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The Klebsiella genus is a group of gut opportunists led by K. pneumoniae. Their ureases are nickel enzymes, and a nickel chelator can slow even multidrug-resistant members.
Klebsiella is a genus of encapsulated Enterobacteriaceae, led by Klebsiella pneumoniae, that colonize the gut and act as opportunistic pathogens in the lungs, urinary tract, and bloodstream. The genus depends on metal acquisition: iron piracy by siderophores and a nickel-dependent urease that nickel chelation can block.
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 MoreKlebsiella is a genus of Gram-negative, encapsulated Enterobacteriaceae that colonize the human gut and mucosa and act as opportunistic pathogens. It is led by Klebsiella pneumoniae, an ESKAPE pathogen responsible for pneumonia, urinary tract infections, and bloodstream infections,[1] and also includes K. oxytoca and K. aerogenes. On this database the genus appears as a differentially abundant gut taxon across many human microbiome studies.
The genus is defined by its capacity to acquire antibiotic resistance and, in hypervirulent lineages, to cause invasive disease, increasingly on the same conjugative plasmids.[1][2] Members also depend on the metal nickel: their ureases are nickel enzymes, and a nickel chelator inhibits Klebsiella urease and slows multidrug-resistant strains, a nutritional immunity angle this database reads pathogens through.[3]
Klebsiella species are Gram-negative, non-motile, rod-shaped bacteria with a prominent polysaccharide capsule.[1] In hypervirulent K. pneumoniae the capsule creates a hypermucoviscous phenotype that resists immune clearance.[1]
The genus is opportunistic: gut colonization is common, and disease follows spread to the lungs, urinary tract, bloodstream, or liver.[1] Classical strains dominate hospital-acquired, carbapenem-resistant infection, while hypervirulent strains cause community-acquired invasive disease, and convergent resistant-and-hypervirulent strains are a recognized threat.[1][2]
The genus pairs an anti-immune capsule with metal piracy and adhesion.
| Virulence factor | Description and role |
|---|---|
| Polysaccharide capsule | The dominant virulence factor; blocks phagocytosis and complement and drives hypermucoviscosity in hypervirulent strains.[1] |
| Siderophores | Iron-scavenging molecules (aerobactin, yersiniabactin, salmochelin) that pirate host iron; aerobactin marks hypervirulence.[1] |
| Urease | A nickel-dependent enzyme supporting colonization, inhibited by nickel chelation (see Metallomics).[3] |
| Resistance/virulence plasmids | Conjugative plasmids move carbapenem resistance and hypervirulence together across strains.[2] |
Klebsiella fights the host for iron, which it pirates with siderophores, and nickel, which powers its urease.
| Metal / ion | Key features in Klebsiella |
|---|---|
| Iron (Fe) | The primary virulence metal; siderophores strip iron from host proteins, and output tracks with hypervirulence.[1] |
| Nickel (Ni) | Urease is nickel-dependent; the chelator dimethylglyoxime inhibits Klebsiella urease and is bacteriostatic against multidrug-resistant strains.[3] |
| Host metal withholding | The host restricts iron, zinc, and nickel to starve invaders; the genus's siderophore and nickel systems are its countermeasures.[1][3] |
The metal-acquisition systems that make Klebsiella invasive are also targets.
| Weak point | Why it is exploitable |
|---|---|
| Nickel and urease dependence | Nickel chelation inhibits urease and slows even multidrug-resistant strains, sidestepping conventional resistance.[3] |
| Iron and siderophore dependence | Reliance on siderophores makes iron restriction and siderophore targeting attractive against hypervirulent strains.[1] |
| Antibiotic therapy | Infections are treated with antibiotics, but spreading carbapenem resistance narrows options.[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 metal restriction.
| Intervention | Class | Status |
|---|---|---|
| Antibiotic therapy (culture-directed) | Drug | Validated |
| Nickel chelation / urease inhibition | Concept | Validation In Progress |
| Iron restriction / siderophore targeting | Concept | Validation In Progress |
Untargeted dietary nickel loading, which could feed the nickel-dependent urease and work against the host's metal-withholding defense.[3]
Where Klebsiella (NCBI:txid570) 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 140 conditions and 162 studies, the signal is genuinely mixed: enriched in 71, depleted in 43, and direction-conflicting in 26 (directional agreement 0.59). Because Klebsiella is a low-abundance gut colonizer that blooms opportunistically, its differential signal usually reflects an Enterobacteriaceae shift rather than a fixed community role, so the aggregate evidence tier is Low.
How to read these. Klebsiella is usually a minor gut resident that expands under dysbiosis, antibiotics, or inflammation, and genus-level detection groups several species. A differential signal most often marks that bloom rather than a stable ecological role. This is why direction can conflict between cohorts and the aggregate tier stays Low.
Internal summaries of the 162 studies we reviewed in which Klebsiella 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: Tuberculosis (TB) and COVID-19 are both respiratory diseases, and understanding their interaction is important for effective co-infection management. Although some studies have investigated TB and COVID-19 co-infection in terms of immune responses, microbial dysbiosis in such cases remains unexplored. In this study, we understand the interface between TB and COVID-19 by systematically inspecting the microbial composition of sputum samples collected from four groups of individuals: TB only, COVID-19 only, and both TB and COVID-19 (TBCOVID) infected patients, and uninfected group (Controls). Besides metagenomic analysis of the microbiome of these sputum samples, we also performed whole-genome sequencing analysis of a subset of TB-positive samples. Different bioinformatic analyses ensured data quality and revealed significant differences in the microbial composition between Control vs disease groups. To understand the effect of COVID-19 on TB, we compared TBCOVID vs TB samples and observed (i) higher read counts of TB-causing bacteria in the TBCOVID group, and (ii) differential abundance of several taxa, including Capnocytophaga gingivalis. Functional profiling with PICRUSt2 revealed elevated pathways, including the pulmonary surfactant lipid metabolism pathway (with a fold change of 7.46) in the TBCOVID group. Further clustering of these pathways revealed a sub-cluster of individuals with adverse treatment outcomes. Two individuals in this sub-cluster had a respiratory pathogen, Stenotrophomonas maltophilia-knowing such information on key respiratory pathogens in a patient can help personalize the patient's antibiotic regimen. Overall, our study reveals the effect of COVID-19 on the airway microbiome of TB patients and encourages the use of co-microbial/co-pathogen profiling to personalize TB treatment. IMPORTANCE: The community of microbes in an individual's airway tract can play a complex role in respiratory diseases like tuberculosis (TB) and COVID-19. Although changes in microbial composition in TB and COVID-19 patients have been studied separately, we present a first-of-its-kind investigation of the airway-tract microbiome of individuals simultaneously infected with TB and COVID-19 pathogens. Our results highlight that co-infection with COVID-19 in TB patients alters the abundance of certain bacterial species and their related pathways. For instance, Capnocytophaga gingivalis is abundant in co-infected patients, but not in TB-only patients. This species and other differentially abundant species we identified in the co-morbid condition, if replicated in independent cohorts, can help explain how COVID-19 could exacerbate the severity of lung infection in TB patients. Our study also stimulates future longitudinal studies using expanded data sets to understand the role of concomitant pathogens and assess whether adjusting the antibiotic regimen accordingly can improve TB treatment outcomes.
Azithromycin is a widely used antibiotic and was frequently used to treat hospitalized patients during the COVID-19 pandemic. The impact of empiric azithromycin use on the respiratory microbiome in patients with viral respiratory infections is unclear. Here we used longitudinal metatranscriptomics on nasal swabs from a prospective multicentre cohort of 1,164 patients hospitalized for COVID-19. We compared the upper respiratory microbiome, resistome and systemic immune response in patients treated with azithromycin (n = 366) with those who received no antibiotics (n = 474) or other antibiotics (n = 324). We found that azithromycin altered microbiome composition and increased the expression and relative proportion of macrolide/lincosamide/streptogramin (MLS) resistance genes. These changes occurred after 1 day of exposure and persisted for over a week. MLS resistance gene expression was associated with commensals and potential pathogens, while there were no differences in host inflammatory gene expression in blood and airways. This demonstrates that empiric azithromycin treatment impacts the upper respiratory microbiome and resistome without apparent anti-inflammatory benefit.
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.
Background: The real-world risk profiles of newly defined steatotic liver disease (SLD) subtypes-MASLD, MetALD, and ALD-remain incompletely described in community settings. Methods: A cross-sectional analysis of 950 health-checkup participants was conducted. SLD (CAP ≥ 248 dB/m) and significant fibrosis (LSM ≥ 7.0 kPa) were evaluated by transient elastography. Associations between alcohol intake, cardiometabolic factors, fibrosis, and gut microbiota (16S rRNA sequencing) were assessed. Results: Among 950 participants, 310 (33%) had SLD (MASLD, n = 222; MetALD, n = 41; ALD, n = 23). Treated as a continuous exposure, higher alcohol intake was significantly correlated with elevated systolic/diastolic blood pressure, triglycerides, AST, and γ-GTP, but inversely correlated with HOMA-IR (all p < 0.05). In multivariable logistic regression adjusting for cardiometabolic factors, BMI was the only independent predictor of fibrosis (adjusted OR 1.22, 95% CI 1.11-1.35, p < 0.01), whereas alcohol intake showed no independent association. Furthermore, microbiota analysis revealed that ALD-related SLD was characterized by significant depletion of Blautia and enrichment of Gemella (FDR q < 0.05) compared to non-SLD controls, indicating an alcohol-associated dysbiosis signature. Conclusions: In early-stage SLD, alcohol intake continuously exacerbates cardiometabolic risk factors, whereas fibrosis is predominantly driven by BMI. These findings support quantitative alcohol/BMI integration for risk stratification, alongside microbiota profiling to detect ALD-related dysbiosis.
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.
With the improvement of living standards, alcoholic liver disease caused by long-term drinking has been a common multiple disease. Probiotic interventions may help mitigate liver damage caused by alcohol intake, but the mechanisms need more investigation.
This study involved 70 long-term alcohol drinkers (18-65 years old, alcohol consumption ≥20 g/day, lasting for more than one year) who were randomly assigned to either the BC99 group or the placebo group. Two groups were given BC99 (3 g/day, 1 × 1010 CFU) or placebo (3 g/day) for 60 days, respectively. Before and after the intervention, blood routine indicators, liver function, renal function, inflammatory factors and intestinal flora were evaluated.
The results showed that intervention with Weizmannia coagulans BC99 reduced the levels of alanine aminotransferase, aspartate aminotransferase, glutamyl transpeptidase, serum total bilirubin, blood urea nitrogen, uric acid and 'blood urea nitrogen/creatinine'. Weizmannia coagulans BC99 also reduced the levels of pro-inflammatory factors TNF-α and IL-6 and increased the levels of anti-inflammatory factor IL-10. The results of intestinal flora analysis showed that Weizmannia coagulans BC99 regulated the imbalance of intestinal flora, increased the beneficial bacteria abundance (Prevotella, Faecalibacterium and Roseburia) and reduced the conditionally pathogenic bacteria abundance (Escherichia-Shigella and Klebsiella). Both LEfSe analysis and random forest analysis indicated that the increase in the abundance of Muribaculaceae induced by BC99 was a key factor in alleviating alcohol-induced liver damage.
These findings demonstrate that Weizmannia coagulans BC99 has the potential to alleviate alcoholic liver injury and provide an effective strategy for liver protection in long-term drinkers.
This study examined whether the probiotic Bifidobacterium longum subsp. longum BL21 could mitigate symptoms of polycystic ovary syndrome (PCOS) in a DHT-induced (prenatal androgen-induced) mouse model. The researchers focused on BL21's effects on metabolic dysregulation, inflammation, and neuroprotection, framed through the gut-brain-ovary axis. Mice received a daily oral dose of 1 x 10^9 CFU of BL21 for a continuous 8-week treatment period. Outcomes assessed included body weight, glucose tolerance, serum BDNF, inflammatory markers, sex hormone levels, and gut microbiota composition via 16S rRNA gene sequencing.
The subjects were twenty-four ICR mice with prenatal androgen (DHT)-induced PCOS, an established animal model rather than human patients. The abstract does not specify how the 24 mice were divided among treatment and control groups. All findings therefore come from a controlled mouse model of PCOS, not from a human cohort.
BL21 significantly increased sex hormone levels, particularly follicle-stimulating hormone (FSH) and estradiol (E2), suggesting improved ovarian function (P < 0.05). The probiotic also curbed weight gain and improved glucose tolerance in the PCOS mice (P < 0.05). Additionally, BL21 reduced inflammatory markers, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and lipopolysaccharides (LPS), while increasing the anti-inflammatory marker IL-10. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so this study is summarized on its own terms.
These results position Bifidobacterium longum subsp. longum BL21 as a novel candidate approach for addressing hormonal, metabolic, and inflammatory disturbances in PCOS. The findings support the concept of a gut-brain-ovary axis, in which a targeted probiotic can influence ovarian hormone output and systemic inflammation together. Because this work was conducted in a mouse model, further research would be needed to establish whether similar effects occur in humans with PCOS.
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 characterized the peripheral blood microbiome of tuberculosis (TB) patients using RNA sequencing, aiming to find non-sputum biomarkers for TB diagnosis. The researchers focused on identifying Mycobacterium tuberculosis (Mtb) genome-derived small RNA molecules, specifically rRNA-derived small RNAs (rsRNAs), circulating in blood. They analyzed blood microbiome RNA signals across bacteria, fungi, archaea, and viruses, and then tested candidate Mtb rsRNAs as potential diagnostic markers. Small RNA sequencing was also performed on plasma exosomes to further probe these RNA signatures.
The initial analysis used RNA sequencing data from the blood of TB patients and healthy controls retrieved from the NCBI-SRA public database. Small RNA sequencing was additionally performed on plasma exosomes from TB patients and healthy controls. Candidate Mtb rsRNA levels were then validated by RT-qPCR in a separate cohort of 73 TB patients and 62 healthy controls. Together these groups combined public sequencing data with a defined clinical validation cohort.
The blood microbiome of TB patients contained RNA signals from bacteria, fungi, archaea, and viruses, with bacteria making up more than 97% of the total signal. TB patients showed reduced blood microbial diversity and reduced abundance of six Mycobacterium-associated bacterial genera, including Mycobacterium and Priestia. Mtb-derived rsRNAs were detectable in blood and plasma exosomes, distinguishing TB patients from healthy controls in the validation cohort of 73 patients and 62 controls.
These findings suggest that blood microbiome signatures and circulating Mtb-derived rsRNAs could serve as non-sputum, blood-based diagnostic biomarkers for tuberculosis. This approach could help address the ongoing challenge of early TB diagnosis, particularly for patients who cannot easily produce sputum samples. The reduced microbial diversity and altered Mycobacterium-associated genera also point to broader shifts in the blood microbiome accompanying active TB infection. Validating these markers in a defined patient cohort supports their potential clinical translation as a diagnostic test.
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.
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.
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.
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.
Obesity-related cognitive decline is linked to gut microbiota dysbiosis, with emerging evidence suggesting that dietary interventions may ameliorate cognitive impairment via gut-brain axis modulation. The role of microglial cells in this process remains underexplored. To investigate how diet-induced changes in gut microbiota influence cognitive function in individuals with obesity and their microglial activity, and to determine the impact of specific dietary interventions.
This study included 96 participants with obesity who were randomised into three dietary intervention groups: Mediterranean diet (Med), alternate-day fasting (ADF) and ketogenic diet (Keto). Cognitive performance and microbiota composition were assessed pre-intervention and post-intervention. The effects of microbiota-related changes on microglial function were further evaluated in mice models through faecal transplantation and in vitro model with microbiota exosome treatment.
Both the Keto and ADF groups demonstrated significant weight loss, but cognitive performance improved most notably in the ADF group, in association with reduced inflammation. Diet-related microbiota composition was correlated with the cognitive outcomes in the human study. Mice models confirmed that the cognitive benefits of ADF were microbiota-dependent and linked to enhanced microglial phagocytic capacity and reduced inflammation, accompanied by changes in microglia morphology.
Fasting-induced modifications in gut microbiota contribute to cognitive improvement in individuals with obesity, with microglial cells playing a crucial mediatory role. Among the interventions, ADF most effectively enhanced microglial function and cognitive performance, suggesting its potential as a therapeutic strategy for obesity-related cognitive decline. Further studies are required to fully elucidate the underlying mechanisms.
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.
This study examined the relationship between peripheral blood cytokine profiles and gut microbiota composition in Graves' disease (GD), the most common autoimmune thyroid disorder. Researchers used 16S rRNA gene sequencing of fecal samples alongside multiplex cytokine array analysis of blood immune markers. Electrochemiluminescence immunoassay was used to quantify thyroid function parameters, and Spearman correlation analysis linked cytokines, thyroid function indices, and microbial taxa. The goal was to clarify how cellular immunity and gut microbial community dynamics interact in GD pathogenesis.
The study enrolled 30 untreated GD patients consecutively admitted to the Department of Endocrinology at the Third Affiliated Hospital of Qiqihar Medical University between January and July 2023. These patients were compared against 30 age- and sex-matched healthy controls. This case-control design allowed direct comparison of microbiota and cytokine profiles between diseased and healthy individuals.
Alpha diversity analysis showed that the abundance and diversity of certain gut microbiota decreased in the GD group compared to healthy controls. Beta diversity analysis also indicated compositional differences between the two groups, though the abstract's full details on which specific taxa and cytokines correlated were not provided. The study framed gut microbiome alterations as linked to immune marker changes in GD patients, consistent with bidirectional communication between the gut microbiome and host immunity.
These findings support the idea that gut microbiota may act as a modulator of autoimmune pathogenesis in Graves' disease through interaction with cellular immune pathways. Identifying correlations between specific cytokines and microbial taxa could eventually help explain mechanisms driving thyroid autoimmunity. This work lays groundwork for future research into whether modifying the gut microbiome could influence immune dysregulation in GD.
Crohn's disease (CD) is a chronic non-specific inflammatory bowel disease with an increasing incidence worldwide. Patients with CD are facing elevated risk for mental disorders (MD) than healthy people, and chronic psychological stress is considered to trigger deterioration and relapse of CD. The microbiome-gut-brain axis (MGBA) is recognized as a crucial factor in unraveling this connection. Whereas, so far, few studies have revealed the relationship of the microbiota communities and tryptophan catabolites of the terminal ileum mucosa on gut-brain communication.
A total of 52 patients with CD, along with 11 patients with colorectal cancers recruited as controls, were enrolled in this study. The participants completed Patient Health Questionnaire-9 and Generalized Anxiety Disorder-7 Questionnaire. The terminal ileal mucosa was collected during surgery. We profiled the microbiota composition of 37 patients and quantified the tryptophan catabolites of 28 patients utilizing 16 S rRNA gene sequencing and liquid chromatography-tandem mass spectrometry, respectively. In addition, bioinformatics methods were used to elucidate the interrelationships between psychological states, microbial communities, and tryptophan catabolites.
CD patients with MD showed a significant reduction in microbial diversity within the ileal mucosa. Regarding microbial composition, Prevotella was relatively enriched in CD patients with MD, along with lower relative abundances of Akkermansia and Faecalibacterium. Furthermore, significant disparities in the levels of Picolinic acid (PA), Kynurenic acid (KYNA), Nicotinic acid (N-Acid), and Indole-3-carbaldehyde (ICAld) were detected within the ileal mucosa of CD patients comorbid with MD. A pronounced correlation was observed between PA levels and anxiety scale scores. The heightened abundance of Prevotella may be closely associated with altered levels of PA, N-Acid, and KYNA.
Alterations in the microbial composition of the terminal ileum may interact with changes in tryptophan metabolism and are associated with MD in patients with CD undergoing surgery.
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.
The gut microbiome is associated with bone mass acquisition, yet evidence in childhood remains limited. Given that lower peak bone mass predicts osteoporosis in later life, understanding early influences is important. This analysis explores the association between the early life gut microbiome and bone health in later childhood. Data were obtained from 700 children recruited in pregnancy and followed prospectively within the Copenhagen Prospective Studies on Asthma in Childhood2010 cohort, a population-based mother-child cohort. The infant gut microbiome was measured at 1 wk (n = 445), 1 mo (n = 492), 1 yr (n = 508), 4 yr (n = 350), and 6 yr (n = 327) of age by 16S ribosomal ribonucleic acid amplicon sequencing targeting the fourth variable region. Total body less head BMD and area-adjusted BMC were measured by DXA at 6 yr of age. Associations were investigated by multiple linear regression, permutational analysis of variance, differential abundance analysis, and Random Forest machine learning. There were few associations between the early-life gut microbiome and bone health outcomes at age 6. We found negative associations between alpha (within-sample) diversity and area-adjusted BMC at 4 yr. Beta (between-sample) diversity of the gut microbiome at 6 yr was associated with concurrent BMD. Escherichia-Shigella abundance at 1 mo of age was associated with lower BMD. Sutterella abundance at 1 yr was associated with lower BMD and area-adjusted BMC at 6 yr. There were no other associations between the gut microbiome and bone outcome measures at any time point. In a well-powered unselected cohort study with longitudinal sampling of the gut microbiome, there were some suggestive but no consistent associations between the early gut microbiome and bone health outcomes at 6 yr of age. Bone health in childhood is important for preventing osteoporosis later in life. This study explored whether gut bacteria (gut microbiome) during infancy and early childhood influences bone health later in childhood. We followed 700 children, measuring their gut microbiome at 1 wk, 1 mo, and at 1, 4, and 6 yr, and their bone health at age 6. While some weak links were found between specific gut microbiome and bone health, the results were inconsistent. Overall, the findings suggest that early gut microbiome may have limited impact on later childhood bone health, and further research is required to confirm this.
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.
This study examined seasonal changes in gut microbiota composition and function across four bear species: giant pandas, Asian black bears, brown bears, and polar bears. Researchers combined comparative seasonal microbiome analysis with fecal microbiota transplantation (FMT) experiments in mice to test whether bear gut microbiota actively drives host energy metabolism. The core question was whether giant pandas, long considered metabolically unique due to their specialized herbivorous diet and low metabolic rate, actually rely on a distinct microbial regulatory mechanism compared to other bears.
The subjects were four Ursidae species: giant pandas (Ailuropoda melanoleuca), Asian black bears (Ursus thibetanus), brown bears (Ursus arctos), and polar bears (Ursus maritimus), sampled across seasons to capture gut microbiota dynamics. The abstract does not specify exact animal counts or sampling sites. Recipient mice were also used as a secondary population in the fecal microbiota transplantation experiments to test the functional effects of bear gut microbiota on host metabolism and appetite.
The gut microbial composition was similar across all four bear species, with Firmicutes and Proteobacteria as the dominant phyla. Firmicutes became enriched in winter, which enhanced lipid metabolism and helped the bears adapt to seasonal dietary differences, pointing to a convergent microbial functional strategy shared across the Ursidae family rather than a panda-specific mechanism. In FMT experiments, winter bear gut microbiota transferred stronger capacity to regulate host energy metabolism and appetite in mice, increasing energy intake, demonstrating that these microbial shifts causally promote seasonal metabolic adaptation.
By showing convergent, shared microbial functional strategies across giant pandas, black bears, brown bears, and polar bears, the findings challenge the long-standing view that giant panda gut microbiota is metabolically unique among bears. This reframes seasonal energy adaptation in Ursidae as a family-wide, diet-responsive microbiome trait rather than an evolutionary novelty confined to pandas. The FMT results also suggest that bear-derived winter microbiota could serve as a model system for studying microbiome-driven regulation of energy intake and appetite in mammals more broadly.
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.
Background: Autism Spectrum Disorder (ASD) is increasingly associated with alterations in gut microbiota, intestinal permeability, and immune dysregulation. However, integrative studies exploring these mechanisms in Latin American populations are lacking. Objective: To characterize gut microbiota profiles in Colombian children with ASD and evaluate the effects of two microbiota-targeted interventions, an anti-inflammatory diet and a probiotic formulation, on microbial diversity and taxonomic composition. Methods: In a two-phase study, shotgun metagenomic sequencing was performed on fecal samples from 23 children with ASD and 7 typically developing (TD) controls. In the second phase, 17 children with ASD were randomized to receive a 12-week intervention (anti-inflammatory diet, probiotics, or no intervention). Alpha diversity indices (Shannon, Pielou, and Chao1) and differential abundance analyses were conducted. Results: Compared to TD children, those with ASD showed a higher Firmicutes/Bacteroidetes ratio and a significantly increased abundance of genera such as Clostridioides, Thomasclavelia, Alistipes, and Coprococcus. The presence of functional gastrointestinal disorders (FGIDs) in ASD patients is associated with reduced microbial richness. POST-intervention, the anti-inflammatory diet group showed that no statistically significant changes in alpha diversity were observed, although a slight upward trend was noted and significant enrichment of six bacterial genera, including Moraxella and Eubacterium. The probiotic group exhibited a significant increase in Romboutsia and a decrease in Lachnospira. Cytokine-microbiota networks in ASD were fragmented and dominated by IFN-γ and MCP-1 hubs, indicating systemic immune activation. Interventions induced functional remodeling: The anti-inflammatory diet increased the number of beneficial genera (Eubacterium, Adlercreutzia) and shifted networks toward positive correlations involving IL-8 and MIP-1β. Probiotics increased Romboutsia, reduced Lachnospira, and restructured networks with regulatory cytokines (SDF-1α, Eotaxin) and SCFA-producing taxa (Blautia, Roseburia). Conclusions: Children with ASD in Colombia displayed distinct microbial profiles characterized by pro-inflammatory taxa and altered richness. Both the anti-inflammatory diet and probiotics produced compositional shifts in the gut microbiota, although global changes in diversity were limited. These findings support the potential of microbiota-targeted nutritional strategies for ASD and underscore the need for precision interventions tailored to specific clinical and microbial phenotypes.
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.
Emerging evidence indicates gut microbiota is essential to chronic kidney disease (CKD) progression. This study investigated the association between gut microbiota profiles, plasma trimethylamine-N-oxide (TMAO), and circulating inflammatory markers in CKD patients according to dietary patterns, particularly low-protein, high-fiber (LP-HF) versus high-protein, low-fiber (HP-LF) diet. In this cross-sectional study, patients with non-dialysis CKD and healthy subjects were enrolled. Dietary patterns among participants were assessed using three-day diet records with detailed nutrient analysis. The 16 S ribosomal RNA sequencing was conducted to examine fecal gut microbiota composition. Plasma samples were analyzed for TMAO concentration and cytokine levels. A total of 135 CKD patients were recruited. A distinct shift in gut microbiota composition in CKD patients was observed compared to 19 healthy controls, particularly a significant reduction of short-chain fatty acid (SCFA)-producing bacteria. TMAO and several cytokine levels were significantly elevated in CKD patients compared to healthy subjects. Within CKD, patients with LP-HF diet displayed a greater abundance of SCFA-producing bacteria, such as the Lachnospiraceae NK4A136 group and Eubacterium ruminantium group, than those with the HP-LF diet. The HP-LF subgroup showed enriched proteolytic bacterial genera such as Klebsiella. The HP-LF subgroup also exhibited significantly higher plasma levels of TMAO, interleukin (IL)-18, and monocyte chemoattractant protein-1 (MCP-1). CKD patients displayed marked alterations in gut bacterial composition compared to healthy controls. Our results also highlighted the potential advantages of adopting a high fiber-rich and low-protein diet intake in reducing gut dysbiosis in CKD patients.
This randomized, placebo-controlled trial examined whether resistant starch (RS), a prebiotic, has therapeutic effects in metabolic dysfunction-associated steatotic liver disease (MASLD). The researchers focused on why RS efficacy was heterogeneous, since about 30% of participants showed limited benefit. Using multi-omics analysis, fecal microbiota transplantation, population stratification, network analysis, and in vitro and in vivo experiments, they sought the microbial basis of this variable response. They then built a predictive model combining baseline microbial and clinical features to forecast who would respond.
Participants were drawn from the original randomized, placebo-controlled trial of resistant starch in MASLD, with the finding of heterogeneous response replicated in a separate multi-center trial (ChiCTR2300074588). The abstract does not give exact participant numbers or demographic details for either trial. A strain, Bifidobacterium pseudocatenulatum RRP01, was isolated from the study cohort for further experimentation.
Baseline gut microbiota composition was the dominant contributor to whether a participant responded to resistant starch. Prevotella was identified as a key cause of low response because it inhibits RS-degrading bacteria, impairing RS utilization. In contrast, the cohort-derived strain Bifidobacterium pseudocatenulatum RRP01 restored RS degradation and improved the RS response that Prevotella had attenuated. A predictive model integrating baseline microbial and clinical features achieved an area under the curve of 0.74 to 0.87 for stratifying likely responders.
The findings show that pre-existing gut microbiota composition, not just the intervention itself, determines whether resistant starch benefits patients with MASLD. This supports moving toward microbiota-oriented precision therapeutics, where baseline microbial and clinical features are used to predict who will respond before treatment begins. It also points to specific microbiota-targeted strategies, such as supplementing Bifidobacterium pseudocatenulatum RRP01, to overcome Prevotella-driven non-response and expand the benefit of prebiotic therapy to more patients.
Irritable bowel syndrome (IBS) is a common disorder of gut-brain interaction, and its pathogenesis remains unclear. Dysbiosis of the gut microbiota is associated with IBS. The gut microbiota may modulate IBS symptoms via the epithelial barrier, mucosal immunity, microbial metabolites (e.g., short-chain fatty acids and bile acids), and gut-brain signaling. Currently, dietary approaches, probiotics, prebiotics, rifaximin, and fecal microbiota transplantation show variable benefit; effects are strain-/context-dependent and evidence certainty varies, with adverse-event reporting inconsistent. This narrative review takes a subtype-aware, mechanism-first perspective to summarize microbiota functions, symptom links, and intervention evidence with safety considerations. This review offers new perspectives and insights for precision treatment and microbiome research in IBS.
This study examined the role of the intestinal microflora in pediatric nonalcoholic fatty liver disease (NAFLD), including its subtypes nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). Researchers used 16S rRNA and metagenomic sequencing on fecal samples to characterize the gut microbiome and its metabolic pathways. The goal was to explore how variation in gut flora correlates with NAFLD-related clinical indexes and metabolic function in children.
The study examined Chinese pediatric patients diagnosed with NAFLD, NASH, and NAFL, compared against healthy child controls. The abstract does not give an exact sample size or age range for these groups. The population reflects a clinical cohort of Chinese children, framed against the backdrop that 45% of Chinese adolescents with obesity develop fatty liver disease.
Certain fecal microbiota showed a negative correlation with body mass index (BMI), meaning higher abundance of these taxa was associated with lower BMI. The study identified several bacteria linked to NAFLD, including Lachnoclostridium, Escherichia-Shigella, and Faecalibacterium prausnitzii. These findings connected specific gut bacterial taxa to NAFLD-related metabolic and clinical indexes in children.
The findings suggest that variation in gut microbiota composition may play a more important role than previously appreciated in the development and progression of NAFLD and NASH in children. This points to the gut microbiome as a potential target for understanding or managing pediatric fatty liver disease, particularly given its long-term risk of progressing to cirrhosis and liver cancer. Because certain bacteria correlated with BMI, the results also reinforce a link between microbiome composition and body weight regulation in this population.
Remodeling eubiosis of the gut microenvironment may contribute to preventing the occurrence and development of depression. Mounting experimental evidence has shown that complement C3 signaling is associated with the pathogenesis of depression, and disruption of the gut microbiota may be an underlying cause of complement system activation. However, the mechanism by which complement C3 participates in gut-brain crosstalk in the pathogenesis of depression remains unknown.
In the present study, we found that chronic unpredictable mild stress (CUMS)-induced mice exhibited obvious depression-like behavior as well as cognitive impairment, which was associated with significant gut dysbiosis, especially enrichment of Proteobacteria and elevation of microbiota-derived lipopolysaccharides (LPS). In addition, peripheral and central complement C3 activation and central C3/CR3-mediated aberrant synaptic pruning in microglia have also been observed. Transplantation of gut microbiota from CUMS-induced depression model mice into specific pathogen-free and germ-free mice induced depression-like behavior and concomitant cognitive impairment in the recipient mice, accompanied by increased activation of the complement C3/CR3 pathway in the prefrontal cortex and abnormalities in microglia-mediated synaptic pruning. Conversely, antidepressants and fecal microbiota transplantation from antidepressant-treated donors improved depression-like behaviors and restored gut microbiome disturbances in depressed mice. Concurrently, inhibition of the complement C3/CR3 pathway, amelioration of abnormal microglia-mediated synaptic pruning, and increased expression of the synapsin and postsynaptic density protein 95 were observed. Collectively, our results revealed that gut dysbiosis induces the development of depression-like behaviors through abnormal synapse pruning in microglia-mediated by complement C3, and the inhibition of abnormal synaptic pruning is the key to targeting microbes to treat depression.
Our findings provide novel insights into the involvement of complement C3/CR3 signaling and aberrant synaptic pruning of chemotactic microglia in gut-brain crosstalk in the pathogenesis of depression. Video Abstract.
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 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.
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.
Recent studies have more focused on gut microbial alteration in tuberculosis (TB) patients. However, no detailed study on gut fungi modification has been reported till now. So, current research explores the characteristics of gut microbiota (bacteria)- and mycobiota (fungi)-dysbiosis in TB patients and also assesses the correlation between the gut microbiome and serum cytokines. It may help to screen the potential diagnostic biomarker for TB.
The results show that the alpha diversity of the gut microbiome (including bacteria and fungi) decreased and altered the gut microbiome composition of TB patients. The bacterial genera Bacteroides and Prevotella were significantly increased, and Blautia and Bifidobacterium decreased in the TB patients group. The fungi genus Saccharomyces was increased while decreased levels of Aspergillus in TB patients. It indicates that gut microbial equilibrium between bacteria and fungi has been altered in TB patients. The fungal-to-bacterial species ratio was significantly decreased, and the bacterial-fungal trans-kingdom interactions have been reduced in TB patients. A set model including Bacteroides, Blautia, Eubacterium_hallii_group, Apiotrichum, Penicillium, and Saccharomyces may provide a better TB diagnostics option than using single bacterial or fungi sets. Also, gut microbial dysbiosis has a strong correlation with the alteration of IL-17 and IFN-γ.
Our results demonstrate that TB patients exhibit the gut bacterial and fungal dysbiosis. In the clinics, some gut microbes may be considered as potential biomarkers for auxiliary TB diagnosis.
The mosquito microbiota is a critical determinant of mosquito life history. It is therefore a target for novel vector control strategies like paratransgenesis. However, the microbiota in Anopheles funestus, a major African malaria vector, is poorly characterized. Thus, the study aimed to investigate the overall bacterial landscape in the salivary glands, ovaries and midguts of three laboratory strains of An. funestus differing in insecticide-resistant phenotype by sequencing the V3-V4 hypervariable region of bacterial 16S rRNA genes. When examining alpha diversity, the salivary glands harbored significantly more bacteria in terms of species richness and evenness compared to ovaries and midguts. On the strain level, the insecticide-susceptible FANG strain had significantly lower bacterial diversity than the insecticide-resistant FUMOZ and FUMOZ-R strains. When looking at beta diversity, the compositions of microbiota between the three tissues as well as between the strains were statistically different. While there were common bacteria across all three tissues and strains of interest, each tissue and strain did exhibit differentially abundant bacterial genera. However, overall, the top five most abundant genera across all tissues and strains were Elizabethkingia, Acinetobacter, Aeromonas, Cedecea and Yersinia. The presence of shared microbiota suggests a core microbiota that could be exploited for paratransgenesis efforts.
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.
Polycystic ovary syndrome (PCOS) is an endocrinopathy in childbearing-age females which can cause many complications, such as diabetes, obesity, and dyslipidemia. The metabolic disorders in patients with PCOS were linked to gut microbial dysbiosis. However, the correlation between the gut microbial community and dyslipidemia in PCOS remains unillustrated. Our study elucidated the different gut microbiota in patients with PCOS and dyslipidemia (PCOS.D) compared to those with only PCOS and healthy women.
In total, 18 patients with PCOS, 16 healthy females, and 18 patients with PCOS.D were enrolled. The 16 S rRNA sequencing in V3-V4 region was utilized for identifying the gut microbiota, which analyzes species annotation, community diversity, and community functions. Our results showed that the β diversity of gut microbiota did not differ significantly among the three groups. Regarding gut microbiota dysbiosis, patients with PCOS showed a decreased abundance of Proteobacteria, and patients with PCOS.D showed an increased abundance of Bacteroidota compared to other groups. With respect to the gut microbial imbalance at genus level, the PCOS.D group showed a higher abundance of Clostridium_sensu_stricto_1 compared to other two groups. Furthermore, the abundances of Faecalibacterium and Holdemanella were lower in the PCOS.D than those in the PCOS group. Several genera, including Faecalibacterium and Holdemanella, were negatively correlated with the lipid profiles. Pseudomonas was negatively correlated with luteinizing hormone levels. Using PICRUSt analysis, the gut microbiota community functions suggested that certain metabolic pathways (e.g., amino acids, glycolysis, and lipid) were altered in PCOS.D patients as compared to those in PCOS patients.
The gut microbiota characterizations in patients with PCOS.D differ from those in patients with PCOS and controls, and those might also be related to clinical parameters. This may have the potential to become an alternative therapy to regulate the clinical lipid levels of patients with PCOS in the future.
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.
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.
This study used deep shotgun metagenomic sequencing to characterize the taxonomic and functional composition of the gut microbiome in older adults from Singapore. The researchers examined how gut microbial communities and their metabolic capabilities relate to aging phenotypes. They performed joint species-level analysis together with other Asian cohorts to identify age-associated shifts in microbial composition and function. The work also linked microbiome features to clinical markers of inflammation, cardiometabolic health, and liver health.
The cohort consisted of 234 community-living octogenarians in Singapore who were described as well-phenotyped. Their gut microbiomes were compared jointly against data from other Asian cohorts to identify consistent age-associated species shifts. The abstract does not specify sex distribution, exact age range beyond octogenarian status, or additional demographic details.
Aging was associated with reduced microbial richness and enrichment of specific Alistipes and Bacteroides species, including Alistipes shahii and Bacteroides xylanisolvens. Functional analysis showed a corresponding expansion of metabolic potential toward pathways synthesizing and utilizing amino-acid precursors, in contrast to the dominant butyrate-producing guilds such as Faecalibacterium prausnitzii and Roseburia inulinivorans that generate butyrate from pyruvate. The study also identified more than ten robust microbial associations with inflammation and with cardiometabolic and liver health markers, including a potential probiotic species, Parabacteroides goldsteinii.
The findings suggest that healthy aging in this population is accompanied by a measurable shift away from butyrate-producing commensals like Faecalibacterium prausnitzii toward microbes with alternate amino-acid metabolic capacity. This shift, combined with the identified links to inflammation and cardiometabolic and liver health markers, points to specific microbial species and pathways that could serve as biomarkers or targets for supporting healthy aging. The results also highlight potential probiotic candidates, such as Parabacteroides goldsteinii, for further investigation in aging-related interventions.
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 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 visceral adipose tissue (VAT) area relates to the gut bacterial microbiome and circulating markers of metabolic endotoxemia in aging women. Metabolic endotoxemia is chronic low-grade inflammation driven by elevated circulating lipopolysaccharide (LPS), a component of gram-negative bacterial cell walls. Researchers measured VAT by dual x-ray absorptiometry, assessed diet quality with a food frequency questionnaire, quantified plasma LPS, LPS-binding protein, and anti-LPS, anti-flagellin, and anti-lipoteichoic acid antibodies by ELISA, and performed metagenomic sequencing on fecal DNA. A parallel mouse experiment modeled metabolic endotoxemia by feeding female C57BL/6 mice diet-derived fecal LPS on high-fat or low-fat diets.
The human cohort consisted of fifty postmenopausal women with a mean age of 78.8 years who already had existing DXA-based adipose measurements. Participants were selected from the extremes of visceral adiposity: twenty-five women with low VAT area (about 45.6 cm2) and twenty-five with high VAT area (about 177.5 cm2). This extreme-groups design allowed comparison of gut microbiome and endotoxemia markers across a wide range of visceral fat. The companion animal experiment used female C57BL/6 mice on high-fat or low-fat diets to model the human findings.
The abstract indicates that high visceral adiposity in these postmenopausal women was linked to a gut bacterial microbiome shifted toward a pro-inflammatory profile compared to women with low VAT area. This shift accompanied signs of immunogenic metabolic endotoxemia, reflected in circulating LPS, LPS-binding protein, and antibody markers measured by ELISA. The provided abstract text is truncated before reporting the specific taxa, antibody levels, or mouse-model outcomes, so those detailed results cannot be stated here.
The findings support a model in which visceral fat accumulation after menopause is accompanied by microbiome-driven inflammatory signaling, not just local adipose tissue changes. Pairing human cohort data with a mouse model of diet-derived LPS exposure suggests the gut microbiome and endotoxemia pathway may be a mechanistic link between visceral obesity and chronic disease risk in older women. This points to the gut barrier and circulating bacterial products as potential targets for reducing inflammation associated with abdominal obesity in aging populations.
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.
This study tested whether a healthy low-carbohydrate diet (HLCD) and time-restricted eating (TRE), alone or combined, affect body weight and the gut microbiome beyond what caloric restriction alone produces. It used a 12-week two-by-two factorial randomized controlled feeding trial with a 28-week follow-up period. The design let researchers isolate the added effects of carbohydrate restriction and eating-window timing on top of isocaloric-restricted feeding.
The trial enrolled 96 participants with overweight or obesity. Participants were assigned across the two-by-two factorial design to receive isocaloric-restricted feeding with or without HLCD and with or without TRE. The abstract does not give further demographic detail such as age or sex distribution.
Isocaloric-restricted feeding produced significant weight loss ranging from 2.57 to 4.11 kg across groups, and both HLCD and TRE produced additional reductions in body mass index beyond caloric restriction alone. HLCD led to additional fat mass loss, while TRE led to more lean mass loss, showing the two strategies affect body composition differently. HLCD also decreased fecal branched-chain amino acids, and TRE tended to increase the abundance of probiotic species that synthesize short-chain fatty acids. The fat-mass-reducing effect of HLCD persisted through the post-intervention follow-up period.
The findings suggest that dietary carbohydrate composition and meal timing each add measurable value to weight management beyond simple calorie counting. HLCD and TRE produce distinct effects on body composition (fat versus lean mass) and distinct, profound alterations to the gut microbiome and metabolome. The persistence of HLCD's fat-loss effect after the intervention ended points to potential durability of low-carbohydrate approaches. These results support tailoring weight-management strategies to specific metabolic and microbiome-related goals rather than treating all caloric-restriction approaches as equivalent.
The gut microbiota has emerged as an independent risk factor for diabetes and its complications. This research aimed to delve into the intricate relationship between the gut microbiome and diabetic retinopathy (DR) through a dual approach of cross-sectional and prospective cohort studies. In our cross-sectional study cross-sectional investigation involving ninety-nine individuals with diabetes, distinct microbial signatures associated with DR were identified. Specifically, gut microbiome profiling revealed decreased levels of Butyricicoccus and Ruminococcus torques group, alongside upregulated methanogenesis pathways among DR patients. These individuals concurrently exhibited lower concentrations of short-chain fatty acids in their plasma. Leveraging machine learning models, including random forest classifiers, we constructed a panel of microbial genera and genes that robustly differentiated DR cases. Importantly, these genera also demonstrated significant correlations with dietary patterns and the molecular profiles of peripheral blood mononuclear cells. Building upon these findings, our prospective cohort study followed 62 diabetes patients over a 2-year period to assess the predictive value of these microbial markers. The results underlined the panel's efficacy in predicting DR incidence. By stratifying patients based on the predictive genera and metabolites identified in the cross-sectional phase, we established significant associations between reduced levels of Butyricicoccus, plasma acetate, and increased susceptibility to DR. This investigation not only deepens our understanding of how gut microbiota influences DR but also underscores the potential of microbial markers as early indicators of disease risk. These insights hold promise for developing targeted interventions aimed at mitigating the impact of diabetic complications. KEY POINTS: • Microbial signatures are differed in diabetic patients with and without retinopathy • DR-related taxa are linked to dietary habits and transcriptomic profiles • Lower abundances of Butyricicoccus and acetate were prospectively associated with DR.
This study examined the biogeography of the mucosa-associated microbiome (MAM) across different segments of the upper and lower gastrointestinal tract. Researchers compared microbial composition and bacterial load between patients with inflammatory bowel disease (IBD) and controls. They also looked at how the MAM related to proton pump inhibitor (PPI) use, gastrointestinal symptom severity, and symptom response to a standardised nutrient challenge. Microbial composition was assessed with 16S rRNA gene amplicon sequencing, and bacterial load was measured by qPCR on mucosal biopsies.
The study included 59 controls without structural gastrointestinal abnormalities or symptoms, 44 patients with ulcerative colitis, and 31 patients with Crohn's disease. Biopsies were collected from multiple segments of both the upper and lower gastrointestinal tract in these participants. This gives a total of 134 individuals across three clinical groups.
Microbial communities differed between the upper and lower gastrointestinal tract in their mucosal composition. IBD patients showed relative and absolute depletion of numerous genera known to produce butyrate and/or propionate compared with controls. The largest difference observed was depletion of Faecalibacterium in the lower gastrointestinal tract of patients with Crohn's disease. The abstract also indicates that PPI users showed a notable difference in the MAM, though the specific finding is cut off in the provided text.
The findings suggest that loss of short-chain fatty acid producing bacteria, particularly Faecalibacterium, is a hallmark of mucosal dysbiosis in Crohn's disease at the site of tissue contact rather than only in stool. Mapping microbiome differences by gastrointestinal segment highlights that biogeography matters when interpreting mucosal microbiome studies in IBD. The association with PPI use also points to medication exposure as a factor that should be accounted for when characterizing the mucosa-associated microbiome in these patients.
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.
This study used metagenomic sequencing to examine how chemotherapy affects the gut microbiota and antibiotic resistance genes (ARGs) in patients with acute leukemia (AL). Researchers compared stool samples collected before and after chemotherapy to track shifts in microbial composition and resistance gene carriage. The analysis also explored how antibiotic dosage shapes microbiota and ARG networks, and how gut microbial species relate to circulating inflammatory markers.
The subjects were patients diagnosed with acute leukemia who provided stool samples both before and after undergoing chemotherapy. The abstract does not give an exact number of patients, so the precise cohort size cannot be stated. Blood samples from these same patients were also analyzed for inflammatory biomarkers alongside the paired stool metagenomes.
Post-chemotherapy stool samples showed decreased alpha diversity and greater sample-to-sample dispersion compared with pre-chemotherapy samples, along with shifts in the abundance of specific bacterial taxa. Enterococcus, Klebsiella, and Escherichia coli were identified as the most prevalent carriers of antibiotic resistance genes. Correlation analysis linked specific microbial species to inflammatory markers, including C-reactive protein (CRP) and adenosine deaminase (ADA), and co-occurrence networks connected 179 microbial and ARG nodes across 206 edges. Treatment with cephamycin and sulfonamide antibiotics was associated with the emergence of multidrug-resistant Klebsiella colonization.
The findings suggest that chemotherapy in acute leukemia patients disrupts gut microbial balance in ways that favor colonization by resistant, potentially pathogenic Enterobacteriaceae members such as Klebsiella and E. coli. The observed links between specific antibiotics, resistant bacteria, and inflammatory biomarkers highlight the need for careful antibiotic selection and dosing during leukemia treatment to limit multidrug-resistant colonization. These data support closer monitoring of gut microbiota and ARG dynamics as a tool for anticipating infection risk and inflammatory complications in immunocompromised leukemia patients.
This study investigated whether the gut microbiome contributes to the progression of adult T-cell leukemia/lymphoma (ATLL), a refractory blood cancer caused by HTLV-1 retroviral infection. The researchers analyzed the taxonomic and functional profiles of gut microbiota to identify microbial pathways and metabolites associated with ATLL. They then tested whether a candidate microbial metabolite could directly affect the growth of ATLL cells in vitro.
The study analyzed gut microbiota from 28 patients with adult T-cell leukemia/lymphoma and 37 individuals infected with HTLV-1 who had not developed ATLL. High-risk HTLV-1-infected individuals were also examined as part of the comparison. ATLL cell lines were used for the functional proliferation experiments.
The succinic semialdehyde (SSA) synthesis pathway was significantly enriched in the gut microbiome of ATLL patients (P = 0.000682). Klebsiella was identified as the main bacterial contributor to this pathway and was significantly more abundant in both ATLL patients and high-risk HTLV-1-infected individuals (P = 0.0326). When ATLL cell lines were treated with SSA, the cells showed significant proliferation.
These findings suggest the gut microbiome can actively promote ATLL progression through a specific bacterial metabolite rather than merely reflecting disease state. Klebsiella-driven succinic semialdehyde production emerges as a potential mechanistic link between gut microbial function and malignant T-cell proliferation in HTLV-1-infected individuals. This raises the possibility that monitoring or targeting this microbial pathway could help identify high-risk individuals or inform future interventions to slow ATLL development.
This study examined the gut microbiome in people who inject drugs, comparing those with and without HIV-1 infection. Researchers used amplicon-based 16S rDNA sequencing to identify amplicon sequence variants (ASVs) and detect shifts in bacterial community composition. The goal was to disentangle how HIV status and injection drug use, separately and together, shape the gut microbiota. Effects of multiple drug use on the microbiome were also assessed in both HIV-infected and non-infected participants.
The study drew on a well-established cohort of people who inject drugs in Puerto Rico, a region with historically high rates of injection drug use and an HIV incidence disproportionately linked to it. Participants included both HIV-positive and HIV-negative individuals, and both drug-injecting and non-injecting individuals, allowing comparison across these groups. The abstract does not give an exact sample size.
HIV-positive individuals had a higher abundance of ASVs from the genera Prevotella, Alloprevotella, Sutterella, Megasphaera, Fusobacterium, and Mitsuokella. In contrast, Bifidobacteria and Lactobacillus ASVs were more abundant in people who inject drugs compared to non-injectors, regardless of HIV status. The study also found that using multiple drugs significantly affected the composition of the gut microbial community. These patterns show that HIV status and drug use each leave distinct, identifiable signatures on the gut microbiome.
The findings suggest that HIV infection and injection drug use independently reshape the gut microbiome, producing distinguishable bacterial signatures rather than a single combined effect. Identifying HIV-associated genera separately from drug-use-associated genera could help researchers understand how each factor contributes to health outcomes in this population. Recognizing that multiple drug use further alters the microbial community underscores the need to account for drug use patterns in microbiome research on people with HIV. This work supports using gut microbiota profiling as a tool to better understand the intersecting effects of infection and substance use.
This study examined the gut microbiome of patients with Peutz-Jeghers syndrome (PJS), a rare hereditary disorder marked by intestinal polyposis and a high risk of intussusception. Researchers used 16S rRNA sequencing to characterize overall microbiome composition and metagenomic sequencing on a subset of samples to assess functional pathway changes. The goal was to determine whether gut microbiota imbalance is associated with PJS and, specifically, with the complication of intussusception.
Stool samples were collected from 168 patients with PJS and 68 healthy family members who lived in the same household. For the deeper metagenomic functional analysis, a representative subset of 61 PJS patients and 27 healthy family members was used. Using cohabitating relatives as controls helps account for shared diet and environment.
The fecal microbiome of PJS patients showed greater variation in beta-diversity compared with healthy family members. PJS patients had an enhancement of Escherichia coli and a reduction of Faecalibacterium prausnitzii, an anti-inflammatory, butyrate-associated commensal. Among PJS patients, those with intussusception showed a further reduction in Faecalibacterium prausnitzii, marking it as a distinguishing microbial feature of this complication. Functional analysis found propanoate metabolism enriched in PJS patients overall and further enriched in those with intussusception, with Escherichia coli identified as the major contributor to this pathway.
These findings suggest gut microbiome imbalance, particularly loss of Faecalibacterium prausnitzii and expansion of Escherichia coli, may play a role in PJS pathogenesis and specifically in the development of intussusception. The progressive depletion of this anti-inflammatory commensal alongside enriched propanoate metabolism points to a possible microbial signature that could help identify PJS patients at greater risk for this complication. This raises the possibility that restoring depleted commensals or targeting E. coli-driven metabolic pathways could be explored as future strategies, though the abstract does not report interventional data.
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.
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.
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.
Captive koala breeding programmes are essential for long-term species management. However, breeding efficacy is frequently impacted by high neonatal mortality rates in otherwise healthy females. Loss of pouch young typically occurs during early lactation without prior complications during parturition and is often attributed to bacterial infection. While these infections are thought to originate from the maternal pouch, little is known about the microbial composition of koala pouches. As such, we characterised the koala pouch microbiome across the reproductive cycle and identified bacteria associated with mortality in a cohort of 39 captive animals housed at two facilities.
Using 16S rRNA gene amplicon sequencing, we observed significant changes in pouch bacterial composition and diversity between reproductive time points, with the lowest diversity observed following parturition (Shannon entropy - 2.46). Of the 39 koalas initially sampled, 17 were successfully bred, after which seven animals lost pouch young (overall mortality rate - 41.18%). Compared to successful breeder pouches, which were largely dominated by Muribaculaceae (phylum - Bacteroidetes), unsuccessful breeder pouches exhibited persistent Enterobacteriaceae (phylum - Proteobacteria) dominance from early lactation until mortality occurred. We identified two species, Pluralibacter gergoviae and Klebsiella pneumoniae, which were associated with poor reproductive outcomes. In vitro antibiotic susceptibility testing identified resistance in both isolates to several antibiotics commonly used in koalas, with the former being multidrug resistant.
This study represents the first cultivation-independent characterisation of the koala pouch microbiota, and the first such investigation in marsupials associated with reproductive outcomes. Overall, our findings provide evidence that overgrowth of pathogenic organisms in the pouch during early development is associated with neonatal mortality in captive koalas. Our identification of previously unreported, multidrug resistant P. gergoviae strains linked to mortality also underscores the need for improved screening and monitoring procedures aimed at minimising neonatal mortality in future. Video Abstract.
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.
Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder characterized by chronic low-grade inflammation. Previous studies have demonstrated that the gut microbiome can affect the host tissue cells' mRNA N6-methyladenosine (m6A) modifications. This study aimed to understand the role of intestinal flora in ovarian cells inflammation by regulating mRNA m6A modification particularly the inflammatory state in PCOS. The gut microbiome composition of PCOS and Control groups was analyzed by 16S rRNA sequencing, and the short chain fatty acids were detected in patients' serum by mass spectrometry methods. The level of butyric acid was found to be decreased in the serum of the obese PCOS group (FAT) compared to other groups, and this was correlated with increased Streptococcaceae and decreased Rikenellaceae based on the Spearman's rank test. Additionally, we identified FOSL2 as a potential METTL3 target using RNA-seq and MeRIP-seq methodologies. Cellular experiments demonstrated that the addition of butyric acid led to a decrease in FOSL2 m6A methylation levels and mRNA expression by suppressing the expression of METTL3, an m6A methyltransferase. Additionally, NLRP3 protein expression and the expression of inflammatory cytokines (IL-6 and TNF-α) were downregulated in KGN cells. Butyric acid supplementation in obese PCOS mice improved ovarian function and decreased the expression of local inflammatory factors in the ovary. Taken together, the correlation between the gut microbiome and PCOS may unveil crucial mechanisms for the role of specific gut microbiota in the pathogenesis of PCOS. Furthermore, butyric acid may present new prospects for future PCOS treatments.
Functional constipation (FC) in children affects their growth, development and quality of life. L-pipecolic acid (L-PA) was decreased in FC children based on gut microbiome and serum metabolomic. In this study, loperamide-induced constipation in mice was used to evaluate the effects of L-PA on constipated mice.
26 FC and 28 healthy children were recruited. Stool samples and serum samples were subjected to 16S rDNA sequencing and ultra-performance liquid chromatography/quadrupole time of flight (UPLC-Q/TOF-MS) approach, respectively. A loperamide-induced mouse constipation model was developed, and all mice were randomly divided into control (Con), loperamide (Lop) and L-PA (Lop + L-PA) treatment groups (6 mice per group). The mice in the Lop + L-PA group were given L-PA (250 mg/kg, once a day) and loperamide; the Lop group was given loperamide for 1 week, and the Con group was given saline. The fecal parameters and intestinal motility of mice in each group were detected. serum 5-HT levels and colon 5-HT expression were detected by ELISA and immunohistochemistry, respectively; qRT-PCR was used to detect the expression of AQP3 and 5-HT4R mRNA in each group.
45 differential metabolites and 18 significantly different microbiota were found in FC children. The α and β diversity of gut microbiota in FC children was significantly reduced. Importantly, serum L-PA was significantly reduced in FC children. The KEGG pathway enrichment were mainly enriched in fatty acid biosynthesis, lysine degradation, and choline metabolism. L-PA was negatively associated with Ochrobactrum, and N6, N6, N6-trimethyl-l-lysine was positively associated with Phascolarcrobacterium. In addition, L-PA improved the fecal water content, intestinal transit rate, and increased the serum 5-HT levels in constipated mice. Moreover, L-PA increased the expression of 5-HT4R, reduced AQP3, and regulated constipation-associated genes.
Gut microbiota and serum metabolites were significantly altered in children with FC. The abundance of Phascolarctobacterium and Ochrobactrum and serum L-PA content were decreased in FC children. L-PA was found to alleviate the fecal water content, increase intestinal transit rate and the first black stool defecation time. L-PA improved constipation by increasing 5-HT and 5-HT4R expression while down-regulating AQP3 expression.
Bacterial and viral infections are commonly implicated in the development of pneumonia. We aimed to compare the diversity and composition of lung bacteria among severe pneumonia patients who were influenza virus positive (IFVP) and influenza virus negative (IFVN).
Bronchoalveolar lavage fluid specimens were procured from patients diagnosed with severe pneumonia to investigate the microbiome utilizing 16S-rDNA sequencing. The alpha diversity of the microbiome was evaluated employing Chao1, Shannon, and Simpson indexes, while the beta diversity was assessed using principal component analysis and principal coordinate analysis. Linear discriminant analysis effect size (LEfSe) was employed to determine the taxonomic differences between the IFVP and IFVN groups.
A total of 84 patients with 42 in the IFVP group and 42 in the IFVN group were enrolled. Slightly higher indexes of Shannon and Simpson were observed in the IFVP group without statistically significant difference. The dominant bacterial genera were Streptococcus, Klebsiella, Escherichia-Shigella in the IFVN group and Acinetobacter, Streptococcus, Staphylococcus in the IFVP group. Streptococcus pneumoniae and Acinetobacter baumannii were the most abundant species in the IFVN and IFVP groups, respectively. LEfSe analysis indicated a greater abundance of Klebsiella in the IFVN group.
Individuals with severe pneumonia infected with IFV exhibit heightened susceptibility to certain bacteria, especially Acinetobacter baumannii, and the underlying mechanism of the interaction between IFV and Acinetobacter baumannii in the progression of pneumonia needs further investigation.
This study investigated the duodenal mucosa-associated microbiota and its surrounding microenvironment in relation to hyperglycemia, an area far less studied than stool microbiota in metabolic disease. The researchers compared paired stool and duodenal microbial samples between hyperglycemic and normoglycemic individuals. They also assessed the duodenal microenvironment directly by measuring tissue oxygen saturation, serum inflammatory markers, and zonulin as a marker of gut permeability. The goal was to determine whether duodenal, rather than stool, microbial changes track more closely with glycemic status.
The study population consisted of 33 subjects with hyperglycemia, defined as HbA1c of 5.7% or higher and fasting plasma glucose above 100 mg/dl, compared against 21 normoglycemic subjects. Both groups contributed paired stool and duodenal samples, allowing direct comparison of microbiota across two body sites within the same individuals. No further demographic details are given in the abstract.
Hyperglycemic subjects had a significantly higher duodenal bacterial count than normoglycemic subjects, along with increased pathobionts and reduced beneficial flora. This bacterial overload correlated with elevated serum zonulin and higher TNF-alpha, suggesting a link to increased gut permeability and inflammation. The hyperglycemic group also showed reduced duodenal oxygen saturation, higher total leukocyte count, and lower IL-10, indicating a systemic proinflammatory state. Notably, unlike stool flora, duodenal bacterial profile variability was specifically associated with glycemic status.
These findings suggest the duodenal microbiome and its local microenvironment, rather than stool alone, may play a distinct role in the pathogenesis of hyperglycemia and prediabetes. The association between bacterial overload, reduced oxygen saturation, and systemic inflammatory markers points to a possible mechanistic pathway linking small intestinal dysbiosis to metabolic dysfunction. This work highlights the duodenum as an underexplored but potentially important site for understanding and possibly intervening in early glycemic disturbances.
This study examined whether the gut microbiota is associated with the development of Graves' disease (GD), an autoimmune thyroid condition. Researchers profiled gut microbiota composition using 16S rRNA sequencing, comparing samples taken before and after treatment in GD patients. They also measured interleukin-17 levels to explore a possible immune link, and used a random forest model to see whether specific bacterial genera could distinguish GD patients from healthy individuals.
The study included 65 patients newly diagnosed with Graves' disease, sampled both before and after treatment. A comparison group of 33 physical examination personnel (presumed healthy individuals) was also profiled. All participants underwent gut microbiota analysis via 16S rRNA sequencing.
Gut microbiota composition differed significantly between GD patients and the comparison group, with differences spanning 1 class, 1 order, 5 families, and 14 genera. After treatment, bacterial taxa that had been enriched in GD patients decreased, while taxa that had been depleted increased, alongside a significant decrease in interleukin-17 levels. A random forest analysis identified 12 genera capable of distinguishing GD patients from healthy controls. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, sulfide, or sulfur metabolism.
The findings suggest that gut microbiota alterations in Graves' disease are linked to immune imbalance, given the parallel changes in microbiota composition and interleukin-17 levels after treatment. The identification of 12 discriminating genera raises the possibility that gut microbiota profiling could help distinguish GD patients from healthy individuals. The partial normalization of microbiota after treatment suggests gut microbiota may be a dynamic marker worth monitoring alongside thyroid disease activity.
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.
Gastric cancer is one of the leading causes of death worldwide, and resections are performed to cure the disease. We have previously reported the changes in the gastric microbiota after gastric cancer resection, which may be associated with the oral microbiota; however, the changes in the oral microbiota remain uncharacterized. This study aimed to characterize the changes in the salivary microbiota caused by gastric cancer resection and to evaluate their association with the gastric fluid microbiota. Saliva and gastric fluid samples were collected from 63 patients who underwent gastrectomy before and after surgery, and a 16S rRNA metagenomic analysis was performed to compare the microbiota composition. The number of bacterial species in the salivary microbiota decreased, and the bacterial composition changed after the resection of gastric cancer. In addition, we identified several bacterial genera that varied significantly in the salivary microbiota, some of which also showed similar changes in the gastric fluid microbiota. These findings indicate that changes in the gastric environment affect the oral microbiota, emphasizing the close association between the oral and gastric fluid microbiota. Our study signifies the importance of focusing on the oral microbiota in the perioperative period of gastrectomy in patients with gastric cancer.
The gut and salivary microbiomes have been widely reported to be significantly associated with a number of neurological disorders. The stability of the microbiome in the oral cavity makes it a potentially ideal sample that can be conveniently obtained for the investigation of microbiome-based pathogenesis in diseases. In the present study, we used a single-molecule long-read sequencing technique to study the distribution of the salivary microbiota in patients with pituitary adenoma (PA) and healthy individuals, as well as among four clinical phenotypes of PA. We found that the diversity of salivary microbes was more abundant in PA patients than in healthy individuals. We also observed some unique genera in different PA phenotypes. The bioinformatics-based functional predictions identified potential links between microbes and different clinical phenotypes of PA. This study improves the existing understanding of the pathogenesis of PA and may provide diagnostic and therapeutic targets for PA.
This study examined how surgery-induced gut microbial dysbiosis contributes to perioperative neurocognitive disorders (PND), a common but poorly treated postoperative complication. The researchers investigated the mechanisms linking postoperative changes in the gut microbiota to disruptions in intestinal barrier function, serum metabolism, and cognitive outcomes. Behavioral testing, 16S rRNA gene sequencing, non-target metabolomics, intestinal permeability assays, protein analysis, and immunofluorescence staining were used to trace this gut-brain pathway. The metabolite palmitic amide was identified as a specific link between microbial changes and cognitive effects.
The study was conducted in mice, comparing aged and young animals subjected to surgery. Aged mice were the primary focus, since surgery-induced cognitive impairment occurred predominantly in this group. Interventions including fecal microbiota transplantation from young donors, dexamethasone, Lactobacillus supplementation, indole propionic acid, and palmitic amide administration were tested in these mouse models.
Surgery altered gut microbiota composition and worsened intestinal barrier disruption specifically in aged mice, which corresponded with the cognitive impairment seen mainly in this group. These adverse effects could be reduced by transferring microbiota from young donors or by strengthening intestinal barrier function with dexamethasone, Lactobacillus, or indole propionic acid. The abstract also points to microbiota-linked changes in metabolism, including the metabolite palmitic amide, as part of the mechanism connecting gut dysbiosis to cognitive outcomes.
The findings suggest that age-related vulnerability to postoperative cognitive decline may be driven in part by how surgery disrupts the gut microbiota and intestinal barrier. Because microbiota transfer, probiotic supplementation, and metabolite-targeted interventions each improved outcomes in this model, gut-directed strategies could represent a therapeutic avenue for PND. This supports viewing perioperative cognitive complications through a gut-brain axis lens rather than treating them as purely neurological events.
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 study examined the uterine microbiome of post-partum dairy cows using deep shotgun metagenomic sequencing. Researchers compared microbial ecology and diversity in cows with metritis, purulent vaginal discharge, and no disease. The goal was to characterize taxonomic composition and identify differences in community structure associated with metritis.
The study drew on intrauterine swab samples from post-partum dairy cows across 24 commercial California dairy farms. A subset of 95 samples was analyzed out of a larger collection of 307 individual cow samples. Cows within 21 days post-partum were classified into three clinical groups: control (n = 32), metritis (n = 33), and purulent discharge (n = 31), based on the appearance and odor of vaginal discharge.
All three clinical groups showed highly diverse uterine microbial communities, with the top 12 most abundant genera accounting for only about 8.8 to 10.3 percent of mean relative abundance across groups. Alpha diversity was lower in samples from cows with metritis and purulent discharge compared to control cows. PERMANOVA testing showed a statistically significant difference in overall microbial community composition (beta diversity) between groups.
The findings suggest that uterine disease states in post-partum dairy cows are associated with reduced microbial diversity rather than dominance by a single pathogen, reflecting a broader ecological shift in the uterine environment. Deep shotgun sequencing offers a more complete picture of this community than earlier culture-based or amplicon-based approaches. These results could inform future work on diagnosing and managing metritis through microbiome-based markers rather than single-organism detection.
This study investigated the gut microbiome and fecal metabolite profile in functional constipation (FC), a condition whose underlying mechanisms remain unclear. The researchers combined 16S rDNA sequencing with non-targeted metabolomic detection using liquid chromatography-mass spectrometry (LC-MS/MS) to characterize fecal samples. The goal was to identify how gut microbiota and metabolites are altered in FC and how the two are interrelated, since this relationship had received limited attention in prior literature.
The study compared fecal samples from patients with functional constipation to samples from healthy individuals, referred to as the healthy control (HC) group. The abstract does not specify exact participant numbers, age range, or geographic setting. The comparison design indicates a case-control human cohort study rather than an animal or purely computational dataset.
Gut microbiota richness and diversity were significantly increased in FC patients compared to healthy controls (p < 0.01). Eighteen bacterial genera showed statistically significant changes between groups, including Intestinibacter, Klebsiella, and Akkermansia (p < 0.05). Metabolomic analysis revealed 79 differentially abundant metabolites, such as (-)-caryophyllene oxide, chenodeoxycholic acid, and biliverdin, with primary bile acid biosynthesis and porphyrin and chlorophyll metabolism emerging as the most significantly enriched pathways (FDR < 0.01).
The findings suggest that functional constipation involves coordinated shifts in both gut microbial composition and metabolic output, particularly involving bile acid metabolism. Because chenodeoxycholic acid and related bile acids are implicated, altered microbial processing of bile acids may contribute to disrupted bowel function in FC. Mapping these microbiome-metabolite relationships could help identify biomarkers or microbiome-targeted strategies for diagnosing or managing functional constipation.
While dysbiosis within the intestinal ecosystem has been associated with functional constipation (FC), the mechanisms underlying the interactions between FC and the microbiome remain poorly elucidated. Recent investigations suggested that host microRNAs (miRNAs) can modulate bacterial growth and influence the composition of the gut microbiome. To explore the connection between gut microbiota and fecal miRNAs in FC patients, we initially employed 16S rRNA sequencing to assess the gut microbial landscape in 30 FC patients and 30 healthy controls (HCs). The α-diversity within the FC group exhibited some alterations, and the β-diversity significantly differed, signifying distinctive variations in gut microbiota composition between FC patients and HCs. Subsequently, we identified 44 differentially expressed (DE) miRNAs in feces from FC patients and HCs. Through correlation analysis between DE miRNAs and FC-associated microbiota, we detected an interaction involving nine DE miRNAs (miR-205-5p, miR-493-5p, miR-215-5p, miR-184, miR-378c, miR-335-5p, miR-514a-3p, miR-141-3p, and miR-34c-5p) with seven bacterial genera (Oscillibacter, Escherichia.Shigella, UCG.002, Lachnospiraceae_NK4A136_group, Lachnospiraceae_UCG.010, Eubacterium_ruminantium_group and Megamonas), as evidenced by a co-occurrence network. Further, a comprehensive panel of seven diagnostic biomarkers (Oscillibacter, Escherichia.Shigella, UCG.002, miR-205-5p, miR-493-5p, miR-215-5p, and Lachnospiraceae_NK4A136_group) demonstrated robust discriminatory capacity in predicting FC status when integrated into a random forest model (AUC = 0.832, 95% CI: 65.73-98.88). Microbiomes correlating with DE miRNAs exhibited enrichment in distinct predicted metabolic categories. Moreover, miRNAs correlated with FC-associated bacteria were found to be enriched in signaling pathways linked to colonic contractility, including Axon guidance, PI3K-Akt signaling pathway, MAPK signaling pathway, and Hippo signaling pathway. Our study offers a comprehensive insight into the global relationship between microbiota and fecal miRNAs in the context of FC, presenting potential targets for further experimental validation and therapeutic interventions.
Preterm birth is associated with the development of acute and chronic disease, potentially, through the disruption of normal gut microbiome development. Probiotics may correct for microbial imbalances and mitigate disease risk. Here, we used amplicon sequencing to characterise the gut microbiome of probiotic-treated premature infants. We aimed to identify and understand variation in bacterial gut flora from admission to discharge and in association with clinical variables.
Infants born <32 weeks gestation and <1500 g, and who received probiotic treatment, were recruited in North Queensland Australia. Meconium and faecal samples were collected at admission and discharge. All samples underwent 16S rRNA short amplicon sequencing, and subsequently, a combination of univariate and multivariate analyses.
71 admission and 63 discharge samples were collected. Univariate analyses showed significant changes in the gut flora from admission to discharge. Mixed-effects modelling showed significantly lower alpha diversity in infants diagnosed with either sepsis or retinopathy of prematurity (ROP) and those fed formula. In addition, chorioamnionitis, preeclampsia, sepsis, necrotising enterocolitis and ROP were also all associated with the differential abundance of several taxa.
The lower microbial diversity seen in infants with diagnosed disorders or formula-fed, as well as differing abundances of several taxa across multiple variables, highlights the role of the microbiome in the development of health and disease. This study supports the need for promoting healthy microbiome development in preterm neonates.
Gut microbiome changes have been associated with human ageing and implicated in age-related diseases including Alzheimer's disease and Parkinson's disease. However, studies to date have used stool samples, which do not represent the entire gut. Although more challenging to access, the small intestine plays critical roles in host metabolism and immune function. In this paper (Leite et al. (2021), Cell Reports, doi: 10.1016/j.celrep.2021.109765), we demonstrate significant differences in the small intestinal microbiome in older subjects, using duodenal aspirates from 251 subjects aged 18-80 years. Differences included significantly decreased microbial diversity in older subjects, driven by increased relative abundance of phylum Proteobacteria, particularly family Enterobacteriaceae and coliform genera Escherichia and Klebsiella. Moreover, while this decreased diversity was associated with the 'ageing process' (comprising chronologic age, number of medications, and number of concomitant diseases), changes in certain taxa were found to be associated with number of medications alone (Klebsiella), number of diseases alone (Clostridium, Bilophila), or chronologic age alone (Escherichia, Lactobacillus, Enterococcus). Lastly, many taxa associated with increasing chronologic age were anaerobes. These changes may contribute to changes in human health that occur during the ageing process.
Yoghurt contains live bacteria that could contribute via modulation of the gut microbiota to its reported beneficial effects such as reduced body weight gain and lower incidence of type 2 diabetes. To date, the association between yoghurt consumption and the composition of the gut microbiota is underexplored. Here we used clinical variables, metabolomics, 16S rRNA and shotgun metagenomic sequencing data collected on over 1000 predominantly female UK twins to define the link between the gut microbiota and yoghurt-associated health benefits.
According to food frequency questionnaires (FFQ), 73% of subjects consumed yoghurt. Consumers presented a healthier diet pattern (healthy eating index: beta = 2.17 ± 0.34; P = 2.72x10-10) and improved metabolic health characterised by reduced visceral fat (beta = -28.18 ± 11.71 g; P = 0.01). According to 16S rRNA gene analyses and whole shotgun metagenomic sequencing approach consistent taxonomic variations were observed with yoghurt consumption. More specifically, we identified higher abundance of species used as yoghurt starters Streptococcus thermophilus (beta = 0.41 ± 0.051; P = 6.14x10-12) and sometimes added Bifidobacterium animalis subsp. lactis (beta = 0.30 ± 0.052; P = 1.49x10-8) in the gut of yoghurt consumers. Replication in 1103 volunteers from the LifeLines-DEEP cohort confirmed the increase of S. thermophilus among yoghurt consumers. Using food records collected the day prior to faecal sampling we showed than an increase in these two yoghurt bacteria could be transient. Metabolomics analysis revealed that B. animalis subsp. lactis was associated with 13 faecal metabolites including a 3-hydroxyoctanoic acid, known to be involved in the regulation of gut inflammation.
Yoghurt consumption is associated with reduced visceral fat mass and changes in gut microbiome including transient increase of yoghurt-contained species (i.e. S. thermophilus and B. lactis).
This study examined how the gut microbiota of Nigerian infants develops over the first year of life, a population underrepresented in existing microbiome research. Researchers characterized bacterial composition using 16S rRNA gene sequencing (V1-V2 region) and measured short chain fatty acids and lactate in faecal samples using gas chromatography. The goal was to track how delivery mode, feeding practices, and weaning shape the developing infant gut microbiota over time.
The cohort consisted of 28 Nigerian infants followed monthly from birth through one year of age, with faecal samples collected at each timepoint. Infants were born by a mix of natural (vaginal) birth and caesarean section, and were either exclusively breast-fed or mixed fed. This represents one of the relatively few longitudinal microbiome datasets from a non-Western infant population.
Microbial differences between vaginally delivered and caesarean-delivered infants were evident only in samples collected within the first 7 days of life, and these differences disappeared in later samples. Exclusively breast-fed infants showed predominance of Ruminococcus gnavus, Collinsella, and Sutterella species, and different Bifidobacterium species dominated in breast-fed compared to mixed-fed infants. Once infants began weaning, Clostridium, Enterococcus, Roseburia, and Coprococcus species emerged, and butyrate was first detected around this transition.
The findings suggest that delivery mode has only a short-lived influence on the early infant gut microbiota, while feeding practices exert a more sustained effect on which bacterial taxa, including specific Bifidobacterium species, come to dominate. The emergence of butyrate-producing genera at weaning highlights diet transition as a key driver of functional microbiota maturation. These results extend infant microbiome knowledge beyond Western cohorts and can inform feeding and care guidance in similarly underrepresented populations.
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.
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.
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.
Microbiota studies have reported changes in the microbial composition of the breast upon cancer development. However, results are inconsistent and limited to the later phases of cancer development (after diagnosis). We analyzed and compared the resident bacterial taxa of histologically normal breast tissue (healthy, H, n = 49) with those of tissues donated prior to (prediagnostic, PD, n = 15) and after (adjacent normal, AN, n = 49, and tumor, T, n = 46) breast cancer diagnosis (n total = 159). DNA was isolated from tissue samples and submitted for Illumina MiSeq paired-end sequencing of the V3-V4 region of the 16S gene. To infer bacterial function in breast cancer, we predicted the functional bacteriome from the 16S sequencing data using PICRUSt2. Bacterial compositional analysis revealed an intermediary taxonomic signature in the PD tissue relative to that of the H tissue, represented by shifts in Bacillaceae, Burkholderiaceae, Corynebacteriaceae, Streptococcaceae, and Staphylococcaceae. This compositional signature was enhanced in the AN and T tissues. We also identified significant metabolic reprogramming of the microbiota of the PD, AN, and T tissue compared with the H tissue. Further, preliminary correlation analysis between host transcriptome profiling and microbial taxa and genes in H and PD tissues identified altered associations between the human host and mammary microbiota in PD tissue compared with H tissue. These findings suggest that compositional shifts in bacterial abundance and metabolic reprogramming of the breast tissue microbiota are early events in breast cancer development that are potentially linked with cancer susceptibility. IMPORTANCE The goal of this study was to determine the role of resident breast tissue bacteria in breast cancer development. We analyzed breast tissue bacteria in healthy breast tissue and breast tissue donated prior to (precancerous) and after (postcancerous) breast cancer diagnosis. Compared to healthy tissue, the precancerous and postcancerous breast tissues demonstrated differences in the amounts of breast tissue bacteria. In addition, breast tissue bacteria exhibit different functions in pre-cancerous and post-cancerous breast tissues relative to healthy tissue. These differences in function are further emphasized by altered associations of the breast tissue bacteria with gene expression in the human host prior to cancer development. Collectively, these analyses identified shifts in bacterial abundance and metabolic function (dysbiosis) prior to breast tumor diagnosis. This dysbiosis may serve as a therapeutic target in breast cancer prevention.
This study performed a meta-analysis of gastric mucosal microbiome data across multiple published studies to determine whether microbial associations with gastric cancer are consistent across different patient populations. The researchers examined compositional and ecological shifts in gastric microbial communities across the stages of gastric carcinogenesis. They also assessed how bacterial co-occurrence patterns and microbial diversity change as the disease progresses from a healthy state toward cancer.
The abstract does not specify a single original cohort, since this was a meta-analysis pooling gastric mucosal microbiome data from multiple prior studies. The comparisons were made between samples representing gastric cancer (GC) and samples representing superficial gastritis (SG), spanning different stages of gastric carcinogenesis. Helicobacter pylori infection status was also used to stratify samples within this pooled dataset.
Opportunistic pathobionts including Fusobacterium, Parvimonas, Veillonella, Prevotella, and Peptostreptococcus were enriched in gastric cancer, while commensals such as Bifidobacterium, Bacillus, and Blautia were depleted compared to superficial gastritis. Co-occurrence correlation strength among GC-enriched bacteria increased with disease progression, while correlations among GC-depleted bacteria weakened. The study newly identified eight bacterial taxa, Veillonella, Dialister, Granulicatella, Herbaspirillum, Comamonas, Chryseobacterium, Shewanella, and Helicobacter, as universal biomarkers that discriminated gastric cancer from superficial gastritis with an area under the curve of 0.85. H. pylori-positive samples showed reduced microbial diversity, altered community composition, and weaker interactions among gastric microbes.
By pooling data across multiple independent studies, this meta-analysis establishes a set of universal, reproducible microbial signatures associated with gastric carcinogenesis rather than findings specific to one cohort. The eight-taxa biomarker panel, with an AUC of 0.85, suggests potential value as a non-invasive or biopsy-based tool for distinguishing gastric cancer from superficial gastritis. The finding that H. pylori infection reshapes microbial diversity and community interactions reinforces its role as a driver of dysbiosis during gastric cancer development, highlighting the broader gastric microbiome as a target for risk stratification.
This observational study examined the gut microbiota and host immune response in elderly patients with schizophrenia compared to healthy controls. Researchers used 16S rRNA gene sequencing targeting the V3-V4 region to profile fecal bacterial communities. They then correlated these microbial profiles with measures of host immune function, including circulating cytokine levels.
The study included 161 fecal samples total, comprising 90 samples from elderly patients with schizophrenia and 71 samples from healthy controls. The abstract identifies the population as Chinese elderly individuals, consistent with the study title. No further demographic details are provided in the abstract.
Beta-diversity analysis separated schizophrenia patients and healthy controls into two distinct bacterial community clusters. Linear discriminant analysis effect size (LEfSe) identified compositional shifts in several genera associated with schizophrenia, including Faecalibacterium, Roseburia, Actinomyces, Butyricicoccus, and Prevotella. Alongside these microbial changes, pro-inflammatory cytokines such as IL-1β were markedly elevated in patients, while anti-inflammatory cytokines such as IFN-γ were markedly reduced. Correlation analysis linked these specific bacterial taxa to the observed immune disturbances.
The findings support a link between gut dysbiosis and immune dysfunction in elderly patients with schizophrenia. The identified bacteria correlated with inflammatory markers could serve as non-invasive biomarkers for this population. This suggests the gut microbiome and host immune signaling may be relevant targets for understanding or monitoring schizophrenia in older adults.
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.
The purpose of this study was to elucidate the characteristics of the gut microbiome in patients with Polycystic ovary syndrome (PCOS) and analyze the alterations of fecal fatty acid metabolism, so as to further provide the pathogenesis of PCOS.
Fecal samples from the PCOS group (n = 31) and healthy control group (n = 27) were analyzed by 16S rRNA gene sequencing and untargeted metabolomics. Peripheral venous blood was collected to measure serum inflammation and intestinal permeability. Finally, the correlation analysis of intestinal flora, fecal metabolites, and laboratory indicators was carried out.
Serum D-lactate content in the PCOS group was higher than that in the control group. There was no significant difference in microbial α diversity and β diversity between PCOS patients and healthy controls. Peptostreptococcaceae and Bacteroidales S24-7 group existed significant differences between PCOS patients and healthy controls. Based on linear discriminant analysis selection, 14 genera including Klebsiella, Enterobacteriaceae, and Gammaproteobacteria were dominant in patients with PCOS, while 4 genera, including rumenococcus (Ruminocaccaceae UCG 013), prewortella (Prevotellaceae UCG 001), and erysipelas (Erysipelatoclostridium), were dominant in healthy controls. Compared with PCOS with Body mass index (BMI) < 24, patients with BMI ≥ 24 have multiple dominant genera including Abiotrophia and Peptostreptococcaceae. Moreover, serum levels of free testosterone and androstenedione were positively correlated with Megamonas, while total testosterone was negatively correlated with Alistipes. Additionally, fecal contents of acetic acid and propionic acid in patients with PCOS were significantly higher than those in healthy controls. Eubacterium_coprostanoligenes_group and Alistipes were positively correlated with 6 kinds of fatty acids.
Specific intestinal flora fecal fatty acids and serum metabolites may mediate the occurrence and development of PCOS. PCOS patients with different body sizes have specific intestinal flora.
This study investigated how probiotic supplementation affects the gut microbiota of extremely preterm infants in the neonatal intensive care unit. Probiotics were already known to reduce necrotizing enterocolitis (NEC) risk in this population, but the underlying mechanism was unclear. The researchers used a prospective cohort design to compare gut microbiota composition between infants who received probiotics and those who did not. They also examined whether probiotic exposure was associated with clinical outcomes such as NEC, late-onset sepsis, and duration of total parenteral nutrition.
The cohort consisted of 120 extremely preterm neonates with a gestational age of 28 weeks or less. Infants were enrolled between August 2019 and December 2021 and divided into a study group that received probiotics and a control group that did not. This was a real-world clinical NICU population rather than a public dataset or animal model.
Neonates who received probiotics had a significantly increased abundance of Lactobacillus compared with the control group (adjusted odds ratio 4.33, 95% CI 1.89 to 9.96, p = 0.009). The probiotic group also spent significantly fewer days on total parenteral nutrition (median 29.0 days versus 35.5 days, p = 0.004). In addition, the probiotic group had a significantly lower rate of late-onset sepsis than the control group.
The findings suggest that probiotics may benefit extremely preterm infants partly by reshaping the gut microbiota toward greater Lactobacillus abundance, alongside reductions in parenteral nutrition duration and late-onset sepsis. This offers a plausible microbiota-mediated mechanism linking probiotic use to previously reported reductions in NEC and other neonatal morbidities. The results support continued clinical use of probiotics in extremely preterm NICU populations and point to gut microbiota composition as a relevant marker for future studies of probiotic mechanisms in this vulnerable group.
Papillary thyroid carcinoma (PTC) has a high incidence, and its proper treatment remains challenging. Therefore, identifying PTC progression markers is essential. Here, using 16S RNA sequences, we analyzed the PTC intratumor microbiome and its role in tumor progression. Substantial microbial abundance was detected in PTC from all patients. The tumor bacterial diversity in patients with advanced lesions (T3/T4) was significantly higher than that in patients with relatively mild lesions (T1/T2). Importantly, we identified signatures of eight tumor bacterial taxa highly predictive of PTC invasion status. Hence, microbial host factors-independent of the genomic composition of the tumor-may determine tumor behaviors and patient outcomes. Furthermore, the correlation between specific bacterial genus and thyroid hormones or autoimmune thyroid disease-related antibodies may indicate the potential contribution of the microbiome in the relationship between autoimmune thyroid disease or irregular thyroid function and PTC progression, intervention of which might therefore be worth exploring for advancing oncology care.
Depression in childhood negatively affects the growth and development, school performance, and peer or family relationships of affected children, and may even lead to suicide. Despite this, its etiology and pathophysiology remain largely unknown. Increasing evidence supports that gut microbiota plays a vital role in the development of childhood depression. However, little is known about the underlying mechanisms, as most clinical studies investigating the link between gut microbiota and depression have been undertaken in adult cohorts. In present study, a total of 140 school-aged children (6-12 years) were enrolled, including 92 with depression (male/female: 42/50) and 48 healthy controls (male/female: 22/26) from Lishui, Zhejiang, China. Illumina sequencing of the V3-V4 region of the 16S rRNA gene was used to investigate gut microbiota profiles while Bio-Plex Pro Human Cytokine 27-plex Panel was employed to explore host immune response. We found that, compared with healthy controls, children with depression had greater bacterial richness and altered β-diversity. Pro-inflammatory genera such as Streptococcus were enriched in the depression group, whereas anti-inflammatory genera such as Faecalibacterium were reduced, as determined by linear discriminant analysis effect size. These changes corresponded to altered bacterial functions, especially the production of immunomodulatory metabolites. We also identified the presence of a complex inflammatory condition in children with depression, characterized by increased levels of pro-inflammatory cytokines such as IL-17 and decreased levels of anti-inflammatory cytokines such as IFN-γ. Correlation analysis demonstrated that the differential cytokine abundance was closely linked to changes in gut microbiota of children with depression. In summary, key functional genera, such as Streptococcus and Faecalibacterium, alone or in combination, could serve as novel and powerful non-invasive biomarkers to distinguish between children with depression from healthy ones. This study was the first to demonstrate that, in Chinese children with depression, gut microbiota homeostasis is disrupted, concomitant with the activation of a complex pro-inflammatory response. These findings suggest that gut microbiota might play an important role in the pathogenesis of depression in school-aged children, while key functional bacteria in gut may serve as novel targets for non-invasive diagnosis and patient-tailored early precise intervention in children with depression.
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.
Postmenopausal women are severely affected by recurrent urinary tract infection (rUTI). The urogenital microbiome is a key component of the urinary environment. However, changes in the urogenital microbiome underlying rUTI susceptibility are unknown. Here, we perform shotgun metagenomics and advanced culture on urine from a controlled cohort of postmenopausal women to identify urogenital microbiome compositional and function changes linked to rUTI susceptibility. We identify candidate taxonomic biomarkers of rUTI susceptibility in postmenopausal women and an enrichment of lactobacilli in postmenopausal women taking estrogen hormone therapy. We find robust correlations between Bifidobacterium and Lactobacillus and urinary estrogens in women without urinary tract infection (UTI) history. Functional analyses reveal distinct metabolic and antimicrobial resistance gene (ARG) signatures associated with rUTI. Importantly, we find that ARGs are enriched in the urogenital microbiomes of women with rUTI history independent of current UTI status. Our data suggest that rUTI and estrogen shape the urogenital microbiome in postmenopausal women.
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.
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in children and adolescents. The gut microbiota plays an important role in the pathophysiology of NAFLD through the gut-liver axis. Therefore, we aimed to investigate the genus and species of gut microbiota and their functions in children and adolescents with NAFLD. From May 2017 to July 2018, a total of 58 children and adolescents, including 27 abnormal weight (AW) (obese) NAFLD patients, 16 AW non-NAFLD children, and 15 healthy children, were enrolled in this study at Shenzhen Children's Hospital. All of them underwent magnetic resonance spectroscopy (MRS) to quantify the liver fat fraction. Stool samples were collected and analysed with metagenomics. According to body mass index (BMI) and MRS proton density fat fraction (MRS-PDFF), we divided the participants into BMI groups, including the AW group (n = 43) and the Lean group (n = 15); MRS groups, including the NAFLD group (n = 27) and the Control group (n = 31); and BMI-MRS 3 groups, including NAFLD_AW (AW children with NAFLD) (n = 27), Ctrl_AW (n = 16) (AW children without NAFLD) and Ctrl_Lean (n = 15). There was no difference in sex or age among those groups (p > 0.05). In the BMI groups, at the genus level, Dialister, Akkermansia, Odoribacter, and Alistipes exhibited a significant decrease in AW children compared with the Lean group. At the species level, Megamonas hypermegale was increased in the AW group, while Akkermansia muciniphila, Dialister invisus, Alistipes putredinis, Bacteroides massiliensis, Odoribacter splanchnicus, and Bacteroides thetaiotaomicron were decreased in AW children, compared to the Lean group. Compared with the Control group, the genus Megamonas, the species of Megamonas hypermegale and Megamonas rupellensis, increased in the NAFLD group. Furthermore, the genus Megamonas was enriched in the NAFLD_AW group, while Odoribacter, Alistipes, Dialister, and Akkermansia were depleted compared with the Ctrl_Lean or Ctrl_AW group at the genus level. Megamonas hypermegale and Megamonas rupellensis exhibited a significant increase in NAFLD_AW children compared with the Ctrl_Lean or Ctrl_AW group at the species level. Compared with healthy children, the pathways of P461-PWY contributed by the genus Megamonas were significantly increased in NAFLD_AW. We found that compared to healthy children, the genus Megamonas was enriched, while Megamonas hypermegale and Megamonas rupellensis were enriched at the species level in children and adolescents with NAFLD. This indicates that the NAFLD status and/or diet associated with NAFLD patients might lead to the enrichment of the genus Megamonas or Megamonas species.
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 gut and oral (salivary) microbial profiles in relation to childhood obesity using 16S rDNA sequencing. Researchers compared microbial diversity and composition between African American (AA) and European American (EA) children. They also correlated microbiome data with salivary amylase and socioeconomic factors such as education and family income. The goal was to identify microbial clades that could serve as indicators of obesity in each ethnic group.
The study population consisted of African American and European American children, divided by obesity status (obese versus non-obese) within each ethnic group. Both gut and saliva samples were collected from these children for microbial profiling. The abstract does not give an exact total sample size, so the precise cohort count cannot be stated.
Gut and oral microbial diversity differed significantly between AA and EA children at the alpha-, beta-, and taxa-diversity levels. In AA children, greater abundance of gut Klebsiella and Megasphaera was associated with obesity, whereas gut microbial diversity did not distinguish obese from non-obese EA children. In EA children, obesity was instead associated with greater abundance of oral Aggregatibacter and Eikenella. Socioeconomic factors also influenced the microbiota in an ethnicity-dependent manner.
The findings suggest that microbial signatures of obesity are not universal but are ethnicity-specific, differing between gut and oral sites depending on population. This implies that a single microbial biomarker panel for childhood obesity may not generalize across ethnic groups. Socioeconomic context appears to shape these microbial associations, meaning interventions to address childhood obesity may need to be tailored separately for different populations rather than applying one universal approach.
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.
This study examined the nasal and oropharyngeal (NOP) microbial community using 16S rRNA gene sequencing. Researchers compared the microbiota composition and diversity across groups differing in COVID-19 status and severity. The goal was to characterize how SARS-CoV-2 infection alters the local respiratory microbiome, since no reliable markers exist to predict disease prognosis in these patients.
The cohort included 21 patients affected by COVID-19, some paucisymptomatic and others admitted to the Intensive Care Unit (ICU). They were compared against 10 controls who tested negative for COVID-19, as well as 8 patients infected with other human coronaviruses (HKU1, NL63, and OC43). All samples were drawn from nasal/oropharyngeal swabs analyzed by 16S rRNA sequencing.
Chao1 index, a measure of microbial richness, was significantly lower in ICU COVID-19 patients compared to paucisymptomatic patients. Chao1 was also decreased across ICU, paucisymptomatic, and other-coronavirus groups relative to controls. Shannon diversity index, which accounts for both richness and evenness, was significantly reduced only in ICU patients compared to controls and paucisymptomatic patients. At the phylum level, Deinococcus-Thermus was detected only in controls and was absent in SARS-CoV-2 and other-coronavirus patient groups.
The progressive loss of microbial diversity in the nasal/oropharyngeal tract, most pronounced in ICU patients, suggests that upper respiratory microbiome disruption tracks with COVID-19 severity. These findings raise the possibility that 16S rRNA-based diversity indices, such as Chao1 and Shannon, could serve as candidate biomarkers to help stratify disease severity. Further research could clarify whether restoring microbial diversity or targeting specific taxa like Deinococcus-Thermus has prognostic or therapeutic relevance in COVID-19 management.
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.
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.
Autism spectrum disorders (ASDs) are a set of complex neurobiological disorders. Growing evidence has shown that the microbiota that resides in the gut can modulate brain development via the gut-brain axis. However, direct clinical evidence of the role of the microbiota-gut-brain axis in ASD is relatively limited.
A case-control study of 71 boys with ASD and 18 neurotypical controls was conducted at China-Japan Friendship Hospital. Demographic information and fecal samples were collected, and the gut microbiome was evaluated and compared by 16S ribosomal RNA gene sequencing and metagenomic sequencing.
A higher abundance of operational taxonomic units (OTUs) based on fecal bacterial profiling was observed in the ASD group. Significantly different microbiome profiles were observed between the two groups. At the genus level, we observed a decrease in the relative abundance of Escherichia, Shigella, Veillonella, Akkermansia, Provindencia, Dialister, Bifidobacterium, Streptococcus, Ruminococcaceae UCG_002, Megasphaera, Eubacterium_coprostanol, Citrobacter, Ruminiclostridium_5, and Ruminiclostridium_6 in the ASD cohort, while Eisenbergiella, Klebsiella, Faecalibacterium, and Blautia were significantly increased. Ten bacterial strains were selected for clinical discrimination between those with ASD and the neurotypical controls. The highest AUC value of the model was 0.947.
Significant differences were observed in the composition of the gut microbiome between boys with ASD and neurotypical controls. These findings contribute to the knowledge of the alteration of the gut microbiome in ASD patients, which opens the possibility for early identification of this disease.
This study examined the relationship between the intestinal microbiota and SARS-CoV-2 infection in a United States hospital cohort. Researchers collected fecal samples and used 16S rRNA sequencing plus qPCR analysis to compare microbial composition across infection states. They compared actively infected patients, recovered patients, and uninfected controls seen for unrelated respiratory conditions, and also tested for fecal viral shedding.
The cohort included 50 patients actively infected with SARS-CoV-2, 9 patients who had recovered from SARS-CoV-2 infection, and 34 uninfected control subjects seen at the hospital for unrelated respiratory medical conditions. The study is described as a United States, majority African American and minority-dominated cohort. Fecal DNA and RNA were collected prospectively from all three groups for microbiota analysis.
Fecal microbial composition differed significantly between SARS-CoV-2 patients and controls, independent of antibiotic exposure, with Peptoniphilus, Corynebacterium, and Campylobacter enriched in COVID-19 patients. Actively infected patients also had a distinct gut microbiota compared to recovered patients, with Campylobacter most enriched during active infection and Agathobacter and Faecalibacterium enriched after recovery. Notably, recovered patients showed no difference in microbial community structure or alpha diversity compared to uninfected controls. Nearly half of the COVID-19 patients (24 of 50, 48%) tested positive by RT-qPCR for fecal viral material.
The findings suggest that SARS-CoV-2 infection is associated with a transient disruption of gut microbial composition that resolves as patients recover, rather than causing lasting dysbiosis. This return to an uninfected-like microbiome state in recovered patients supports the gut as a site of active but reversible interaction with the virus. The high rate of fecal viral detection also reinforces concern about potential fecal-oral transmission during active infection.
In COVID-19 patients, information regarding superinfection, antimicrobial assessment, and the value of metagenomic sequencing (MS) could help develop antimicrobial stewardship.
This retrospective study analyzed 323 laboratory-confirmed COVID-19 patients for co-infection rate and antimicrobial usage in the Shanghai Public Health Clinical Center (SPHCC) from January 23rd to March 14th 2020. The microbiota composition was also investigated in patients with critically severe COVID-19.
The total population co-infection rate was 17/323 (5.3%) and 0/229 (0), 4/78 (5.1%), and 13/16 (81.3%) for the mild, severe, and critically severe subgroups, respectively. Proven fungal infection was significantly associated with a higher mortality rate (p = 0.029). In critically severe patients, the rate of antimicrobials and carbapenem usage were 16/16 (100%) and 13/16 (81.3%), respectively, in which the preemptive and empiric antimicrobial days accounted for 51.6% and 30.1%, respectively. Targeted therapy only accounted for 18.3%. MS was implemented to detect non-COVID-19 virus co-existence and the semi-quantitative surveillance of bacteremia, with clear clinical benefit seen in cases with MS-based precision antimicrobial management. Airway microbiome analysis suggested that the microbiota compositions in critically severe COVID-19 patients were likely due to intubation and mechanical ventilation.
In the SPHCC cohort, we observed a non-negligible rate of super-infection, especially for the critically ill COVID-19 patients. Fungal co-infection requires intensive attention due to the high risk of mortality, and the clinical benefit of MS in guiding antimicrobial management warrants further investigation.
This study characterized the skin and gut bacterial communities of the invasive Asian common toad, Duttaphrynus melanostictus, in Toamasina, Eastern Madagascar. The researchers compared these microbial communities to those of a co-occurring native frog species, Ptychadena mascareniensis. Sampling took place at three sites where the toad had established at different times, allowing the study to assess whether its microbiome changes across the expansion range.
The subjects were skin and gut bacterial communities sampled from the invasive Asian common toad and the native frog Ptychadena mascareniensis, both collected at three sites in Toamasina, Eastern Madagascar. These sites represented different time points in the toad's invasion history. The abstract does not report a specific number of individual animals sampled.
Microbial composition in the invasive toad did not vary among the three sites, indicating that Duttaphrynus melanostictus maintains a stable skin and gut bacterial community as it expands across Madagascar. However, significant differences were observed between the invasive toad and the native frog. The toad harbored richer and more diverse bacterial communities and carried a high percentage of unique taxa not shared with the native species, 80 percent on the skin and 52 percent in the gut.
The stability of the toad's microbiome across its expansion range suggests it travels with a resilient, portable microbial community that may support its colonization success in new habitats. The high proportion of unique taxa carried by the toad raises the possibility that it introduces novel microbes into Malagasy ecosystems, with unknown consequences for native amphibians and the broader environment. These findings underscore the importance of tracking invader-associated microbiomes when assessing threats posed by biological invasions.
This study examined the gut microbiota and fecal metabolome in children with systemic lupus erythematosus (SLE), an autoimmune connective tissue disease with unclear origins. Researchers used 16S rRNA sequencing to profile intestinal bacterial communities and gas chromatography-mass spectrometry (GC-MS) to characterize fecal metabolites. The goal was to correlate microbial composition changes with metabolite shifts to better understand SLE pathogenesis.
The abstract identifies the population as children with systemic lupus erythematosus, compared against healthy controls (referred to as HCs). No specific sample size, age range, or recruitment site is given in the abstract. The comparison design implies a case-control cohort of pediatric SLE patients and matched or unmatched healthy children.
Alpha diversity of the gut microbiota was unchanged in SLE patients, while beta diversity was partially altered compared to controls. Proteobacteria and Enterobacteriales increased and Ruminococcaceae decreased among SLE patients. Fecal metabolite analysis showed enrichment of amino acids and short-chain fatty acids alongside a decrease in long-chain fatty acids, with KEGG pathway analysis highlighting protein digestion and absorption, and association analysis pointing to 3-phenylpropanoic acid and Sphingomonas as key features. Sphingomonas was also found to be less abundant in healthy periodontal sites of SLE patients than in controls, suggesting possible oral-to-gut transmission of this taxon.
These findings suggest that gut microbial imbalance and altered fecal metabolites, particularly involving Ruminococcaceae, Proteobacteria, and short-chain and long-chain fatty acids, may contribute to SLE pathogenesis in children. The identification of Sphingomonas and 3-phenylpropanoic acid as correlated features points to a potential oral-gut microbial axis worth further investigation. This work provides a foundation for exploring microbiome-targeted approaches as potential treatments for pediatric SLE.
This study examined the gut microbiome composition of patients with young-onset colorectal cancer (yCRC), a form of sporadic colorectal cancer whose incidence is rising. Researchers used 16S rRNA gene sequencing to identify microbial markers distinguishing yCRC, then validated these findings in an independent cohort. Metagenome sequencing was also performed to characterize species-level and functional differences in bacterial communities associated with yCRC.
The discovery analysis drew on 728 samples analyzed by 16S rRNA gene sequencing. An independent validation cohort of 310 samples was used to confirm the identified microbial markers. A further subset of 200 samples underwent metagenome sequencing for species-level and functional analysis.
Gut microbial diversity was increased in yCRC compared to other groups studied. Flavonifractor plautii emerged as an important bacterial species associated with yCRC, whereas the genus Streptococcus contained the key phylotype linked to old-onset colorectal cancer. Functional analysis showed that yCRC-associated bacterial communities were distinguished by a dominance of DNA binding and RNA-dependent DNA biosynthetic processes, and a random forest classifier built on these microbial features achieved strong classification performance.
The findings suggest that gut microbiota biomarkers, particularly Flavonifractor plautii abundance and associated functional signatures, could serve as a non-invasive tool for detecting and distinguishing yCRC. This approach could help address the diagnostic gap for younger patients as sporadic colorectal cancer incidence rises in this age group. The distinct microbial and functional profile of yCRC versus old-onset colorectal cancer also points to potentially different underlying disease biology between the two age groups.
Olfactory dysfunction is a pre-motor symptom of Parkinson's disease (PD) that appears years prior to diagnosis and can affect quality of life in PD. Changes in microbiota community in deep nasal cavity near the olfactory bulb may trigger the olfactory bulb-mediated neuroinflammatory cascade and eventual dopamine loss in PD. To determine if the deep nasal cavity microbiota of PD is significantly altered in comparison to healthy controls, we characterized the microbiota of the deep nasal cavity using 16S rRNA gene amplicon sequencing in PD subjects and compared it to that of spousal and non-spousal healthy controls. Correlations between microbial taxa and PD symptom severity were also explored. Olfactory microbial communities of PD individuals were more similar to those of their spousal controls than to non-household controls. In direct comparison of PD and spousal controls and of PD and non-spousal controls, significantly differently abundant taxa were identified, and this included increased relative abundance of putative opportunistic-pathobiont species such as Moraxella catarrhalis. M. catarrhalis was also significantly correlated with more severe motor scores in PD subjects. This proof-of-concept study provides evidence that potential pathobionts are detected in the olfactory bulb and that a subset of changes in the PD microbiota community could be a consequence of unique environmental factors associated with PD living. We hypothesize that an altered deep nasal microbiota, characterized by a putative pro-inflammatory microbial community, could trigger neuroinflammation in PD.
Patients with pulmonary tuberculosis (TB) undergoing anti-tuberculosis (anti-TB) treatment were previously reported to present gut bacterial microbiota dysbiosis, but the role of the mycobiota has not been reported. Here, we conducted a follow-up study of 29 naive TB patients who received first-line anti-TB drug treatment; we collected their fecal samples at different time points, as well as 22 fecal samples from healthy subjects. Fungal ITS2 and bacterial 16S rRNA amplicon sequencing were used to analyze the effects of active TB and anti-TB treatment on the gut microbiota. We found that naive TB patients had bacterial and fungal dysbiosis with altered community composition and a decreased density of the transkingdom correlation network. Anti-TB drug treatment significantly decreased the diversity of bacteria and fungi with altered composition. Notably, we observed that the abundance of Purpureocillium lilacinum tended to decrease and Nakaseomyces spp. tended to increase in the anti-TB treatment, and all of them had increased proportions in the three TB groups compared with healthy subjects. We found that the fungal-bacterial transkingdom network was severely altered in TB patients after 2 months of treatment, and new fungal-enriched connections that were not observed in other groups after 6 months of treatment. This study provides the first detailed analysis of dysbiosis of the gut mycobiota due to active TB and anti-TB treatment. The results suggest that fungi play an important role in the balance of the gut microbiota and may be associated with the progression of TB, influencing the microbiota and immunity homeostasis in those receiving anti-TB treatment. IMPORTANCE Numerous studies have shown that the gut bacterial microbiota is altered in active TB patients and that anti-TB drugs have profound and long-term impacts. However, as an integral part of the microbiota, fungi have rarely been studied. The need to investigate both the bacterial and fungal microbiota, as well as the relationship between them is apparent. The significance of our study is in our examination of the changes in the bacterial and fungal microbiota simultaneously in both active TB and patients receiving anti-TB treatment. We found that fungi play an important role in the bacterial-fungal transkingdom network, especially during the anti-TB therapy. These findings underscore the importance of fungi in gut microbiota dysbiosis during active TB and anti-TB treatment processes. In addition, our findings suggest it is meaningful to research potential adjunctive therapies that reduce fungal expansion and increase commensal bacterial abundance after anti-TB treatment, which would help the recovery of TB patients.
Allergic rhinitis (AR) is a common heterogeneous chronic disease with a high prevalence and a complex pathogenesis influenced by numerous factors, involving a combination of genetic and environmental factors. To gain insight into the pathogenesis of AR and to identity diagnostic biomarkers, we combined systems biology approach to analyze microbiome and serum composition. We collected inferior turbinate swabs and serum samples to study the microbiome and serum metabolome of 28 patients with allergic rhinitis and 15 healthy individuals. We sequenced the V3 and V4 regions of the 16S rDNA gene from the upper respiratory samples. Metabolomics was used to examine serum samples. Finally, we combined differential microbiota and differential metabolites to find potential biomarkers. We found no significant differences in diversity between the disease and control groups, but changes in the structure of the microbiota. Compared to the HC group, the AR group showed a significantly higher abundance of 1 phylum (Actinobacteria) and 7 genera (Klebsiella, Prevotella and Staphylococcus, etc.) and a significantly lower abundance of 1 genus (Pelomonas). Serum metabolomics revealed 26 different metabolites (Prostaglandin D2, 20-Hydroxy-leukotriene B4 and Linoleic acid, etc.) and 16 disrupted metabolic pathways (Linoleic acid metabolism, Arachidonic acid metabolism and Tryptophan metabolism, etc.). The combined respiratory microbiome and serum metabolomics datasets showed a degree of correlation reflecting the influence of the microbiome on metabolic activity. Our results show that microbiome and metabolomics analyses provide important candidate biomarkers, and in particular, differential genera in the microbiome have also been validated by random forest prediction models. Differential microbes and differential metabolites have the potential to be used as biomarkers for the diagnosis of allergic rhinitis.
The significance of the liver-microbiome axis has been increasingly recognised as a major modulator of autoimmunity. The aim of this study was to take advantage of a large well-defined corticosteroids treatment-naïve group of patients with autoimmune hepatitis (AIH) to rigorously characterise gut dysbiosis compared with healthy controls.
We performed a cross-sectional study of individuals with AIH (n=91) and matched healthy controls (n=98) by 16S rRNA gene sequencing. An independent cohort of 28 patients and 34 controls was analysed to validate the results. All the patients were collected before corticosteroids therapy.
The gut microbiome of steroid treatment-naïve AIH was characterised with lower alpha-diversity (Shannon and observed operational taxonomic units, both p<0.01) and distinct overall microbial composition compared with healthy controls (p=0.002). Depletion of obligate anaerobes and expansion of potential pathobionts including Veillonella were associated with disease status. Of note, Veillonella dispar, the most strongly disease-associated taxa (p=8.85E-8), positively correlated with serum level of aspartate aminotransferase and liver inflammation. Furthermore, the combination of four patients with AIH-associated genera distinguished AIH from controls with an area under curves of approximately 0.8 in both exploration and validation cohorts. In addition, multiple predicted functional modules were altered in the AIH gut microbiome, including lipopolysaccharide biosynthesis as well as metabolism of amino acids that can be processed by bacteria to produce immunomodulatory metabolites.
Our study establishes compositional and functional alterations of gut microbiome in AIH and suggests the potential for using gut microbiota as non-invasive biomarkers to assess disease activity.
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.
Aim: To identify intestinal microbiota compositions in elderly functional constipation (FC) patients. Materials and methods: Fecal samples from 61 FC patients and 48 healthy age-matched volunteers were analyzed through 16S rRNA gene sequencing. Results: The intestinal microbiota compositions of FC patients were significantly different from healthy controls. Additionally, the species diversity of healthy controls was greater than that of FC patients. Indeed, the abundance of Firmicutes and Proteobacteria was significantly decreased, whereas that of Bacteroides, Prevotella, Lactococcus, Ruminococcus and Butyricimonas was remarkably increased in FC patients. Conclusion: Elderly FC patients appear to have a unique intestinal microbiota profile. Our findings should provide insight regarding the pathogenic mechanism of FC and evidence for exploring new therapeutic strategies in elderly FC patients.
This study examined whether fecal gut microbiota composition differs between patients with Parkinson's disease (PD) who have mild cognitive impairment (PD-MCI) and those with normal cognition (PD-NC), as well as healthy controls (HC). Researchers analyzed fecal bacterial composition using 16S ribosomal RNA sequencing alongside short-chain fatty acid levels measured by gas chromatography-mass spectrometry. The study also investigated whether specific microbiota alterations were associated with cognitive ability in PD patients.
The study included 13 patients with PD-MCI, 14 patients with PD-NC, and 13 healthy spouses serving as controls. Using spouses as the healthy control group suggests an effort to account for shared household and dietary environment. Statistical adjustments were made for age, sex, body mass index, education, and constipation to isolate microbiota differences related to cognitive status.
Fecal microbial diversity was higher in both the PD-MCI and PD-NC groups compared with healthy controls. After adjusting for confounders, the PD-MCI group showed higher relative abundances of the families Rikenellaceae and Ruminococcaceae and the genera Alistipes, Barnesiella, Butyricimonas, and Odoribacter compared with the other two groups. The abundance of the genera Blautia and Ruminococcus decreased in association with cognitive impairment, indicating a distinct microbial signature linked to PD-MCI.
These findings suggest that gut microbiota alterations may be linked specifically to cognitive impairment in Parkinson's disease, not just to PD status itself. Identifying distinct bacterial taxa associated with PD-MCI raises the possibility that fecal microbiota could serve as a biomarker for cognitive decline in PD patients. This work supports further investigation into the gut-brain axis as a factor in PD-related cognitive outcomes, though the small sample size means findings require validation in larger cohorts.
Rationale: Long-term antibiotic use for managing chronic respiratory disease is increasing; however, the role of the airway resistome and its relationship to host microbiomes remains unknown.Objectives: To evaluate airway resistomes and relate them to host and environmental microbiomes using ultradeep metagenomic shotgun sequencing.Methods: Airway specimens from 85 individuals with and without chronic respiratory disease (severe asthma, chronic obstructive pulmonary disease, and bronchiectasis) were subjected to metagenomic sequencing to an average depth exceeding 20 million reads. Respiratory and device-associated microbiomes were evaluated on the basis of taxonomical classification and functional annotation including the Comprehensive Antibiotic Resistance Database to determine airway resistomes. Co-occurrence networks of gene-microbe association were constructed to determine potential microbial sources of the airway resistome. Paired patient-inhaler metagenomes were compared (n = 31) to assess for the presence of airway-environment overlap in microbiomes and/or resistomes.Measurements and Main Results: Airway metagenomes exhibit taxonomic and metabolic diversity and distinct antimicrobial resistance patterns. A "core" airway resistome dominated by macrolide but with high prevalence of β-lactam, fluoroquinolone, and tetracycline resistance genes exists and is independent of disease status or antibiotic exposure. Streptococcus and Actinomyces are key potential microbial reservoirs of macrolide resistance including the ermX, ermF, and msrD genes. Significant patient-inhaler overlap in airway microbiomes and their resistomes is identified where the latter may be a proxy for airway microbiome assessment in chronic respiratory disease.Conclusions: Metagenomic analysis of the airway reveals a core macrolide resistome harbored by the host microbiome.
This cross-sectional study used shotgun metagenomic sequencing of fecal samples to identify gut microbial species associated with polycystic ovary syndrome (PCOS). Researchers compared the gut microbiota composition of women with PCOS to that of women without the condition. They also collected clinical parameters, including body mass index, endocrine hormone levels, and glycemia, to test for correlations with the microbial findings.
The study included 14 reproductive-aged women diagnosed with PCOS and 14 control women, all recruited from an academic Centre for Reproductive Medicine. Fecal samples from these 28 participants underwent shotgun metagenomic sequencing. Clinical and metabolic data were gathered from the same women for correlation analysis.
Several microbial strains were significantly more abundant in the PCOS group, including Parabacteroides merdae, Bacteroides fragilis, and strains of Escherichia and Shigella, while Faecalibacterium prausnitzii was enriched in controls. Metagenomic species analysis showed that the microbial profiles of the PCOS group were negatively correlated with those of the control group. Microbial species associated with PCOS were positively correlated with endocrine disturbances, including higher body mass index and elevated serum testosterone levels.
The findings support a pathological association between gut dysbiosis and PCOS, linking specific bacterial taxa to hormonal and metabolic disturbances seen in the condition. The enrichment of Escherichia and Shigella strains alongside depletion of the beneficial species Faecalibacterium prausnitzii suggests a shift toward a more pro-inflammatory gut environment in PCOS. These results point to the gut microbiome as a potential target for understanding or managing the endocrine and metabolic features of PCOS, though further work is needed to establish causality.
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.
This study examined gut microbiota composition and fecal metabolite profiles in people with Parkinson's disease compared to controls. Researchers used next-generation sequencing to characterize bacterial taxa and gas chromatography-mass spectrometry to measure fecal metabolites. The goal was to identify microbiome and metabolome alterations associated with Parkinson's disease, a neurodegenerative disorder marked by misfolded alpha-synuclein aggregates along the cerebral axis. The abstract notes that a cause-effect relationship between intestinal dysbiosis and Parkinson's disease has not yet been established.
The study included 64 Italian patients with Parkinson's disease and 51 controls. Both groups underwent gut microbiota sequencing and fecal metabolite analysis. No further demographic details, such as age or sex distribution, are given in the abstract.
Parkinson's disease patients showed reduced levels of bacterial taxa linked to anti-inflammatory and neuroprotective effects, particularly within the Lachnospiraceae family, including Butyrivibrio, Pseudobutyrivibrio, Coprococcus, and Blautia. Fecal metabolite analysis revealed changes across several compound classes. These included lipids such as linoleic acid, oleic acid, succinic acid, and sebacic acid, vitamins such as pantothenic acid and nicotinic acid, amino acids such as isoleucine, leucine, phenylalanine, glutamic acid, and pyroglutamic acid, and other organic compounds such as cadaverine, ethanolamine, and hydroxy propionic acid. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, or hydrogen sulfide.
The findings reinforce that Parkinson's disease is accompanied by a distinct pattern of gut dysbiosis and metabolic disturbance, with depletion of beneficial, anti-inflammatory Lachnospiraceae members standing out as a key feature. The combined microbiota and metabolome approach suggests that fecal biomarkers could eventually help characterize or monitor the disease. Because the abstract states that causality remains unestablished, these results should be viewed as associative rather than proof that gut changes drive Parkinson's disease pathology.
This study investigated whether BDB, a natural bromophenol isolated from the marine red alga Rhodomela confervoides, could alleviate type 2 diabetes mellitus (T2DM) by modulating the gut microbiota. Researchers used 16S rRNA gene pyrosequencing of the V3-V4 regions along with metagenomic analysis to characterize microbial community changes during BDB treatment. The study compared BDB against metformin, a standard antidiabetic drug, and a vehicle control to assess effects on fasting blood glucose and gut microbial composition.
The study used 24 diabetic BKS db mice, randomly assigned in a blinded manner to receive BDB (n = 6), metformin (n = 6), or vehicle (n = 6) for seven weeks. Non-diabetic BKS mice (n = 6) served as a normal control group. This was an animal model study, not a human cohort.
Diabetic mice treated with BDB or metformin showed significant reductions in fasting blood glucose by the seventh week compared with vehicle-treated diabetic mice. Gut microbiota analysis revealed that short-chain fatty acid (SCFA) producing bacteria, including Lachnospiraceae and Bacteroides, were significantly more abundant in the BDB and metformin groups than in the vehicle group. Notably, Akkermansia was significantly elevated at the genus level in the BDB-treatment group specifically. No sulfate-reducing bacteria, Desulfovibrio, hydrogen sulfide, or sulfur metabolism findings were reported in this abstract.
These findings suggest that BDB's antidiabetic effects in this mouse model may be linked to favorable shifts in gut microbiota composition, particularly increases in SCFA-producing bacteria and Akkermansia. This positions BDB as a candidate natural compound worth further investigation for T2DM management through a gut-microbiota-mediated mechanism. The metagenomic data point toward specific microbial pathways that could be explored in future mechanistic and translational studies.
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.
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.
Chronic constipation is one of the most prevalent functional gastrointestinal disorders, yet its etiology is multifactorial, and the pathophysiological mechanism is still unclear. Previous studies have shown that the gut microbiota of constipated patients differs from healthy controls; however, many discrepancies exist in the findings, and no clear link has been confirmed between chronic constipation and changes in the gut microbiota. Growing evidence indicates that age, gender, and hormone levels can affect the composition of gut microbiota. The aim of this study is to examine the overall changes in gut microbiota within a specific sub-population of patients, namely, constipated women of reproductive age.
We carried out a cross-sectional study comparing the fecal microbial composition of 30 healthy women and 29 constipated women using 16S rRNA gene sequencing. Only women of reproductive age were recruited to reduce the effects of age, gender, and hormone levels on the microbiome, and to prevent conflating the impact of these factors with the effects of constipation.
There were obvious differences in the gut microbiota in constipated women of reproductive age compared with the healthy controls, manifesting mainly as a significant increase in the abundance of Bacteroides (p < 0.05) and a significant decrease in the abundance of Proteobacteria (p < 0.01). The overall composition of the gut microbiota in each group was different, which was reflected in the ratios of Firmicutes to Bacteroidetes (F/B), which was 1.52 in the constipated group vs. 2.21 in the healthy group. Additionally, there was a significant decrease in butyrate-producing bacteria, like Roseburia and Fusicatenibacter (p < 0.01).
The overall composition of the gut microbiota changed in constipated women of reproductive age, characterized by a loss in Proteobacteria and an increase in Bacteroidetes. Furthermore, the abundance of some butyrate-producing bacteria also reduced. These changes may reflect the unique interactions between host and some bacteria, or some bacterial metabolic products, which may be important targets for future studies to explore the pathogenesis of constipation.
This cross-sectional study examined whether the gut microbiota is associated with extraintestinal joint inflammation in patients with inflammatory bowel disease (IBD). Stool samples were collected and DNA was sequenced on the Illumina platform, with reads quality-controlled using SHI7 and processed with SHOGUN. Microbial abundance and diversity were assessed with QIIME, and compositional biomarkers distinguishing groups were identified using LEfSe. The study also evaluated microbial functional pathways, including tyrosine degradation, and examined history of bowel surgery as a possible source of variability.
One hundred eighty patients were included in the analysis, divided into four groups: those with IBD-associated arthropathy (IBD-A), IBD without arthropathy (IBD-N), rheumatoid arthritis (RA), and non-IBD, nonarthritis controls. The abstract does not give a numeric breakdown of how many patients fell into each of the four groups. This design allowed direct comparison of gut microbial composition across intestinal and joint-related inflammatory phenotypes.
IBD-A was associated with an increased abundance of microbial tyrosine degradation pathways compared with IBD-N (P = 0.02). IBD-A and RA patients both showed an increased abundance of Clostridiaceae compared with controls (P = 0.045), suggesting a shared microbial signature across two distinct arthritis-associated conditions. History of bowel surgery was also identified as a significant source of variability among IBD patients (P = 0.001) and was linked to decreased alpha diversity.
The shared enrichment of Clostridiaceae in both IBD-associated arthritis and rheumatoid arthritis suggests a common gut microbial feature may underlie joint inflammation across different autoimmune and inflammatory contexts. Altered tyrosine degradation pathways in IBD-A point to a possible metabolic mechanism linking gut microbes to extraintestinal disease manifestations. The findings also highlight bowel surgery history as an important confounder to account for in future microbiome studies of IBD patients. Together, these results support further investigation of Clostridiaceae and related microbial pathways as potential targets or biomarkers for arthritis in IBD.
This study investigated the composition of the intestinal (gut) microbiota in patients with gastric cancer compared with healthy individuals. The researchers used 16S rRNA gene sequencing on fecal samples to characterize microbial community differences. They also examined correlations between the intestinal microbiota and cellular immunity, including peripheral T lymphocyte subpopulations and NK cells, measured by flow cytometry.
The study included 116 gastric cancer patients and 88 healthy controls from Shanxi Province, China, who provided fecal samples for microbiota analysis. A subset of this group, 66 gastric cancer patients and 46 healthy controls, also provided peripheral blood samples for immune cell profiling. All participants were drawn from a single geographic region in China.
Gastric cancer patients showed increased intestinal species richness compared with healthy controls. Butyrate-producing bacteria were decreased, while other symbiotic bacteria were enriched, particularly Lactobacillus, Escherichia, and Klebsiella. Lactobacillus and Lachnospira emerged as key species within the network of gastric cancer associated bacterial genera, and a combination of five genera, Lachnospira, Lactobacillus, Streptococcus, Veillonella, and Tyzzerella_3, performed well in distinguishing gastric cancer patients from controls based on the information provided.
These findings suggest that gastric cancer is associated with a distinct pattern of intestinal dysbiosis, marked by loss of butyrate producers and enrichment of specific symbiotic genera. The identified microbial signature, especially the five-genus combination, points toward potential use of gut microbiota profiling as a non-invasive tool to help distinguish gastric cancer patients from healthy individuals. The proposed links to cellular immunity also support the broader concept that host-microbial interactions may influence immune regulation relevant to gastric cancer development.
This study used 16S rRNA gene sequencing to characterize the gut microbiota across the colorectal cancer disease course. It compared microbial diversity, overall community composition, and taxonomic abundance among colorectal adenoma patients, colorectal cancer (CRC) patients, and CRC patients after surgical treatment. The study also examined how postoperative gut microbiota related to colonoscopy findings and to CRC prognosis.
The comparison groups were colorectal adenoma patients, CRC patients, CRC postoperative (post-surgical) patients, and healthy controls. Postoperative patients were further divided into those with newly developed adenoma on colonoscopy versus those with a clean intestine. The abstract does not give specific sample sizes, so exact cohort numbers cannot be stated.
Gut microbiota composition shifted progressively along the adenoma-carcinoma sequence, with marked changes occurring before or during CRC development. The gut microbiota of postoperative patients differed significantly from that of CRC patients, showing that surgery does not restore a healthy-control-like microbial profile. Among postoperative patients, those who developed new adenomas had a microbiota more similar to carcinoma patients than to healthy controls, and differences between postoperative subgroups corresponded to CRC prognosis.
Persistent microbiota alterations after CRC surgery suggest the gut microbiome could serve as a monitoring tool for recurrence risk and prognosis in postoperative patients. A microbiota signature resembling carcinoma in patients with new adenomas points to the gut microbiome as a potential early warning marker distinct from clean-intestine recovery. This abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so no sulfide-related angle applies here.
This study investigated the relationship between gut microbiota composition, microbial metabolic pathways, and metabolite profiles in thyroid carcinoma (TC). Researchers used 16S rRNA gene sequencing to characterize fecal microbial communities and applied PICRUSt to predict functional metabolic pathways. In a subset of participants, liquid chromatography mass spectrometry was also performed to characterize circulating or fecal metabolite profiles and correlate them with microbial genera.
The primary comparison included 30 patients with thyroid carcinoma and 35 healthy controls, whose fecal samples were used for 16S rRNA sequencing. A smaller, matched subset of the same population, 15 TC patients and 15 healthy controls, was then analyzed in more depth for combined microbiota and metabolite profiling. All participants were human subjects recruited for direct comparison between disease and healthy states.
Gut microbiota composition differed significantly between TC patients and healthy controls, with 19 genera enriched and 8 genera depleted in TC samples. Six differentially abundant genera distinguished TC patients from healthy controls with an area under the curve of 0.94, indicating strong discriminatory potential. Twelve metabolic pathways predicted by PICRUSt were significantly altered, and in the smaller matched subset, 21 differential genera and 72 significantly changed metabolites were identified and found to correlate with one another. Several genera also correlated with clinical parameters such as lipoprotein A and apolipoprotein B.
The findings suggest that gut microbiota alterations and their associated metabolite changes are linked to thyroid carcinoma and may reflect or contribute to underlying metabolic disturbances in these patients. The high discriminatory accuracy of the six-genus panel raises the possibility that gut microbiota signatures could serve as non-invasive biomarkers for thyroid carcinoma. The correlations between specific genera, metabolites, and clinical lipid parameters point toward a potential mechanistic link between the gut microbiome and host lipid metabolism in thyroid carcinoma that warrants further investigation.
This study examined the relationship between gut microbiome composition and childhood eczema using 16S rRNA gene sequencing. Researchers compared microbial profiles between healthy children and children with eczema, stratifying samples into four age groups (0-0.5, 0.5-1, 1-2, and 2-3 years) to account for developmental and environmental influences on the gut microbiome. Findings from sequencing were further verified using quantitative polymerase chain reaction targeting Bifidobacterium and Bacteroides.
The cohort included 172 subjects under age three, divided into a healthy group of 123 children and an eczema group of 49 children. Samples were further split across four narrower age brackets to examine how the microbiome-eczema relationship changed over early development. No further demographic or geographic details were given in the abstract.
Lower relative abundance of Bifidobacterium was associated with childhood eczema, though this difference was not significant in infants younger than six months old. From 0.5 to 3 years of age, decreased Bifidobacterium was a major and consistent finding in the eczema group compared to age-matched healthy controls. Decreased microbial diversity was also observed in eczema samples across all age groups, most significantly in children aged 2-3 years. Bifidobacterium operational taxonomic units showed strong predictive power for eczema status, with a Random Forest model achieving an AUC of 0.83 in ROC analysis.
The findings suggest that reduced Bifidobacterium levels in the gut, emerging after the first six months of life, may be linked to the development of childhood eczema. Because Bifidobacterium abundance showed high predictive accuracy for eczema status, it may serve as a candidate microbial marker for risk assessment in early childhood. The age-stratified design also indicates that timing matters: the microbiome-eczema association strengthens as children move past infancy, pointing to a developmental window relevant to future preventive or diagnostic strategies.
Excessive alcohol intake can alter the gut microbiota, which may underlie the pathophysiology of alcohol-related diseases. We examined gut microbiota composition and functions in patients with alcohol overconsumption for >10 years, compared to a control group of patients with a history of no or low alcohol intake. Faecal microbiota composition was assessed by 16S rRNA sequencing. Gut microbiota functions were evaluated by quantification of short-chain fatty acids (SCFAs) and predictive metagenome profiling (PICRUSt). Twenty-four patients, mean age 64.8 years (19 males), with alcohol overconsumption, and 18 control patients, mean age 58.2 years (14 males) were included. The two groups were comparable regarding basic clinical variables. Nutritional assessment revealed lower total score on the screening tool Mini Nutritional Assessment, lower muscle mass as assessed by handgrip strength, and lower plasma vitamin C levels in the alcohol overconsumption group. Bacteria from phylum Proteobacteria were found in higher relative abundance, while bacteria from genus Faecalibacterium were found in lower relative abundance in the group of alcohol overconsumers. The group also had higher levels of the genera Sutterella, Holdemania and Clostridium, and lower concentration and percentage of butyric acid. When applying PICRUSt to predict the metagenomic composition, we found that genes related to invasion of epithelial cells were more common in the group of alcohol overconsumers. We conclude that gut microbiota composition and functions in patients with alcohol overconsumption differ from patients with low consumption of alcohol, and seem to be skewed into a putative pro-inflammatory direction.
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.
The gut microbiota plays an important role in the development and progression of colorectal cancer (CRC). To learn more about the dysbiosis of carcinogenesis, we assessed alterations in gut microbiota in patients with CRC. A total of 23 subjects were enrolled in this study: 9 had CRC (CRC group) and 14 had normal colons (normal group). The microbiome of the mucosal-luminal interface of each subject was sampled and analyzed using 16S rRNA gene amplicon sequencing. We also used Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) to predict microbial functional profiles. The microbial composition of the mucosal lumen differed between the groups, and the presence of specific bacteria may serve as a potential biomarker for colorectal carcinogenesis. We identified a significant reduction in Eubacterium, which is a butyrate-producing genera of bacteria, and a significant increase in Devosia in the gut microbiota of CRC patients. Different levels of gut microflora in healthy and CRC samples were identified. The observed abundance of bacterial species belonging to Eubacterium and Devosia may serve as a promising biomarker for the early detection of CRC.
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.
Gastric cancer (GC) is one of the common malignant tumors in China, with a high morbidity and mortality. With the development and application of high-throughput sequencing technologies and metagenomics, a great quantity of studies have shown that gastrointestinal microbiota is closely related to digestive system diseases. Although some studies have reported the effect of long-term follow-up after subtotal gastrectomy on intestinal flora changes in patients with GC. However, the features of gut microbiota and their shifts in patients with GC in perioperative period remain unclear.This study was designed to characterize fecal microbiota shifts of the patients with GC before and after the radical distal gastrectomy (RDG) during their hospital staying periods. Furthermore, fecal microbiota was also compared between the GC patients and healthy individuals.Patients who were diagnosed with advanced gastric adenocarcinoma at distal stomach were enrolled in the study. The bacterial burden within fecal samples was determined using quantitative polymerase chain reaction. To analyze the diversity and composition of gut microbiota from fecal DNA of 20 GC patients and 22 healthy controls, amplicons of the 16S rRNA gene from all subjects were pyrosequenced. To study gut microbiota shifts, the fecal microbiota from 6 GC patients before and after RDG was detected and subsequently analyzed. Short-chain fatty acids were also detected by chromatography spectrometer in these 6 GC patients.RDG had a moderate effect on bacterial richness and evenness, but had pronounced effects on the composition of postoperative gut microbiota compared with preoperative group. The relative abundances of genera Akkermansia, Esherichia/Shigella, Lactobacillus, and Dialister were significant changed in perioperative period. Remarkably, higher abundances of Escherichia/Shigella, Veillonella, and Clostridium XVIII and lower abundances of Bacteroides were observed in gut microbiota of overall GC patients compared to healthy controls.This study is the first study to characterize the altered gut microbiota within fecal samples from GC patients during perioperative period, and provide a new insights on such microbial perturbations as a potential effector of perioperative period phenotype. Further research must validate these discoveries and may evaluate targeted microbiota shifts to improve outcomes in GC patients.
This study examined how the gut microbiome of Hispanic adults living in the USA is shaped by birthplace, migration history, and lifestyle factors. Researchers used 16S rRNA gene V4 amplicon sequencing to profile bacteria and ITS1 fragment sequencing to profile fungi in self-collected stool samples. The analysis was cross-sectional, looking at sociodemographic and migration-related variables alongside obesity status to explain differences in microbiome composition.
The study drew on 1,674 participants from four centers of the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), aged 18 to 74 years old at recruitment. Participants included people born in the USA as well as those who relocated from Latin America at different points in life, including early childhood and adulthood over age 45. This design allowed comparison across USA-born individuals, childhood arrivals, and adult migrants.
Those who relocated to the USA early in life showed reduced Prevotella to Bacteroides ratios that persisted throughout their lives, along with low Shannon diversity for both bacteria and fungi. In contrast, adults who relocated after age 45 had high bacterial and fungal diversity and high Prevotella to Bacteroides ratios compared to USA-born individuals and childhood arrivals. Low bacterial diversity was associated with obesity, and unlike prior studies in other populations, this Latino cohort showed an increasing Prevotella to Bacteroides ratio with greater obesity. Several taxa, including Acidaminococcus, Megasphaera, Ruminococcaceae, Coriobacteriaceae, and Clostridiales, were also implicated in these patterns.
The findings suggest that age at migration is a durable determinant of gut microbiome composition, with effects that persist across the life course rather than fading with time in a new country. Because the Prevotella to Bacteroides and obesity relationship ran counter to patterns seen in other populations, the results caution against generalizing microbiome-obesity associations across ethnic and migration backgrounds. This points to a need for population-specific reference ranges when interpreting gut microbiome signatures tied to metabolic health.
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 case-control study examined the fecal microbiota composition of patients with Parkinson's disease (PD) in a Chinese cohort. Researchers used high-throughput Illumina Miseq sequencing targeting the V3-V4 region of the 16S ribosomal RNA gene to profile bacterial communities. The study aimed to characterize gut microbiota dysbiosis in Chinese PD patients, a population not previously examined for this question, and to relate microbiota features to clinical characteristics of the disease.
The study included 45 patients with Parkinson's disease and their healthy spouses, who served as controls. Using spouses as controls helps account for shared household diet and environment. Clinical characteristics analyzed alongside the microbiota data included age, gender, body mass index (BMI), constipation status, disease duration, levodopa equivalent dose (LED), and non-motor symptoms such as cognitive impairment.
The structure and richness of the fecal microbiota differed between PD patients and healthy controls. After adjusting for age, gender, BMI, and constipation, the genera Clostridium IV, Aquabacterium, Holdemania, Sphingomonas, Clostridium XVIII, Butyricicoccus, and Anaerotruncus were enriched in PD patients. Escherichia/Shigella were negatively associated with disease duration, Dorea and Phascolarctobacterium were negatively associated with levodopa equivalent dose, and Butyricicoccus and Clostridium XlVb were associated with cognitive impairment. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings confirm that gut microbiota dysbiosis occurs in Chinese patients with Parkinson's disease, extending prior evidence from other populations. The associations between specific genera and disease duration, medication dosing, and cognitive symptoms suggest the microbiome may track with clinical progression and treatment response rather than being a static feature. These patterns support further investigation of fecal microbiota as a potential biomarker or contributor to PD's motor and non-motor manifestations.
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.
Emerging evidence suggests the microbiome may affect a number of diseases, including lung cancer. However, the direct relationship between gut bacteria and lung cancer remains uncharacterized. In this study, we directly sequenced the hypervariable V1-V2 regions of the 16S rRNA gene in fecal samples from patients with lung cancer and healthy volunteers. Unweighted principal coordinate analysis (PCoA) revealed a clear difference in the bacterial community membership between the lung cancer group and the healthy control group. The lung cancer group had remarkably higher levels of Bacteroidetes, Fusobacteria, Cyanobacteria, Spirochaetes, and Lentisphaerae but dramatically lower levels of Firmicutes and Verrucomicrobia than the healthy control group (P < 0.05). Despite significant interindividual variation, eight predominant genera were significantly different between the two groups. The lung cancer group had higher levels of Bacteroides, Veillonella, and Fusobacterium but lower levels of Escherichia-Shigella, Kluyvera, Fecalibacterium, Enterobacter, and Dialister than the healthy control group (P < 0.05). Most notably, correlations between certain specific bacteria and serum inflammatory biomarkers were identified. Our findings demonstrated an altered bacterial community in patients with lung cancer, providing a significant step in understanding the relationship between gut bacteria and lung cancer. To our knowledge, this is the first study to evaluate the correlations between certain specific bacteria and inflammatory indicators. To better understand this relationship, further studies should investigate the underlying mechanisms of gut bacteria in lung cancer animal models.
This study examined the gut microbiota of women in relation to obesity, focusing on the ecological co-occurrence network structure of microbial communities and the relationship between short chain fatty acids (SCFAs) and body weight status. Researchers compared microbial alpha-diversity, beta-diversity, fecal SCFA concentrations, and network topology (density, connectivity, stability) between lean and obese participants. They also profiled taxonomic composition and predicted microbial genes involved in butyric acid production via pyruvate or branched amino-acid fermentation.
The study included 100 women of African origin, drawn from rural Ghana and the urban United States. Half of the women were lean (BMI under 25 kg/m2) and half were obese (BMI 30 kg/m2 or greater), split evenly across the two geographic populations. This design allowed comparison of diet, microbiota, and metabolic markers across both BMI status and country of residence.
Ghanaian women consumed significantly more dietary fiber and had greater microbial alpha-diversity, distinct beta-diversity, and higher total fecal SCFA concentrations than US women. Lean Ghanaians showed significantly greater microbial network density, connectivity, and stability than obese Ghanaians and than both lean and obese US women. Bacteroides uniformis was more abundant in lean women regardless of country, while lean Ghanaians also had greater proportions of Ruminococcus callidus, Prevotella copri, and Escherichia coli, and lower proportions of Lachnospiraceae, Bacteroides, and Parabacteroides. Lean Ghanaians additionally showed a significantly greater abundance of predicted microbial genes catalyzing butyric acid production via fermentation of pyruvate or branched amino acids, compared with obese Ghanaians and US women of either BMI status.
The findings suggest that a less stable, less connected gut microbial ecosystem, together with reduced capacity for butyrate production, may be associated with obesity in women of African origin. Diet, particularly fiber intake, appears linked to both microbial network stability and SCFA output, pointing to diet-driven ecological resilience as a factor in metabolic health. These results support further investigation into microbial network stability and butyrate-producing pathways as potential markers or targets related to obesity.
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.
The diagnosis of major depression disorder (MDD) and other mental disorders were depended on some subjective survey scales. There are confirmed relationship between the gut flora and the mental states of MDD patients.
The V3-V4 region of the 16S rRNA gene was extracted from the fecal microbial communities in MDD patients, PCR amplified and sequenced on the Illumina Miseq platform.
More phylum Firmicutes, less Bacteroidetes, and more genus Prevotella, Klebsiella, Streptococcus and Clostridium XI were found in MDD patients. The changes of the proportion of Prevotella and Klebsiella were consistent with Hamilton depression rating scale.
Human microbial communities are characterized by their taxonomic, metagenomic and metabolic diversity, which varies by distinct body sites and influences human physiology. However, when and how microbial communities within each body niche acquire unique taxonomical and functional signatures in early life remains underexplored. We thus sought to determine the taxonomic composition and potential metabolic function of the neonatal and early infant microbiota across multiple body sites and assess the effect of the mode of delivery and its potential confounders or modifiers. A cohort of pregnant women in their early third trimester (n = 81) were prospectively enrolled for longitudinal sampling through 6 weeks after delivery, and a second matched cross-sectional cohort (n = 81) was additionally recruited for sampling once at the time of delivery. Samples across multiple body sites, including stool, oral gingiva, nares, skin and vagina were collected for each maternal-infant dyad. Whole-genome shotgun sequencing and sequencing analysis of the gene encoding the 16S rRNA were performed to interrogate the composition and function of the neonatal and maternal microbiota. We found that the neonatal microbiota and its associated functional pathways were relatively homogeneous across all body sites at delivery, with the notable exception of the neonatal meconium. However, by 6 weeks after delivery, the infant microbiota structure and function had substantially expanded and diversified, with the body site serving as the primary determinant of the composition of the bacterial community and its functional capacity. Although minor variations in the neonatal (immediately at birth) microbiota community structure were associated with the cesarean mode of delivery in some body sites (oral gingiva, nares and skin; R2 = 0.038), this was not true for neonatal stool (meconium; Mann-Whitney P > 0.05), and there was no observable difference in community function regardless of delivery mode. For infants at 6 weeks of age, the microbiota structure and function had expanded and diversified with demonstrable body site specificity (P < 0.001, R2 = 0.189) but without discernable differences in community structure or function between infants delivered vaginally or by cesarean surgery (P = 0.057, R2 = 0.007). We conclude that within the first 6 weeks of life, the infant microbiota undergoes substantial reorganization, which is primarily driven by body site and not by mode of delivery.
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.
Few studies have analyzed the gut microbiota of child in unindustrialized countries, but none during the first month of life. Stool samples were collected from healthy newborns in hospitals of Gabon (n = 6) and Republic of the Congo (n = 9) at different time points during the first month of life: meconium, day 2 (D02), day 7 (D07) and day 28 (D28). In addition, one fecal sample was collected from each mother after delivery. Metagenomic sequencing was performed to determine the bacterial communities, and multiplex real-time PCR was used to detect the presence of seven enteric viruses (rotavirus a, adenovirus, norovirus I and II, sapovirus, astrovirus, enterovirus) in these samples. Bacterial diversity was high in the first days of life, and was dominated by the genus Prevotella. Then, it rapidly decreased and remained low up to D28 when the gut flora was composed almost exclusively of strictly anaerobic bacteria. Each infant's fecal bacterial microbiota composition was significantly closer to that of their mother than to that of any other woman in the mothers' group, suggesting an intrauterine, placental or amniotic fluid origin of such bacteria. Moreover, bacterial communities differed according to the delivery mode. Overall, the bacterial microbiota communities displayed a similar diversification and expansion in newborns within and between countries during the first four weeks of life. Moreover, six of the fifteen infants of this study harbored enteric viruses (rotavirus, enterovirus and adenovirus) in fecal samples, but never in the meconium. A maternal source for the viruses detected at D02 and D07 can be excluded because none of them was found also in the child's mother. These findings improve our knowledge on the gut bacterial and viral communities of infants from two Sub-Saharan countries during their first month of life.
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.
Pancreatic carcinoma (PC) is a lethal cancer. Gut microbiota is associated with some risk factors of PC, e.g. obesity and types II diabetes. However, the specific gut microbial profile in clinical PC in China has never been reported. This prospective study collected 85 PC and 57 matched healthy controls (HC) to analyze microbial characteristics by MiSeq sequencing. The results showed that gut microbial diversity was decreased in PC with an unique microbial profile, which partly attributed to its decrease of alpha diversity. Microbial alterations in PC featured by the increase of certain pathogens and lipopolysaccharides-producing bacteria, and the decrease of probiotics and butyrate-producing bacteria. Microbial community in obstruction cases was separated from the un-obstructed cases. Streptococcus was associated with the bile. Furthermore, 23 microbial functions e.g. Leucine and LPS biosynthesis were enriched, while 13 functions were reduced in PC. Importantly, based on 40 genera associated with PC, microbial markers achieves a high classification power with AUC of 0.842. In conclusion, gut microbial profile was unique in PC, providing a microbial marker for non-invasive PC diagnosis.
This study compared the colonic microbial composition of patients with systemic sclerosis (SSc) to that of healthy controls. Researchers used 16S ribosomal RNA sequencing on mucosal lavage samples collected from the cecum and sigmoid colon during colonoscopy. They also examined whether specific bacterial genera were associated with the presence and severity of gastrointestinal tract symptoms in the SSc patients.
The study included 17 adult patients with systemic sclerosis, 88 percent of whom were female, with a median age of 52.1 years. Healthy controls were matched to the SSc patients by age and sex on a one-to-one basis. Gastrointestinal symptom burden in the SSc group was assessed with the GI Tract 2.0 score, which averaged 0.7 with a standard deviation of 0.6.
Principal coordinate analysis showed significant differences in microbial community structure between SSc patients and healthy controls in both the cecum and sigmoid regions. Patients with SSc had decreased levels of commensal bacteria such as Faecalibacterium and Clostridium, a pattern similar to that seen in other inflammatory disease states. The abstract text provided is cut off before detailing which genera were increased in SSc patients or which specific genera correlated with GI symptoms, so those findings cannot be reported here.
The findings suggest that systemic sclerosis is associated with a distinct colonic microbial consortium that departs from that of healthy individuals, marked by loss of beneficial commensal genera. Because this shift parallels patterns observed in other inflammatory conditions, it raises the possibility that the gut microbiome contributes to or reflects the inflammatory processes underlying SSc. This supports further investigation into the colonic microbiota as a potential factor in SSc-related gastrointestinal symptoms and as a possible target for future research or intervention.
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.
The study examined how a single, low-concentration dose of the organophosphate insecticide trichlorfon affects the gastrointestinal microbiome of the Japanese quail. Researchers used next-generation sequencing of 16S rRNA gene amplicons to characterize bacterial communities in three sample origins: caecum, large intestine, and faeces. The design captured short-term microbial community responses following oral insecticide exposure, mimicking how birds encounter organophosphates in agricultural settings through ingestion of treated invertebrates.
The subjects were Japanese quail (Coturnix japonica), used as an avian model rather than wild birds directly. The abstract indicates both treated and untreated (control) quail of both sexes were compared, since sex-dependent differences are reported, but it does not give an exact number of birds. Sampling was drawn from three gastrointestinal compartments (caecum, large intestine, faeces) within this quail cohort.
Ingestion of the insecticide caused significant changes in gut microbiome composition and diversity between treated and untreated quail. The caecal microbiota showed sex-dependent responses that were not seen in the large intestine or faecal samples. Specifically, only treated females exhibited significant shifts in several genera within the Lachnospiraceae and Enterobacteriaceae families in the caecum.
The findings show that even a low, sublethal dose of an organophosphate insecticide can disrupt the avian gut microbiome, with effects that depend on both sex and gut region sampled. Because shifts occurred within the Enterobacteriaceae family, a group that includes Salmonella enterica and other enteric pathogens, insecticide-driven dysbiosis could plausibly alter colonization resistance against such organisms in exposed birds. This suggests pesticide exposure may have previously underappreciated indirect effects on avian gut health and disease susceptibility, warranting further study of GIT microbiota as a pathway linking agricultural chemical exposure to bird population declines.
This study used pyrosequencing to analyze the intestinal microflora of healthy Thai vegetarians and non-vegetarians. The researchers identified 893 operational taxonomic units (OTUs) covering 189 species. They compared the core gut microbiota composition between the two dietary groups and examined correlations between personal characteristics, consumption behavior, and microbial groups.
The subjects were healthy Thai adults divided into two dietary groups: vegetarians and non-vegetarians. The abstract does not give an exact number of participants, so a precise sample size cannot be stated. The comparison was structured around diet type as the key distinguishing variable between the two cohorts.
Prevotella copri was the strongest species indicator of vegetarians, present at 16.9% relative abundance, while Bacteroides vulgatus and bacteria related to Escherichia hermanii were the strongest indicators of non-vegetarians, at 4.5 to 4.7% relative abundance. The vegetarian group's core gut microbiota consisted of 11 species, compared to 20 species in the non-vegetarian group, spanning Actinobacteria, Firmicutes, and Proteobacteria common to both. Faecalibacterium prausnitzii and Gemmiger formicilis were present in 100% of subjects in both groups, while Clostridium nexile, Eubacterium eligens, and P. copri were common in most vegetarians, and non-vegetarians showed greater diversity including various Escherichia, Bacteroides, and Parabacteroides species. Age in non-vegetarians correlated strongly with Bacteroides uniformis abundance (coefficient 0.54, p = 0.001) and moderately with Alistipes finegoldii.
The findings suggest that a vegetarian diet is associated with a more Prevotella-dominant, less diverse core microbiota, while a non-vegetarian diet supports a broader core community that includes multiple Escherichia species. Because Escherichia and related Enterobacteriaceae are implicated in opportunistic and pathogenic risk, their greater representation and diversity in non-vegetarians may carry implications for gut pathogen risk. This work supports the idea that habitual diet shapes both the composition and the potential pathogen-associated risk profile of the human gut microbiome.
This study examined whether the composition of the gut microbiota in infants differs between those with eczema and those without. Researchers used high-throughput sequencing of the V3-V4 hypervariable regions of the 16S rRNA gene to profile bacterial communities in fecal samples. The analysis identified 12,386 operational taxonomic units (OTUs) at 97% similarity and compared taxa abundance and composition between groups.
The study was a case-control comparison of 50 infants with eczema (cases) and 51 healthy infants without eczema (controls). Fecal samples from these 101 infants were the source material for the 16S rRNA sequencing analysis. No further demographic details are given in the abstract.
Gut microbiota differed between groups in taxa abundance, though not in overall taxonomic composition. Healthy infants showed enrichment of Bifidobacterium, Megasphaera, Haemophilus and Streptococcus. Infants with eczema showed enrichment of Escherichia/Shigella, Veillonella, Faecalibacterium, Lachnospiraceae incertae sedis and Clostridium XlVa, with Faecalibacterium prausnitzii and Ruminococcus gnavus, taxa associated with atopy or inflammation, significantly enriched in the eczema group. Higher abundance of Akkermansia muciniphila in eczematous infants was also noted and may relate to reduced intestinal barrier integrity.
The findings support a link between altered gut bacterial abundance and eczema in infancy, pointing to specific genera and species as candidate markers of the atopic gut. The enrichment of Faecalibacterium prausnitzii alongside other inflammation-associated taxa in eczema cases suggests that microbiota composition changes may accompany, or contribute to, atopic disease processes rather than protect against them in this context. These results could inform future research into microbiota-targeted approaches for eczema risk assessment or intervention in infants.
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.
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 was aimed to assess the diversity of the meconium microbiome and determine if the bacterial community is affected by maternal diabetes status.
The first intestinal discharge (meconium) was collected from 23 newborns stratified by maternal diabetes status: 4 mothers had pre-gestational type 2 diabetes mellitus (DM) including one mother with dizygotic twins, 5 developed gestational diabetes mellitus (GDM) and 13 had no diabetes. The meconium microbiome was profiled using multi-barcode 16S rRNA sequencing followed by taxonomic assignment and diversity analysis.
All meconium samples were not sterile and contained diversified microbiota. Compared with adult feces, the meconium showed a lower species diversity, higher sample-to-sample variation, and enrichment of Proteobacteria and reduction of Bacteroidetes. Among the meconium samples, the taxonomy analyses suggested that the overall bacterial content significantly differed by maternal diabetes status, with the microbiome of the DM group showing higher alpha-diversity than that of no-diabetes or GDM groups. No global difference was found between babies delivered vaginally versus via Cesarean-section. Regression analysis showed that the most robust predictor for the meconium microbiota composition was the maternal diabetes status that preceded pregnancy. Specifically, Bacteroidetes (phyla) and Parabacteriodes (genus) were enriched in the meconium in the DM group compared to the no-diabetes group.
Our study provides evidence that meconium contains diversified microbiota and is not affected by the mode of delivery. It also suggests that the meconium microbiome of infants born to mothers with DM is enriched for the same bacterial taxa as those reported in the fecal microbiome of adult DM patients.
This study examined the structure of the gut microbiota in patients with colorectal cancer (CRC) compared with healthy controls, using pyrosequencing-based analysis of 16S rRNA genes. The researchers separately characterized microbiota from the intestinal lumen, cancerous tissue, and matched noncancerous normal tissue. They also examined mucosa-adherent microbial composition using rectal swab samples, since tissue-adherent bacterial communities can be altered by bowel cleansing prior to biopsy.
The study population consisted of patients diagnosed with colorectal cancer, whose intestinal lumen, tumor tissue, and adjacent noncancerous tissue samples were compared against matched microbiota from healthy individuals. Rectal swab samples were used specifically to capture mucosa-adherent bacteria in these patients. The abstract does not provide a specific sample size or demographic details for the cohort.
The microbial structure of the intestinal lumen differed significantly from that of cancerous tissue, with the lumen showing greater abundance of Firmicutes and lower abundance of Bacteroidetes and Proteobacteria, along with more phylotypes associated with energy harvest and host metabolic exchange. Cancerous and noncancerous tissue had broadly similar overall microbial structures, but tumor tissue showed lower microbial diversity. Both the intestinal lumen microbiota and the mucosa-adherent microbiota differed in CRC patients compared to matched microbiota in healthy individuals, and Lactobacillales was enriched in cancerous tissue.
By distinguishing luminal, tumor, and mucosa-adherent microbial communities, the findings suggest that CRC is associated with site-specific shifts in gut microbiota rather than a single uniform dysbiosis pattern. The reduced diversity in tumor tissue and altered mucosa-adherent communities point to a tumor microenvironment that selects for or is shaped by particular bacterial taxa. These distinctions underscore the importance of sampling method and anatomical site when investigating microbiota-CRC relationships in future research.
This study looked at how the oral microbiome (the bacteria in the mouth) is affected by human papillomavirus (HPV) infection, especially in people with and without HIV. Researchers analyzed mouth rinse samples from 63 men, comparing their bacterial composition based on whether they had HPV and/or HIV. They found that HPV infection changes the diversity and types of bacteria in the mouth, but these changes were different depending on whether the person also had HIV. In HIV-negative individuals, certain bacteria were more common when HPV was present, while in HIV-positive individuals, different bacterial shifts were observed. The study suggests that HPV infection interacts with the oral microbiome in unique ways, and this interaction may be influenced by HIV status.
2026-07-04
Klebsiella majorTaxon page created: genus biology (morphology, pathogenicity, capsule and siderophore virulence), the iron and nickel metallome, interventions, the data-derived Conditions table across 140 conditions, and the full research feed.
Lee CR, Lee JH, Park KS, Jeon JH, Kim YB, Cha CJ, Jeong BC, Lee SH.
Antimicrobial resistance of hypervirulent Klebsiella pneumoniae: epidemiology, hypervirulence-associated determinants, and resistance mechanisms.Front Cell Infect Microbiol. 2017
Yang X, Dong N, Chan EW, Zhang R, Chen S.
Carbapenem resistance-encoding and virulence-encoding conjugative plasmids in Klebsiella pneumoniae.Trends Microbiol. 2021
Benoit SL, Schmalstig AA, Glushka J, Maier SE, Edison AS, Maier RJ.
Nickel chelation therapy as an approach to combat multi-drug resistant enteric pathogens.Sci Rep. 2019
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