = 144), serrated polyp cases (n = 73), or polyp-free controls (n = 323). Conventional adenoma cases were further divided by location (proximal, n = 87; distal, n = 55) and stage (non-advanced, n = 121; advanced, n = 22), and serrated polyp cases were subdivided into hyperplastic polyp (n = 40) and sessile serrated adenoma (n = 33).
Conventional adenoma cases had lower gut microbial species richness in stool than polyp-free controls, and this association was strongest among advanced conventional adenoma cases. In terms of overall microbiota composition, differences from controls were seen specifically among distal or advanced conventional adenoma cases. These patterns indicate that the gut microbiota relationship to colorectal cancer precursors is not uniform but varies by polyp type, location, and severity.
By distinguishing microbiota associations between conventional adenomas and serrated polyps, this study suggests that colorectal cancer's different developmental pathways may have distinct microbial signatures. The stronger association with advanced and distal conventional adenomas points to species richness and composition as potentially useful features for identifying higher-risk precursor lesions. These findings support future research treating colorectal cancer precursors as biologically distinct subtypes rather than a single category when studying the gut microbiota.
Evidence suggests a correlation between the gut microbiota composition and weight loss caused by caloric restriction. Laparoscopic sleeve gastrectomy (LSG), a surgical intervention for obesity, is classified as predominantly restrictive procedure. In this study we investigated functional weight loss mechanisms with regard to gut microbial changes and energy harvest induced by LSG and a very low calorie diet in ten obese subjects (n = 5 per group) demonstrating identical weight loss during a follow-up period of six months. For gut microbiome analysis next generation sequencing was performed and faeces were analyzed for targeted metabolomics. The energy-reabsorbing potential of the gut microbiota decreased following LSG, indicated by the Bacteroidetes/Firmicutes ratio, but increased during diet. Changes in butyrate-producing bacterial species were responsible for the Firmicutes changes in both groups. No alteration of faecal butyrate was observed, but the microbial capacity for butyrate fermentation decreased following LSG and increased following dietetic intervention. LSG resulted in enhanced faecal excretion of nonesterified fatty acids and bile acids. LSG, but not dietetic restriction, improved the obesity-associated gut microbiota composition towards a lean microbiome phenotype. Moreover, LSG increased malabsorption due to loss in energy-rich faecal substrates and impairment of bile acid circulation. This trial is registered with ClinicalTrials.gov NCT01344525.
Chemotherapy is commonly used as myeloablative conditioning treatment to prepare patients for haematopoietic stem cell transplantation (HSCT). Chemotherapy leads to several side effects, with gastrointestinal (GI) mucositis being one of the most frequent. Current models of GI mucositis pathophysiology are generally silent on the role of the intestinal microbiome. To identify functional mechanisms by which the intestinal microbiome may play a key role in the pathophysiology of GI mucositis, we applied high-throughput DNA-sequencing analysis to identify microbes and microbial functions that are modulated following chemotherapy.
We amplified and sequenced 16S rRNA genes from faecal samples before and after chemotherapy in 28 patients with non-Hodgkin's lymphoma who received the same myeloablative conditioning regimen and no other concomitant therapy such as antibiotics.
We found that faecal samples collected after chemotherapy exhibited significant decreases in abundances of Firmicutes (P = 0.0002) and Actinobacteria (P = 0.002) and significant increases in abundances of Proteobacteria (P = 0.0002) compared to samples collected before chemotherapy. Following chemotherapy, patients had reduced capacity for nucleotide metabolism (P = 0.0001), energy metabolism (P = 0.001), metabolism of cofactors and vitamins (P = 0.006), and increased capacity for glycan metabolism (P = 0.0002), signal transduction (P = 0.0002) and xenobiotics biodegradation (P = 0.002).
Our study identifies a severe compositional and functional imbalance in the gut microbial community associated with chemotherapy-induced GI mucositis. The functional pathways implicated in our analysis suggest potential directions for the development of intestinal microbiome-targeted interventions in cancer patients.
Studies using animal models have demonstrated that probiotics may have a beneficial role in the prevention of colorectal cancer (CRC); however, the underlying mechanism of the beneficial effects of interventional probiotic treatment on gut microbiota has remained elusive. In the present study, pyrosequencing of the V3 region of the 16S rRNA genes was conducted in order to determine the extent to which probiotics alter the microbiota. The observations of the present study indicated that the microbial structure of cancerous tissue differed significantly from that of healthy individuals and that the CRC microbiota exhibited lower diversity. It was indicated that interventional treatment with probiotics increased the density and diversity of mucosal microbes, and altered the mucosa‑associated microbiota. Pyrosequencing demonstrated that probiotics significantly reduced (5‑fold) the abundance of a bacterial taxon assigned to the genus Fusobacterium, which had been previously suggested to be a contributing factor to increase tumorigenesis. Accordingly, interventional probiotic therapy is suggested to be able to improve the composition of the mucosal microbial flora and significantly reduce the abundance of mucosa-associated pathogens in patients with CRC.
Accumulating evidence links colorectal cancer (CRC) with the intestinal microbiota. However, the disturbance of intestinal microbiota and the role of Fusobacterium nucleatum during the colorectal adenoma-carcinoma sequence have not yet been evaluated.
454 FLX pyrosequencing was used to evaluate the disturbance of intestinal microbiota during the adenoma-carcinoma sequence pathway of CRC. Intestinal microbiota and mucosa tumor-immune cytokines were detected in mice after introducing 1,2-dimethylhydrazine (DMH), F. nucleatum or Berberine (BBR), using pyrosequencing and Bio-Plex Pro™ cytokine assays, respectively. Protein expressions were detected by western blotting.
The levels of opportunistic pathogens, such as Fusobacterium, Streptococcus and Enterococcus spp. gradually increased during the colorectal adenoma-carcinoma sequence in human fecal and mucosal samples. F. nucleatum treatment significantly altered lumen microbial structures, with increased Tenericutes and Verrucomicrobia (opportunistic pathogens) (P < 0.05 = in wild-type C57BL/6 and mice with DMH treatment). BBR intervention reversed the F. nucleatum-mediated increase in opportunistic pathogens, and the secretion of IL-21/22/31, CD40L and the expression of p-STAT3, p-STAT5 and p-ERK1/2 in mice, compared with mice fed with F. nucleatum alone.
F. nucleatum colonization in the intestine may prompt colorectal tumorigenesis. BBR could rescue F. nucleatum-induced colorectal tumorigenesis by modulating the tumor microenvironment and blocking the activation of tumorigenesis-related pathways.
Increasing evidence suggests that perturbations in the intestinal microbiota composition of infants are implicated in the pathogenesis of food allergy (FA), while the actual structure and composition of the intestinal microbiota in human beings with FA remain unclear. Microbial diversity and composition were analyzed with parallel barcoded 454 pyrosequencing targeting the 16S rRNA gene hypervariable V1-V3 regions in the feces of 34 infants with FA (17 IgE mediated and 17 non-IgE mediated) and 45 healthy controls. Here, we showed that several key FA-associated bacterial phylotypes, but not the overall microbiota diversity, significantly changed in infancy fecal microbiota with FA and were associated with the development of FA. The proportion of abundant Bacteroidetes, Proteobacteria, and Actinobacteria phyla were significantly reduced, while the Firmicutes phylum was highly enriched in the FA group (P < 0.05). Abundant Clostridiaceae 1 organisms were prevalent in infants with FA at the family level (P = 0.016). FA-enriched phylotypes negatively correlated with interleukin-10, for example, the genera Enterococcus and Staphylococcus. Despite profound interindividual variability, levels of 20 predominant genera were significantly different between the FA and healthy control groups (P < 0.05). Infants with IgE-mediated FA had increased levels of Clostridium sensu stricto and Anaerobacter and decreased levels of Bacteroides and Clostridium XVIII (P < 0.05). A positive correlation was observed between Clostridium sensu stricto and serum-specific IgE (R = 0.655, P < 0.001). The specific microbiota signature could distinguish infants with IgE-mediated FA from non-IgE-mediated ones. Detailed microbiota analysis of a well-characterized cohort of infants with FA showed that dysbiosis of fecal microbiota with several FA-associated key phylotypes may play a pathogenic role in FA.
Preterm birth is the second leading cause of death in children under the age of five years worldwide, but the etiology of many cases remains enigmatic. The dogma that the fetus resides in a sterile environment is being challenged by recent findings and the question has arisen whether microbes that colonize the fetus may be related to preterm birth. It has been posited that meconium reflects the in-utero microbial environment. In this study, correlations between fetal intestinal bacteria from meconium and gestational age were examined in order to suggest underlying mechanisms that may contribute to preterm birth.
Meconium from 52 infants ranging in gestational age from 23 to 41 weeks was collected, the DNA extracted, and 16S rRNA analysis performed. Resulting taxa of microbes were correlated to clinical variables and also compared to previous studies of amniotic fluid and other human microbiome niches.
Increased detection of bacterial 16S rRNA in meconium of infants of <33 weeks gestational age was observed. Approximately 61·1% of reads sequenced were classified to genera that have been reported in amniotic fluid. Gestational age had the largest influence on microbial community structure (R = 0·161; p = 0·029), while mode of delivery (C-section versus vaginal delivery) had an effect as well (R = 0·100; p = 0·044). Enterobacter, Enterococcus, Lactobacillus, Photorhabdus, and Tannerella, were negatively correlated with gestational age and have been reported to incite inflammatory responses, suggesting a causative role in premature birth.
This provides the first evidence to support the hypothesis that the fetal intestinal microbiome derived from swallowed amniotic fluid may be involved in the inflammatory response that leads to premature birth.
This study examined the early development of the gut microbiome in young children carrying high genetic risk for type 1 diabetes (T1D). Researchers used high throughput 16S rRNA gene sequencing on monthly stool samples collected from 4 to 6 months of age until 2.2 years of age. The goal was to identify compositional changes in the gut microbiome that occur before children develop T1D related autoimmunity. Both low abundance taxa and highly abundant groups, including two closely related Bacteroides species, were assessed for their relationship to later seroconversion.
The cohort consisted of 76 children at high genetic risk for T1D, all born in the same hospital in Turku, Finland. Of these children, 29 later seroconverted to T1D related autoimmunity, and 22 of those went on to develop T1D, forming the case group. The remaining 47 children stayed healthy throughout the study period and served as controls.
Several low abundance bacterial species showed significant compositional differences between children who later seroconverted and those who remained healthy. Notably, a highly abundant group made up of two closely related species, Bacteroides dorei and a related Bacteroides species, stood out as dominant in the gut microbiome prior to the onset of autoimmunity. This finding points to an early, high abundance microbial signal associated with the path toward T1D related autoimmunity, distinct from the more subtle low abundance differences.
The early presence and dominance of Bacteroides dorei before autoimmune seroconversion suggests the gut microbiome may play an active role in the processes leading to T1D in genetically susceptible children. Because the sampling began in infancy and continued monthly, these findings support the idea that microbiome monitoring during early childhood could help identify children at elevated risk before clinical autoimmunity appears. This work adds to the broader case that environmental factors, particularly the developing gut microbiome, interact with genetic predisposition to influence autoimmune disease risk. The Salmonella and Enterobacteriaceae groups were not mentioned in this abstract, so no claims are made about them here.
Background: Accumulating evidence indicates that diet is one of the most important environmental factors involved in the progression from advanced colorectal adenoma (A-CRA) to colorectal cancer. Objective: We evaluated the possible effects of dietary fiber on the fecal microbiota of patients with A-CRA. Design: Patients with a diagnosis of A-CRA by pathological examination were enrolled in the A-CRA group. Patients with no obvious abnormalities or histopathological changes were enrolled in the healthy control (HC) group. Dietary fiber intake was assessed in all patients. Short-chain fatty acids (SCFAs) in feces were detected by gas chromatography. The fecal microbiota community was analyzed by 454 pyrosequencing based on 16S ribosomal RNA. Results: Lower dietary fiber patterns and consistently lower SCFA production were observed in the A-CRA group (n = 344). Principal component analysis showed distinct differences in the fecal microbiota communities of the 2 groups. Clostridium, Roseburia, and Eubacterium spp. were significantly less prevalent in the A-CRA group (n = 47) than in the HC group (n = 47), whereas Enterococcus and Streptococcus spp. were more prevalent in the A-CRA group (n = 47) (all P < 0.05). Butyrate and butyrate-producing bacteria were more prevalent in a subgroup of HC subjects with a high fiber intake than in those in both the low-fiber HC subgroup and the high-fiber A-CRA subgroup (all P < 0.05). Conclusion: A high-fiber dietary pattern and subsequent consistent production of SCFAs and healthy gut microbiota are associated with a reduced risk of A-CRA. This trial was registered at www.chictr.org as ChiCTR-TRC-00000123.
Several evidences indicate that gut microbiota is involved in the control of host energy metabolism. To evaluate the differences in the composition of gut microbiota in rat models under different nutritional status and physical activity and to identify their associations with serum leptin and ghrelin levels.
In a case control study, forty male rats were randomly assigned to one of these four experimental groups: ABA group with food restriction and free access to exercise; control ABA group with food restriction and no access to exercise; exercise group with free access to exercise and feed ad libitum and ad libitum group without access to exercise and feed ad libitum. The fecal bacteria composition was investigated by PCR-denaturing gradient gel electrophoresis and real-time qPCR.
In restricted eaters, we have found a significant increase in the number of Proteobacteria, Bacteroides, Clostridium, Enterococcus, Prevotella and M. smithii and a significant decrease in the quantities of Actinobacteria, Firmicutes, Bacteroidetes, B. coccoides-E. rectale group, Lactobacillus and Bifidobacterium with respect to unrestricted eaters. Moreover, a significant increase in the number of Lactobacillus, Bifidobacterium and B. coccoides-E. rectale group was observed in exercise group with respect to the rest of groups. We also found a significant positive correlation between the quantity of Bifidobacterium and Lactobacillus and serum leptin levels, and a significant and negative correlation among the number of Clostridium, Bacteroides and Prevotella and serum leptin levels in all experimental groups. Furthermore, serum ghrelin levels were negatively correlated with the quantity of Bifidobacterium, Lactobacillus and B. coccoides-Eubacterium rectale group and positively correlated with the number of Bacteroides and Prevotella.
Nutritional status and physical activity alter gut microbiota composition affecting the diversity and similarity. This study highlights the associations between gut microbiota and appetite-regulating hormones that may be important in terms of satiety and host metabolism.
Despite a long-suspected role in the development of human colorectal cancer (CRC), the composition of gut microbiota in CRC patients has not been adequately described. In this study, fecal bacterial diversity in CRC patients (n=46) and healthy volunteers (n=56) were profiled by 454 pyrosequencing of the V3 region of the 16S ribosomal RNA gene. Both principal component analysis and UniFrac analysis showed structural segregation between the two populations. Forty-eight operational taxonomic units (OTUs) were identified by redundancy analysis as key variables significantly associated with the structural difference. One OTU closely related to Bacteroides fragilis was enriched in the gut microbiota of CRC patients, whereas three OTUs related to Bacteroides vulgatus and Bacteroides uniformis were enriched in that of healthy volunteers. A total of 11 OTUs belonging to the genera Enterococcus, Escherichia/Shigella, Klebsiella, Streptococcus and Peptostreptococcus were significantly more abundant in the gut microbiota of CRC patients, and 5 OTUs belonging to the genus Roseburia and other butyrate-producing bacteria of the family Lachnospiraceae were less abundant. Real-time quantitative PCR further validated the significant reduction of butyrate-producing bacteria in the gut microbiota of CRC patients by measuring the copy numbers of butyryl-coenzyme A CoA transferase genes (Mann-Whitney test, P<0.01). Reduction of butyrate producers and increase of opportunistic pathogens may constitute a major structural imbalance of gut microbiota in CRC patients.
It is debated whether a low total diversity of the gut microbiota in early childhood is more important than an altered prevalence of particular bacterial species for the increasing incidence of allergic disease. The advent of powerful, cultivation-free molecular methods makes it possible to characterize the total microbiome down to the genus level in large cohorts. We sought to assess microbial diversity and characterize the dominant bacteria in stool during the first year of life in relation to atopic eczema development.
Microbial diversity and composition were analyzed with barcoded 16S rDNA 454-pyrosequencing in stool samples at 1 week, 1 month, and 12 months of age in 20 infants with IgE-associated eczema and 20 infants without any allergic manifestation until 2 years of age (ClinicalTrials.gov ID NCT01285830).
Infants with IgE-associated eczema had a lower diversity of the total microbiota at 1 month (P = .004) and a lower diversity of the bacterial phylum Bacteroidetes and the genus Bacteroides at 1 month (P = .02 and P = .01) and the phylum Proteobacteria at 12 months of age (P = .02). The microbiota was less uniform at 1 month than at 12 months of age, with a high interindividual variability. At 12 months, when the microbiota had stabilized, Proteobacteria, comprising gram-negative organisms, were more abundant in infants without allergic manifestation (Empirical Analysis of Digital Gene Expression in R [edgeR] test: P = .008, q = 0.02).
Low intestinal microbial diversity during the first month of life was associated with subsequent atopic eczema.
This study examined how diet shapes gut microbial composition by comparing the fecal microbiota of children eating different diets. Researchers used high-throughput 16S rDNA sequencing together with biochemical analyses to characterize bacterial community composition and short-chain fatty acid output. The design set a fiber-rich, agrarian-style diet against a modern European diet to test whether microbiota differ along with dietary pattern.
The study compared fecal samples from European children (EU) with those from children living in a rural African village in Burkina Faso (BF). The BF children's diet was high in fiber content and described as similar to the diet of early human settlements around the birth of agriculture. Exact sample sizes are not given in the abstract, but the comparison was structured as two defined pediatric cohorts, one European and one rural Burkinabe.
BF children showed significant enrichment in Bacteroidetes and depletion in Firmicutes compared to EU children (P < 0.001). BF children also had a unique abundance of Prevotella and Xylanibacter, genera known to carry genes for cellulose and xylan hydrolysis, which were completely absent in EU children. BF children produced significantly more short-chain fatty acids than EU children (P < 0.001). Enterobacteriaceae, specifically Shigella and Escherichia, were significantly underrepresented in BF children relative to EU children (P < 0.05).
The findings support the idea that gut microbiota coevolved with a polysaccharide-rich diet, helping BF children extract more energy from fiber through bacterial fermentation to short-chain fatty acids. The reduced abundance of Enterobacteriaceae, including Shigella and Escherichia, in the high-fiber BF group suggests diet may also influence the balance between beneficial fiber-degrading bacteria and potentially pathogenic Enterobacteriaceae. Together these results indicate that dietary pattern is a major driver of gut microbial ecology in children, with possible downstream effects on metabolic energy harvest and gut colonization resistance.
2026-07-04
Enterococcus majorTaxon page created: genus biology (morphology, pathogenicity, virulence and resistance), the manganese metallome and vulnerabilities, interventions, the data-derived Conditions table across 193 conditions, and the full research feed.
Rödenbeck M, Ayobami O, Eckmanns T, Pletz MW, Bleidorn J, Markwart R.
Clinical epidemiology and case fatality due to antimicrobial resistance in Germany: a systematic review and meta-analysis, 1 January 2010 to 31 December 2021.Euro Surveill. 2023
Chilambi GS, Nordstrom HR, Evans DR, Ferrolino JA, Hayden RT, Maron GM, Vo AN, Gilmore MS, Wolf J, Rosch JW, Van Tyne D.
Evolution of vancomycin-resistant Enterococcus faecium during colonization and infection in immunocompromised pediatric patients.Proc Natl Acad Sci U S A. 2020
Colomer-Winter C, Flores-Mireles AL, Baker SP, Frank KL, Lynch AJL, Hultgren SJ, Kitten T, Lemos JA.
Manganese acquisition is essential for virulence of Enterococcus faecalis.PLoS Pathog. 2018
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