Klebsiella pneumoniae

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

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.

What was studied?

This study examined whether alterations in the gut microbiome track the development of Parkinson's disease (PD) in people who carry GBA1 gene variants but have not (yet) developed PD symptoms. The researchers combined clinical data with fecal metagenomics and used an analysis method that assessed both differential abundance of microbial species and the coherence of that abundance variation across groups, measured with Cliff's delta. The goal was to determine whether microbiome composition could serve as an early marker of PD risk in genetically at-risk individuals.

Who was studied?

The primary cohort included 271 patients with PD, 43 carriers of GBA1 variants who had not developed PD symptoms (GBA-NMC), and 150 healthy controls. Findings were then checked against three independent cohorts from the United States, Korea, and Turkey, together comprising 638 additional PD patients and 319 additional healthy controls. In total, the study drew on clinical and fecal metagenomic data from close to 1,400 individuals across four countries.

What were the most important findings?

About 25% of the gut microbiome in GBA-NMC individuals showed a composition that was intermediate between healthy controls and patients with PD. This intermediate microbiome signature was strongly correlated with disease progression in patients who already had PD, and with prodromal symptoms suggestive of future PD in both GBA-NMC and healthy individuals. Similar microbiome alterations were reproduced across the three independent international cohorts, strengthening confidence that the pattern is not specific to one population.

What are the greatest implications of this study?

The findings suggest gut microbiome changes can flag both genetically at-risk (GBA1 carriers) and non-genetically at-risk people in the general population who may be on a trajectory toward developing PD. This positions the microbiome as a potential early, non-invasive marker during the premanifest phase of disease, before clinical symptoms appear. Such a marker could eventually help identify candidates for early monitoring or intervention trials aimed at delaying or preventing PD onset.

What was studied?

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.

What was studied?

The colonization and evolution of gut microbiota early in life play a vital role in shaping a healthy, robust immune system for infant health, whether in combating short-term illness or improving long-term health outcomes. Early-life clinical practices may interrupt or disrupt the normal colonization process of the infant gut microbiota, thereby increasing disease susceptibility. In this prospective cohort study, we analyzed the gut microbiota of 46 term and 23 preterm infants using 16S rRNA gene metagenomic sequencing. Fecal samples were collected at six timepoints during the first three months of life. Notably, gestational age was the main factor contributing to differences in the meconium microbial composition. Intriguingly, our study unveiled a more homogeneous microbial composition in preterm infants with more abundant Bifidobacterium from the postnatal age (PNA) of one month. Concurrently, the beneficial bacteria Bifidobacterium and Lactobacillus gradually increased, and the potentially pathogenic bacteria Clostridium, Enterobacter, Enterococcus, Klebsiella, and Pseudomonas gradually decreased. Furthermore, our study underscored a link between decreased microbial diversity of preterm infants and exclusive breastfeeding and antibiotic exposure. Moreover, preterm infants with patent ductus arteriosus (PDA) exhibited reduced microbial diversity but higher abundances of Streptococcus oralis and Streptococcus mitis.

What was studied?

This meta-analysis examined the gut microbiome in obese children with metabolic dysfunction-associated steatotic liver disease (MASLD) or metabolic dysfunction-associated steatohepatitis (MASH). Researchers searched electronic databases for studies providing shotgun metagenomic sequencing data on the gut microbiome in children with obesity, with or without MASLD or MASH. The analysis combined data from multiple existing studies with an additionally recruited cohort to compare microbiome composition and function across disease states.

Who was studied?

The pooled analysis included obese children with MASLD (n = 153) and MASH (n = 70), compared against obese children without liver disease (n = 58) and healthy controls (n = 132). This population was assembled from nine identified studies plus one additionally recruited cohort, all using shotgun metagenomic sequencing. The study therefore draws on a multi-cohort pediatric dataset rather than a single trial population.

What were the most important findings?

Fecal microbiomes of children with MASLD and MASH differed significantly in alpha- and beta-diversity compared to obese and healthy children (p < 0.001). Faecalibacterium prausnitzii and Prevotella copri were differentially abundant across the obese, MASLD, and MASH groups. Machine-learning models (XGBoost and random forest) accurately distinguished MASLD from obesity (AUROC 87%) and MASH from MASLD (AUROC 89%), with pathway-abundance-based models performing similarly well (81% and 88%, respectively). Increasing hepatic fibrosis was accompanied by further gut microbiome alteration and a concomitant rise in Prevotella copri abundance (p = 0.0082).

What are the greatest implications of this study?

The findings suggest that gut microbiome composition, including shifts in species such as Faecalibacterium prausnitzii and Prevotella copri, tracks with the progression from obesity to MASLD to MASH and fibrosis severity in children. The high predictive accuracy of microbiome-based machine-learning models points to potential non-invasive tools for staging pediatric liver disease. These results also support the gut microbiome as a plausible target for future diagnostic or therapeutic strategies in pediatric metabolic liver disease.

What was studied?

COVID-19 has had a profound impact on public health globally. However, most studies have focused on patients with long COVID or those in the acute phase of infection, with limited research on the health of individuals who have recovered from mild COVID-19. This study investigates the long-term changes in bacterial and fungal communities in individuals recovering from mild COVID-19 and their clinical relevance.

Who was studied?

Healthy individuals from Hainan Province were enrolled before the COVID-19 outbreak, along with individuals recovering from COVID-19 at 3 months and 6 months post-recovery. Stool, blood samples, and metadata were collected. Metagenomic sequencing and Internal Transcribed Spacer (ITS) analysis characterized bacterial and fungal communities, while bacterial-fungal co-occurrence networks were constructed. A random forest model evaluated the predictive capacity of key taxa.

What were the most important findings?

The gut microbiota of COVID-19 recoverees differed significantly from that of healthy individuals. At 3 months post-recovery, probiotics (e.g., Blautia massiliensis and Kluyveromyces spp.) were enriched, linked to improved metabolism, while at 6 months, partial recovery of probiotics (e.g., Acidaminococcus massiliensis and Asterotremella spp.) was observed alongside persistent pathogens (e.g., Streptococcus equinus and Gibberella spp.). Dynamic changes were observed, with Acidaminococcus massiliensis enriched at both baseline and 6 months but absent at 3 months. Co-occurrence network analysis revealed synergies between bacterial (Rothia spp.) and fungal (Coprinopsis spp.) taxa, suggesting their potential roles in gut restoration. The bacterial random forest model (10 taxa) outperformed the fungal model (8 taxa) in predicting recovery status (AUC = 0.99 vs. 0.80).

What are the greatest implications of this study?

These findings highlight the significant long-term impacts of mild COVID-19 recovery on gut microbiota, with key taxa influencing metabolism and immune regulation, supporting microbiome-based strategies for recovery management.

What was studied?

The gut microbiota is a complex microbial ecosystem with a major impact on health and disease. Some gut unicellular eukaryotes (particularly Blastocystis) have been linked to features of intestinal eubiosis. Meanwhile, little is known regarding associations between gut-pathogenic protozoa, such as Giardia, and gut microbiota signatures. We therefore characterized and compared gut microbiota profiles of 60 Giardia-positive and 31 Giardia-negative Algerian individuals using amplicon-based next-generation sequencing of prokaryotic and eukaryotic ribosomal genes and stratifying for co-colonization with other unicellular eukaryotes, such as species of Archamoebae or Blastocystis. Overall, we found that alpha and beta microbiota diversity did not differ significantly between Giardia-positive and Giardia-negative individuals, regardless of the presence or absence of Archamoebae and Entamoeba (p > 0.05). However, significant differences were observed in both alpha and beta diversity between Giardia-positive, Blastocystis-negative and Giardia-positive, Blastocystis-positive individuals (observed richness, p = 0.0016; ANOSIM = 0.001), and similar differences were noticed between Blastocystis-negative and-positive carriers (p < 0.05), regardless of Giardia carrier status. Importantly, these differences in gut microbiota were considered to be independent of factors such as sex, age, and location (p > 0.05). Conclusively, Giardia-positive individuals may exhibit features of eubiosis, but whether this depends on the presence of Blastocystis should be confirmed by future studies. These findings combined might indicate that Blastocystis could be an active driver of gut microbiota diversity.

What was studied?

The process of in vitro fertilization-embryo transfer (IVF-ET) induces a maternal supraphysiological estradiol environment during embryo implantation and early development. Estrogen is crucial in modulating the colonization of microbiota within the vaginal epithelium. However, the impact of supraphysiological estradiol levels on the vaginal microbiome and the relationship with pregnancy outcomes remains unclear.

What were the most important findings?

The study aimed to characterize the vaginal microbiota under supraphysiological hormonal conditions. A total of 67 patients undergoing fresh embryo transfer were divided into three groups based on their peak estradiol levels: high-estradiol (HE) group (E2 > 11,000 pmol/L), median-estradiol (ME) group (E2 5,000-11,000 pmol/L), and low-estradiol (LE) group (E2 < 5,000 pmol/L). Twenty-five patients undergoing frozen-thawed embryo transfer were categorized into natural cycle (NC) group and hormone replacement cycle (HRT) group according to endometrial preparation protocols. Using 16S rRNA sequencing, we found that the vaginal microbiome exhibited variations with changes in peak estradiol levels. The elevated estradiol levels during ovarian stimulation or exogenous estrogen supplementation, significantly reduced alpha diversity, altered beta diversity within the vaginal microbiome, and shifted the vaginal community state types (CSTs) in Chinese infertile women toward Lactobacillus-dominant profiles, resembling those observed in most Asian women previously. However, the reproductive outcomes were not improved by these variations. The Streptococcus_anginosus and Akkermansia abundance correlated with estradiol levels positively, whereas Escherichia-Shigella showed a negative correlation. The abundance of Streptococcus, Atopobium, and Bifidobacterium on the day of embryo transfer may serve as predictors for adverse pregnancy outcomes, as determined by calculating the area under the curve (AUC) values.

What are the greatest implications of this study?

Supraphysiological estradiol levels induced by IVF-ET significantly alter vaginal microbiota and shift the CSTs in Chinese infertile women toward patterns of most Asian women. The Lactobacillus dominance under supraphysiological estradiol conditions does not help improve assisted reproductive outcomes. The abundance of Streptococcus, Atopobium, and Bifidobacterium on the day of embryo transfer may serve as predictors for adverse pregnancy outcomes. Among them, Streptococcus correlates positively with peak estradiol levels and may act as a microbial mediator impairing reproductive success under hyperestrogenic conditions. However, further larger-scale researches are needed to identify and elucidate the potential mechanisms.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study examined the longitudinal development of infant gut microbiota and its relationship to tetanus toxoid vaccine responses. Researchers used 16S rRNA gene sequencing to profile gut microbiota at two early-life time points, under one week and 15 weeks of age. They evaluated whether HIV exposure without infection altered microbiota composition and succession, and whether these microbiota patterns were linked to anti-tetanus antibody titers measured by enzyme-linked immunosorbent assay.

Who was studied?

The study included 278 infants total, drawn from two cohorts: 82 South African infants (61 exposed to HIV but uninfected, and 21 HIV-unexposed and uninfected) and 196 Nigerian infants (141 exposed to HIV but uninfected, and 55 HIV-unexposed and uninfected). All infants were assessed at both the under-one-week and 15-week time points. Feeding practice was also documented, noting that the Nigerian infants were exclusively breastfed.

What were the most important findings?

Gut microbiota composition and its succession over the first 15 weeks of life were shaped more strongly by geographic location and infant age than by HIV exposure status. Nigerian infants underwent a dramatic microbiota shift over this period, becoming dominated by Bifidobacterium longum subspecies infantis, a shift not seen in South African infants even when the analysis was restricted to exclusively breastfed babies. Using Least Absolute Shrinkage and Selection Operator (LASSO) regression, the study found that HIV exposure and gut microbiota composition were each independently associated with tetanus antibody titers at 15 weeks, with high passively transferred maternal antibody also playing a role.

What are the greatest implications of this study?

The findings suggest that geography and associated feeding and environmental practices are more powerful drivers of early infant gut microbiota development than HIV-exposure status alone. The emergence of Bifidobacterium longum subspecies infantis dominance in exclusively breastfed Nigerian infants, but not South African infants, points to population-specific factors shaping microbiota maturation beyond breastfeeding alone. Because gut microbiota and HIV exposure independently predicted vaccine antibody responses, these results support further investigation into microbiota-targeted strategies to optimize infant immune and vaccine responses across diverse populations.

What was studied?

Gut microbiome differences between people with Parkinson's disease (PD) and control subjects without Parkinsonism are widely reported, but potential alterations related to PD with mild cognitive impairment (MCI) have yet to be comprehensively explored. We compared gut microbial features of PD with MCI (n = 58) to cognitively unimpaired PD (n = 60) and control subjects (n = 90) with normal cognition. Our results did not support a specific microbiome signature related to MCI in PD.

What was studied?

This study examined how environmental, socioeconomic, and health factors relate to gut microbiome composition at both the species and strain level. Researchers used deeply sequenced metagenomic data to identify associations between bacterial species and a range of host phenotypes and situational factors. They also performed a meta-analysis of species-level profiles across multiple datasets to look for consistent patterns, such as links to body mass index.

Who was studied?

The study drew on a community-based cohort of 1,871 people living in 19 isolated villages in the Mesoamerican highlands of western Honduras. This is a non-industrialized, geographically isolated population, a setting the authors note remains uncommon in deep gut microbiome sequencing studies. Additional comparisons were made using species-level profiles from other, unspecified datasets as part of a meta-analysis.

What were the most important findings?

Socioeconomic factors accounted for 51.44% of all associations found between the gut microbiome and human phenotypes, making them the dominant category of influence. Meta-analysis across datasets identified several bacterial species associated with body mass index, consistent with prior research. Incorporating strain-level phylogenetic information changed the overall picture of host-microbiome relationships, especially for factors like household wealth, where wealthier individuals were found to harbor different strains of Eubacterium rectale than less wealthy individuals.

What are the greatest implications of this study?

The findings suggest that socioeconomic circumstances are a major driver of gut microbiome variation, potentially more so than many other individual health factors. The demonstration that strain-level differences (not just species presence) track with wealth indicates that species-level analysis alone can miss biologically meaningful variation. The authors conclude that gut microbiome surveillance in such populations could help illuminate broader patterns relevant to both individual and public health.

What was studied?

This study used whole-genome shotgun sequencing and gas chromatography/mass spectrometry to profile gut microbial and metabolic signatures across seven different malignancies. The researchers compared taxonomic and metabolomic configurations in cancer patients against sex- and age-matched healthy controls. The goal was to identify both common and cancer-type-specific gut microbiome and metabolite alterations.

Who was studied?

The study included patients with colorectal cancer (40), stomach cancer (45), breast cancer (71), lung cancer (34), melanoma (50), lymphoid neoplasms (60), and acute myeloid leukemia (40). Each cancer group was compared against its own sex- and age-matched healthy control group. In total the analysis spanned 300 cancer patients across seven malignancy types plus their matched controls.

What were the most important findings?

Beta-diversity differed between every cancer group and its healthy controls, while alpha-diversity differed only for the lymphoid neoplasm and acute myeloid leukemia groups. Of 203 unique species identified, 179 were under-represented and 24 were over-represented in cancer patients relative to controls. Faecalibacillus intestinalis was under-represented across all seven cancer groups, and Anaerostipes hadrus was under-represented in all groups except stomach cancer, with a marked reduction in the gut microbiome cancer index in every group except acute myeloid leukemia. Among the short-chain fatty acids and amino acids tested, formic acid concentration was significantly altered.

What are the greatest implications of this study?

The consistent depletion of Faecalibacillus intestinalis and altered formic acid levels across seven distinct cancer types suggest these may represent shared, cross-cancer markers of gut dysbiosis rather than disease-specific findings. This points toward a common gut microbial and metabolic signature that could inform future pan-cancer diagnostic or monitoring approaches. Because the pattern held despite differences in cancer biology and location, it strengthens the case for a generalizable link between gut dysbiosis and malignancy.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

At present, the diagnosis of lower respiratory tract infections (LRTIs) is difficult, and there is an urgent need for better diagnostic methods. This study enrolled 136 patients from 2020 to 2021 and collected bronchoalveolar lavage fluid (BALF) specimens. We used metatranscriptome to analyze the lower respiratory tract microbiome (LRTM) and host immune response. The diversity of the LRTM in LRTIs significantly decreased, manifested by a decrease in the abundance of normal microbiota and an increase in the abundance of opportunistic pathogens. The upregulated differentially expressed genes (DEGs) in the LRTIs group were mainly enriched in infection immune response-related pathways. Klebsiella pneumoniae had the most significant increase in abundance in LRTIs, which was strongly correlated with host infection or inflammation genes TNFRSF1B, CSF3R, and IL6R. We combined LRTM and host transcriptome data to construct a machine-learning model with 12 screened features to discriminate LRTIs and non-LRTIs. The results showed that the model trained by Random Forest in the validate set had the best performance (ROC AUC: 0.937, 95% CI: 0.832-1). The independent external dataset showed an accuracy of 76.5% for this model. This study suggests that the model integrating LRTM and host transcriptome data can be an effective tool for LRTIs diagnosis.

What was studied?

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.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study examined how exclusive enteral nutrition (EEN), a first-line therapy for pediatric Crohn's disease, produces its protective effects on the gut. The researchers used integrated multi-omics analysis of fecal microbiota and metabolites to identify functional network clusters associated with treatment response. They further validated these diet-driven microbiome changes using gut chemostat cultures and by transferring microbiota into germ-free Il10-deficient mice.

Who was studied?

The abstract describes a prospective pediatric cohort of treatment-naive Crohn's disease patients, registered as German Clinical Trials DRKS00013306, who were followed as they began EEN therapy. Exact patient numbers are not given in the abstract. Findings from this human cohort were then extended experimentally using gnotobiotic (germ-free) Il10-deficient mice colonized with patient-derived microbiota.

What were the most important findings?

Multi-omics analysis identified individually variable microbiome network clusters, with Lachnospiraceae and medium-chain fatty acids emerging as protective features associated with EEN response. Bioorthogonal non-canonical amino acid tagging pinpointed specific bacterial species that responded to medium-chain fatty acids, and metagenomic analysis revealed high strain-level dynamics during EEN therapy. When patient-derived microbiota were transferred into gnotobiotic Il10-deficient mice, individual patient-specific strain signatures could either prevent or cause inflammatory bowel disease-like inflammation.

What are the greatest implications of this study?

The findings show that EEN operates through explicit, functional, and highly individualized changes in the fecal microbiome rather than a single uniform mechanism. Because protective effects were tied to specific strains and metabolites such as medium-chain fatty acids, this suggests that microbiome and metabolite profiling could help predict or enhance EEN response in pediatric Crohn's disease. The demonstration that individual strain signatures can causally prevent or induce inflammation in a gnotobiotic model also supports strain-level and metabolite-targeted approaches as a path toward more precise dietary or microbial therapies for Crohn's disease.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study investigated the neonatal gut bacterial and viral microbiome in infants exposed to HIV but who remained uninfected, and examined how this exposure relates to inflammatory biomarkers in plasma. The researchers also tested whether HIV exposure alters antibody-microbiota binding in the neonatal gut. Finally, they assessed whether antibodies present in breast milk affect the growth of commensal gut bacteria.

Who was studied?

The study compared neonates exposed to HIV but uninfected (nHEU) with unexposed, uninfected neonates (nHU). Breast milk from mothers living with HIV was also analyzed and compared for its antibody function. The abstract does not give specific sample sizes, so the exact cohort size cannot be stated.

What were the most important findings?

Neonates exposed to HIV but uninfected showed an altered gut bacteriome and a milder change in the enteric DNA virome compared to unexposed neonates. HIV exposure also differentially affected IgA binding to gut microbiota. The relative abundance of Blautia spp., in both whole stool and IgA-bound microbiota, was positively associated with plasma C-reactive protein levels. Breast milk IgA from mothers living with HIV showed a significantly reduced ability to inhibit the growth of Blautia coccoides, and this reduced inhibitory capacity was associated with inflammation in the exposed neonates.

What are the greatest implications of this study?

The findings suggest that elevated inflammation in HIV-exposed but uninfected neonates may stem in part from a weakened capacity of maternal breast milk IgA to control specific commensal bacteria such as Blautia coccoides. This points to a potential antibody-mediated mechanism linking maternal HIV status, infant gut microbiota composition, and systemic inflammation in the infant. Understanding this pathway could inform strategies to support healthy immune development in this vulnerable population.

What was studied?

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a rare acquired immune-mediated neuropathy. Although microbial infection is potentially a contributing factor, a causative link between CIDP and microbial infection remains unclear. There is also no definitive biomarker for CIDP diagnostics and therapies. The present study aimed to characterize the serum metabolic profile and gut microbiome structure in CIDP.

Who was studied?

Targeted metabolomics profiling of serum, using liquid chromatography-mass spectrometry, and metagenomics sequencing of stool samples from a cohort of CIDP and non-CIDP subjects were performed to evaluate serum metabolic profiles and gut microbiome structure in CIDP subjects relative to healthy controls.

What were the most important findings?

Metabolome data revealed that the bile acids profile was perturbed in CIDP with bile acids and arachidonic acid enriched significantly in CIDP versus non-CIDP controls. Metagenome data revealed that opportunistic pathogens, such as Klebsiella pneumonia and Megamonas funiformis, and genes involved in bacterial infection were notably more abundant in CIDP subjects, while gut microbes related to biotransformation of secondary bile acids were abnormal in CIDP versus non-CIDP subjects. Correlation analysis revealed that changes in secondary bile acids were associated with altered gut microbes, including Bacteroides ovatus, Bacteroides caccae, and Ruminococcus gnavus.

What are the greatest implications of this study?

Bile acids and arachidonic acid metabolism were disturbed in CIDP subjects and might be affected by the dysbiosis of gut microbial flora. These findings suggest that the combination of bile acids and arachidonic acid could be used as a CIDP biomarker and that modulation of gut microbiota might impact the clinical course of CIDP.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disease. Increasing evidence indicates that the gut microbiota can play an important role in the pathophysiology of NAFLD. Recently, several studies have tested the predictive value of gut microbiome profiles in NAFLD progression; however, comparisons of microbial signatures in NAFLD or non-alcoholic steatohepatitis (NASH) have produced discrepant results, possibly due to ethnic and environmental factors. Thus, we aimed to characterize the gut metagenome composition of patients with fatty liver disease.

Who was studied?

Gut microbiome of 45 well-characterized patients with obesity and biopsy-proven NAFLD was evaluated using shot-gun sequencing: 11 non-alcoholic fatty liver controls (non-NAFL), 11 with fatty liver, and 23 with NASH.

What were the most important findings?

Our study showed that Parabacteroides distasonis and Alistipes putredenis were enriched in fatty liver but not in NASH patients. Notably, in a hierarchical clustering analysis, microbial profiles were differentially distributed among groups, and membership to a Prevotella copri dominant cluster was associated with a greater risk of developing NASH. Functional analyses showed that although no differences in LPS biosynthesis pathways were observed, Prevotella-dominant subjects had higher circulating levels of LPS and a lower abundance of pathways encoding butyrate production.

What are the greatest implications of this study?

Our findings suggest that a Prevotella copri dominant bacterial community is associated with a greater risk for NAFLD disease progression, probably linked to higher intestinal permeability and lower capacity for butyrate production.

What was studied?

To determine the effects of second-line anti-tuberculosis (TB) drugs on the composition and functions of intestinal microbiota in patients with rifampicin-resistant TB (RR-TB).

Who was studied?

In this cross-sectional study, stool samples and relevant clinical information were collected from patients with RR-TB admitted to the Drug-resistant Specialty Department at Hunan Chest Hospital (Hunan Institute For Tuberculosis Control). The composition and functions of intestinal microbiota were analyzed using metagenomic sequencing and bioinformatics methods.

What were the most important findings?

Altered structural composition of the intestinal microbiota was found when patients from the control, intensive phase treatment, and continuation phase treatment groups were compared (P<0.05). Second-line anti-TB treatment resulted in a decrease in the relative abundance of species, such as Prevotella copri, compared with control treatment. However, the relative abundance of Escherichia coli, Salmonella enterica, and 11 other conditionally pathogenic species increased significantly in the intensive phase treatment group. Based on differential functional analysis, some metabolism-related functions, such as the biosynthesises of phenylalanine, tyrosine, and tryptophan, were significantly inhibited during second-line anti-TB drug treatment, while other functions, such as phenylalanine metabolism, were significantly promoted during the intensive phase of treatment.

What are the greatest implications of this study?

Second-line anti-TB drug treatment caused changes in the structural composition of the intestinal microbiota in patients with RR-TB. In particular, this treatment induced a significant increase in the relative abundance of 11 conditionally pathogenic species, including Escherichia coli. Functional analysis revealed significantly decreased biosynthesises of phenylalanine, tyrosine, and tryptophan and significantly increased phenylalanine metabolism.

What was studied?

This study investigated the role of gut microbiota and their metabolites, particularly short-chain fatty acids (SCFAs), in the pathogenesis of functional constipation (FC). The researchers used shotgun metagenomic sequencing of gut microbiota alongside serum SCFA analysis to examine relationships between microbial composition, butyric acid levels, and defecation frequency. They then tested the direct effects of butyrate on intestinal neurons using an in vitro mouse model to explore a possible mechanistic link between microbial butyrate metabolism and enteric nervous system damage.

Who was studied?

The primary cohort consisted of 460 Chinese women with differing defecation frequencies, who underwent shotgun metagenomic sequencing and serum SCFA measurement. Findings were verified in an independent cohort of 6 patients with functional constipation and 6 controls. In addition, mouse intestinal neurons were used in vitro to test the cellular effects of butyrate exposure at concentrations of 0.1, 0.5, 1, and 2.5 mM.

What were the most important findings?

The abundance of Fusobacterium varium, a butyric acid-producing bacterium, was positively correlated with defecation frequency, while serum butyric acid concentration was negatively correlated with defecation frequency. These findings were confirmed in the independent validation cohort. In vitro, intestinal neurons treated with 0.5 mM butyrate proliferated better than neurons exposed to other tested concentrations, with significant differences observed in cell cycle and oxidative phosphorylation signaling pathways.

What are the greatest implications of this study?

The findings suggest that abnormal butyrate metabolism, including altered production by gut bacteria such as Fusobacterium varium and shifts in serum butyrate levels, may damage the enteric nervous system and contribute to functional constipation. This points to butyrate-modulating microbes and serum butyrate concentration as potential biomarkers or targets for understanding and managing FC. It also highlights that butyrate's effect on enteric neurons is concentration-dependent, meaning both insufficient and excessive levels may be relevant to disease mechanisms.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study examined how the gut microbiota changes with age and how those age-related changes relate to colorectal cancer (CRC). The researchers analyzed 11 metagenomic data sets, correcting for batch effects, then compared species composition and abundance across three age groups in both healthy individuals and CRC samples. They used LEfSe analysis to identify bacteria whose relative abundance differed by age group, then built age-prediction and CRC-risk-prediction models from those age-differentiated species.

Who was studied?

The abstract does not report a single original cohort with a specific sample size. Instead, the study population consisted of previously published metagenomic samples drawn from 11 combined data sets accessed through the curatedMetagenomicData R package, covering both healthy individuals and people with colorectal cancer. These samples were stratified into three age groups for comparison.

What were the most important findings?

The structure and composition of the gut microbiota differed significantly across the three age groups in both healthy and CRC samples. Bacteroides vulgatus abundance was lower in the older group compared to the other two groups, while Bacteroides fragilis abundance increased with aging. The researchers also identified seven bacterial species whose abundance rose with age, and found that abundance of pathogenic bacteria, including Escherichia coli, increased as well.

What are the greatest implications of this study?

By linking specific age-associated shifts in gut microbiota, such as declining Bacteroides vulgatus and rising Bacteroides fragilis and Escherichia coli, to both healthy aging and CRC samples, this work suggests the microbiome could serve as a biomarker for biological aging and CRC risk. The construction of age-prediction and CRC-risk-prediction models based on these age-differentiated bacteria points toward potential microbiota-based tools for estimating cancer risk as people age. This approach could inform future screening or risk-stratification strategies that account for age-related microbial changes.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

Health disparities are driven by underlying social disadvantage and psychosocial stressors. However, how social disadvantage and psychosocial stressors lead to adverse health outcomes is unclear, particularly when exposure begins prenatally. Variations in the gut microbiome and circulating proinflammatory cytokines offer potential mechanistic pathways. Here, we interrogate the gut microbiome of mother-child dyads to compare high-versus-low prenatal social disadvantage, psychosocial stressors and maternal circulating cytokine cohorts (prospective case-control study design using gut microbiomes from 121 dyads profiled with 16 S rRNA sequencing and 89 dyads with shotgun metagenomic sequencing). Gut microbiome characteristics significantly predictive of social disadvantage and psychosocial stressors in the mothers and children indicate that different discriminatory taxa and related pathways are involved, including many species of Bifidobacterium and related pathways across several comparisons. The lowest inter-individual gut microbiome similarity was observed among high-social disadvantage/high-psychosocial stressors mothers, suggesting distinct environmental exposures driving a diverging gut microbiome assembly compared to low-social disadvantage/low-psychosocial stressors controls (P = 3.5 × 10-5 for social disadvantage, P = 2.7 × 10-15 for psychosocial stressors). Children's gut metagenome profiles at 4 months also significantly predicted high/low maternal prenatal IL-6 (P = 0.029), with many bacterial species overlapping those identified by social disadvantage and psychosocial stressors. These differences, based on maternal social and psychological status during a critical developmental window early in life, offer potentially modifiable targets to mitigate health inequities.

What was studied?

The study characterized the upper respiratory tract (URT) microbiome, meaning the combined nasal and oral bacterial communities, in patients infected with the SARS-CoV-2 Delta versus Omicron variant compared with healthy controls. The authors aimed to identify variant-specific microbiome signatures, since prior work had compared COVID-19 patients to controls but had not examined how distinct variants shape the URT microbiome.

Who was studied?

The cohort comprised 43 COVID-19 patients (24 Delta and 19 Omicron) and 19 healthy controls from Eastern India, with samples collected in 2021 to 2022 (average age about 36 years in patients and 33 in controls). URT swabs were profiled by next-generation sequencing of the V3 to V4 variable regions of the 16S rRNA gene on the Illumina NovaSeq 6000 platform, yielding 12,172 amplicon sequence variants across 34 phyla, 924 genera, and 1,429 species.

What were the most important findings?

COVID-19 patients showed significantly lower intra-individual (alpha) diversity and higher inter-individual (beta) diversity than controls, with Proteobacteria dominant in patients (73.57 percent versus 22.24 percent) and genera such as Pseudomonas, Klebsiella, Enterobacter, and Acinetobacter enriched, while control-associated commensals including Streptococcus, Veillonella, Prevotella, Neisseria, and Bifidobacterium were depleted. Delta patients had lower diversity and greater dysbiosis than Omicron patients, and nine control-associated species declined in a consistent trend of control greater than Omicron greater than Delta. A random forest classifier built on core species distinguished the three groups with roughly 90 percent (plus or minus 0.5 percent) accuracy (class error 0 percent for controls, 18 percent for Omicron, 14 percent for Delta).

What are the greatest implications of this study?

The authors conclude that different SARS-CoV-2 variants are associated with variant-specific URT microbiome signatures, with the newer Omicron variant more closely resembling the healthy control microbiome than the older Delta variant, which may inform host-microbiome interaction research and future nasal probiotic strategies. Because this is an observational, cross-sectional comparison in a modest sample, the results reflect association rather than causation and, as the authors note, sample size is a limitation.

What was studied?

Depression and anxiety are common comorbid diseases of constipation. Fecal microbiota transplantation (FMT) significantly relieves gastrointestinal-related symptoms, but its impact on psychiatric symptoms remains uncharted.

Who was studied?

We collected fecal and serum samples before and after FMT from 4 functional constipation patients with psychiatric symptoms and corresponding donor stool samples. We categorized the samples into two groups: before FMT (Fb) and after FMT (Fa). Parameters associated with constipation, depression, and anxiety symptoms were evaluated. Metagenomics and targeted neurotransmitter metabolomics were performed to investigate the gut microbiota and metabolites. 5-hydroxytryptamine (5-HT) biosynthesis was detected in patients' fecal supernatants exposed to the QGP-1 cell model in vitro.

What were the most important findings?

Our study demonstrated that patient's constipation, depression, and anxiety were improved after FMT intervention. At the genus level, relative abundance of g_Bacteroides and g_Klebsiella decreased in the Fa group, while g_Lactobacillus, and g_Selenomonas content increased in the same group. These observations suggest a potential involvement of these genera in the pathogenesis of constipation with psychiatric symptoms. Metabolomics analysis showed that FMT intervention decreased serum 5-HT levels. Additionally, we found that species, including s_Klebsiella sp. 1_1_55, s_Odoribacter splanchnicus, and s_Ruminococcus gnavus CAG:126, were positively correlated with 5-HT levels. In contrast, s_Acetobacterium bakii, s_Enterococcus hermanniensis, s_Prevotella falsenii, s_Propionispira arboris, s_Schwartzia succinivorans, s_Selenomonas artemidis, and s_Selenomonas sp. FC4001 were negatively correlated with 5-HT levels. Furthermore, we observed that patients' fecal supernatants increased 5-HT biosynthesis in QGP-1 cells.

What are the greatest implications of this study?

FMT can relieve patients' constipation, depression, and anxiety symptoms by reshaping gut microbiota. The 5-HT level was associated with an altered abundance of specific bacteria or metabolites. This study provides specific evidence for FMT intervention in constipation patients with psychiatric symptoms.

What was studied?

The lack of a definition of urinary microbiome health convolutes diagnosis of urinary tract infections (UTIs), especially when non-traditional uropathogens or paucity of bacteria are recovered from symptomatic patients in routine standard-of-care urine tests. Here, we used shotgun metagenomic sequencing to characterize the microbial composition of asymptomatic volunteers in a set of 30 longitudinally collected urine specimens. Using permutation tests, we established a range of asymptomatic microbiota states, and use these to contextualize the microbiota of 122 urine specimens collected from patients with suspected UTIs diagnostically categorized by standard-of-care urinalysis within that range. Finally, we used a standard-of-care culture protocol to evaluate the efficiency of culture-based recovery of the urinary microbiota.

What were the most important findings?

The majority of genitourinary microbiota in individals suspected to have UTI overlapped with the spectrum of asymptomatic microbiota states. Longitudinal characterization of the genitourinary microbiome in urine specimens collected from asymptomatic volunteers revealed fluctuations of microbial functions and taxonomy over time. White blood cell counts from urinalysis suggested that urine specimens categorized as 'insignificant', 'contaminated', or 'no-growth' by conventional culture methods frequently showed signs of urinary tract inflammation, but this inflammation is not associated with genitourinary microbiota dysbiosis. Comparison of directly sequenced urine specimens with standard-of-care culturing confirmed that culture-based diagnosis biases genitourinary microbiota recovery towards the traditional uropathogens Escherichia coli and Klebsiella pneumoniae.

What are the greatest implications of this study?

Here, we utilize shotgun metagenomic sequencing to establish a baseline of asymptomatic genitourinary microbiota states. Using this baseline we establish substantial overlap between symptomatic and asymptomatic genitourinary microbiota states. Our results establish that bacterial presence alone does not explain the onset of clinical symptoms. Video Abstract.

What was studied?

This work re-analyzed three previously published shotgun metagenomic datasets (NCBI SRA accessions PRJNA687519, PRJNA724913, and PRJNA395911) to test how geographic location, respiratory sampling niche, and transportation stress shape the cattle (bovine) respiratory microbiome and its predicted function. The authors examined microbial diversity, composition, co-occurrence networks, and KEGG functional profiles, and assessed which opportunistic pathogens shifted after transportation in relation to bovine respiratory disease (BRD).

Who was studied?

A total of 145 respiratory samples were analyzed from feedlot calves aged 5 to 6 months across three geographic locations: Saskatoon (Canada), the cities of Qiqihaer and Guangan (China), and Alberta (Canada). Samples spanned two niches, comprising 130 nasopharyngeal swabs and 15 bronchoalveolar lavage (lung) samples, the latter collected at necropsy from calves that died of BRD. Sequencing used the Illumina HiSeq platform (shotgun metagenomics), yielding an average of 3,374,490 clean reads per sample, with taxonomy assigned via RefSeq and function via the KEGG Orthology database.

What were the most important findings?

Nasopharyngeal alpha diversity (Shannon index) was higher in the China samples (Qiqihaer and Guangan) than in the Saskatoon nasopharynx or the Alberta lung, and composition clustered distinctly by location (for example, ANOSIM R = 0.99, p = 0.001 between Saskatoon and China). Of high-quality reads, 96.72 percent were bacterial across 27 phyla; the Saskatoon nasopharynx was dominated by Proteobacteria (91.19 percent), whereas the China nasopharynx was more balanced (Proteobacteria 48.49 and 61.94 percent, Firmicutes 24.26 and 17.68 percent, Actinobacteria 14.90 and 9.40 percent, Bacteroidetes 6.59 and 6.98 percent) and the Alberta lung was dominated by Proteobacteria (58.27 percent), Firmicutes (17.03 percent), Tenericutes (14.27 percent), and Bacteroidetes (8.41 percent). Long-distance transportation significantly reduced nasopharyngeal richness at unloading and after adaptive feeding and increased BRD-associated pathogens after feedlot arrival, whereas short-distance transportation did not; the 15 BRD lung samples separated into four clusters dominated by different pathogens.

What are the greatest implications of this study?

The authors conclude that geography, sampling niche, and transportation (especially long-distance shipping) are important factors shaping the bovine respiratory microbiome and BRD, and that distinct pathogen-dominated lung clusters may reflect different subtypes of BRD pathogenesis. Because this is an observational re-analysis of existing metagenomic datasets, the results describe associations rather than causation, and the authors note the small number of lung samples as a limitation.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

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.

What was studied?

This study examined the interaction between the gut microbiota and colorectal cancer (CRC) using metagenomic data retrieved from the GMrepo database. Researchers analyzed differences in gut microbiota distribution between CRC cases and controls at the species level, built a co-occurrence network, and assessed microbial interactions with environmental factors. Random forest models were then used to identify significant microbial biomarkers capable of differentiating CRC samples from control samples.

Who was studied?

The analysis drew on 709 metagenomic samples from six projects in the GMrepo database. After matching, the study population consisted of 86 CRC patients and 86 matched healthy controls from six countries. A total of 484 microbial species and 166 related genera were analyzed across these paired samples.

What were the most important findings?

The study confirmed previously recognized associations between Fusobacterium nucleatum and species within the genera Peptostreptococcus, Porphyromonas, and Prevotella with colorectal cancer. It also identified new associations involving the novel species Parvimonas micra and Collinsella. These findings, generated through a paired-sample design and machine learning models, point to an expanded panel of species-level microbial signals tied to CRC status.

What are the greatest implications of this study?

By quantifying and visualizing microbiota-CRC interactions across a multi-country dataset, this work supports the development of a more precise, species-level microbiota panel for CRC diagnosis. The identification of novel associated species such as Parvimonas micra and Collinsella suggests additional candidate biomarkers beyond the well-established Fusobacterium nucleatum signal. This paired-sample, network-based approach offers a template for refining microbial diagnostic panels in colorectal cancer research.

What was studied?

This study examined whether gut microbiome composition is linked to disease severity in patients with COVID-19, and whether any microbiome disturbances resolve after the SARS-CoV-2 virus is cleared. Researchers used shotgun sequencing of total DNA extracted from stool samples to characterize gut microbiome composition. They also measured concentrations of inflammatory cytokines and other blood markers from plasma to relate gut microbial changes to immune dysfunction.

Who was studied?

The study drew on a two-hospital cohort of 100 patients with laboratory-confirmed SARS-CoV-2 infection, from whom blood, stool, and patient records were collected. Serial stool samples were collected from 27 of these 100 patients for up to 30 days after clearance of the virus, allowing the researchers to track whether microbiome changes persisted or resolved over time.

What were the most important findings?

Gut microbiome composition was significantly altered in patients with COVID-19 compared with non-COVID-19 individuals, regardless of whether patients had received medication. Several gut commensals with known immunomodulatory potential, including Faecalibacterium prausnitzii, Eubacterium rectale, and bifidobacteria, were underrepresented in patients with COVID-19. These organisms remained depleted in stool samples collected up to 30 days after disease resolution, indicating the perturbation did not quickly correct itself.

What are the greatest implications of this study?

The persistence of a disturbed gut microbiome for weeks after viral clearance suggests COVID-19 related gut dysbiosis is not merely a transient bystander effect of infection. Because the depleted organisms, including Faecalibacterium prausnitzii, are known for anti-inflammatory and immunomodulatory functions, their loss may contribute to dysfunctional immune responses seen in the disease. This points to the gut microbiome as a potential factor in COVID-19 severity and recovery, meriting further investigation as a target for monitoring or intervention.

What was studied?

Approximately one-third of epilepsy patients suffer from drug-resistant epilepsy. The gut microbiome, which is the total genetic makeup of all of the total microbes inhabiting the gut, can affect the CNS through various mechanisms. However, there are only limited studies about the relationship between the gut microbiome and epilepsy. We investigated the composition and characteristics of the gut microbiota among adult patients who have drug-responsive and drug-resistant epilepsy.

Who was studied?

We prospectively included 44 adult epilepsy patients and classified them into drug-responsive and drug-resistant groups. We collected fecal samples for the next-generation sequencing analysis. We statistically estimated the bacterial differences and alpha and beta diversities in each category.

What were the most important findings?

Although there was no difference in demographic factors between the drug-responsive and drug-resistant groups, there was a significant difference in the composition of the gut microbiota. While the relative abundance of Bacteroides finegoldii and Ruminococcus_g2 increased in the drug-responsive group, the relative abundance of Negativicutes, which belong to Firmicutes increased in the drug-resistant group. Bifidobacterium was relatively abundant in epilepsy patients with a normal electroencephalogram. There was no significant difference between the two groups in analyses of alpha and beta diversities.

What are the greatest implications of this study?

We found a significant difference in the composition of the gut microbiota among adult patients with drug-responsive and drug-resistant epilepsy. Difference in gut microbiota can be used as a novel biomarker to predict prognosis and evaluate treatment response in epilepsy patients. In addition, modification of gut microbiome can be an effective treatment strategy for patient with drug-resistant epilepsy.

What was studied?

This study examined changes in intestinal bacterial communities across healthy people, patients with inflammatory bowel disease (IBD), and patients with colorectal cancer (CRC). The researchers performed metagenome-wide association studies on fecal samples to characterize bacterial community structure, relative abundance, and functional predictions. They also analyzed differentially abundant bacteria and co-occurrence networks to compare the three groups.

Who was studied?

The analysis drew on fecal metagenomic data from 290 healthy subjects, 512 IBD patients, and 285 CRC patients. Healthy and CRC data were obtained from the European Nucleotide Archive under several study accession numbers, while IBD patient data came from the Integrated Human Microbiome Project via the Human Microbiome Project Data Portal. This makes the cohort a large, multi-source pooled metagenomic dataset rather than a single newly recruited study population.

What were the most important findings?

The bacterial community structure in both IBD and CRC patients differed significantly from that of healthy subjects. Notably, IBD patients showed low intestinal bacterial diversity, while CRC patients showed high intestinal bacterial diversity, a contrasting pattern between the two disease states. The abstract does not specify Faecalibacterium prausnitzii, butyrate, or other named commensals, so no claim is made about those organisms here.

What are the greatest implications of this study?

The finding that IBD and CRC involve opposite directions of diversity change suggests these two diseases are associated with distinct, rather than uniform, disruptions of the gut microbiome. This distinction could help refine how metagenomic diversity and community structure are used to distinguish disease states from health and from each other. It also underscores the value of large, pooled public metagenomic datasets for characterizing disease-associated microbial signatures.

What was studied?

This study examined whether the intestinal microbiome influences clinical outcome and treatment side effects in early breast cancer. Researchers used shotgun metagenomics to characterize fecal microbiota composition and paired this with plasma metabolomics. They looked at associations between the gut microbiota, measured at baseline and after chemotherapy, and both breast cancer prognosis and therapy-induced side effects. Findings were then tested for clinical relevance in an immunocompetent mouse model colonized with patient microbiota and challenged with mouse breast cancer and chemotherapy.

Who was studied?

The human cohort consisted of 76 early breast cancer patients contributing 121 fecal specimens, with 45 patients providing paired samples collected before and after chemotherapy. These patients were enrolled in the CANTO prospective study, which was designed to record side effects associated with clinical management of breast cancer. The findings were further validated in immunocompetent mice colonized with breast cancer patient microbiota.

What were the most important findings?

Specific gut commensals were found to be overabundant in breast cancer patients compared with healthy individuals. These overabundant commensals were associated with worse breast cancer prognosis. Chemotherapy modulated the abundance of these gut microbes, and the same microbes appeared to influence weight gain and neurological side effects linked to breast cancer therapies.

What are the greatest implications of this study?

The results suggest that gut microbiota composition could serve as a modifiable factor affecting both cancer prognosis and treatment tolerability in early breast cancer. Because chemotherapy itself reshapes these microbial communities, monitoring or targeting the microbiome during treatment may offer a way to improve outcomes and reduce side effects. The authors note that these findings, obtained in adjuvant and neoadjuvant settings, warrant prospective validation before any clinical application.

What was studied?

This study evaluated the role of oral microbiota in colorectal cancer (CRC) progression by comparing bacterial communities in saliva and stool. Researchers used 16S rRNA analysis and next-generation sequencing to characterize both sample types. Linear discriminant analysis effect size (LEfSe) was applied to identify bacterial species that differed significantly between groups and across CRC stages.

Who was studied?

The study included 52 patients with colorectal cancer and 51 healthy controls, with saliva and stool samples collected from each participant. CRC patients were further divided into an early-stage group (Stage I or II, n = 26) and an advanced-stage group (Stage III or IV, n = 26). This design allowed comparison not only between CRC patients and healthy subjects but also between disease stages.

What were the most important findings?

Indigenous oral bacteria, including Peptostreptococcus, Streptococcus, and Solobacterium species, were present at significantly higher relative abundance in both saliva and stool of CRC patients compared with healthy controls. Among these, Peptostreptococcus stomatis, Streptococcus anginosus, Streptococcus koreensis, and Streptococcus moorei were identified as oral-cavity-derived species shared between the two body sites in CRC patients. Streptococcus moorei was further found at significantly higher relative abundance in advanced-stage (Stage III, IV) patients compared with early-stage (Stage I, II) patients, and this pattern held consistently in both saliva and stool samples.

What are the greatest implications of this study?

The consistent presence of the same four oral-derived bacterial species in both saliva and stool of CRC patients supports a link between oral microbiota and gut microbiota in CRC. The stage-dependent enrichment of Streptococcus moorei suggests these oral bacteria may track with, or contribute to, CRC progression rather than merely being present. These findings raise the possibility that saliva-based microbial signatures could serve as accessible, non-invasive markers related to CRC status or stage.

What was studied?

Accumulating evidence suggests that gut microbiota plays a role in the pathogenesis of schizophrenia via the microbiota-gut-brain axis. This study sought to investigate whether transplantation of fecal microbiota from drug-free patients with schizophrenia into specific pathogen-free mice could cause schizophrenia-like behavioral abnormalities. The results revealed that transplantation of fecal microbiota from schizophrenic patients into antibiotic-treated mice caused behavioral abnormalities such as psychomotor hyperactivity, impaired learning and memory in the recipient animals. These mice also showed elevation of the kynurenine-kynurenic acid pathway of tryptophan degradation in both periphery and brain, as well as increased basal extracellular dopamine in prefrontal cortex and 5-hydroxytryptamine in hippocampus, compared with their counterparts receiving feces from healthy controls. Furthermore, colonic luminal filtrates from the mice transplanted with patients' fecal microbiota increased both kynurenic acid synthesis and kynurenine aminotransferase II activity in cultured hepatocytes and forebrain cortical slices. Sixty species of donor-derived bacteria showed significant difference between the mice colonized with the patients' and the controls' fecal microbiota, highlighting 78 differentially enriched functional modules including tryptophan biosynthesis function. In conclusion, our study suggests that the abnormalities in the composition of gut microbiota contribute to the pathogenesis of schizophrenia partially through the manipulation of tryptophan-kynurenine metabolism.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study investigated the composition of the gut microbiome in renal transplant recipients (RTRs) and compared it with that of healthy controls. The researchers used 16S rRNA sequencing of fecal samples to characterize microbiome composition and diversity. They then applied multivariate association with linear models (MaAsLin) to identify clinical and pharmacological determinants of the gut microbiome in RTRs, including immunosuppressive drugs and antibiotic exposure.

Who was studied?

The study included 139 renal transplant recipients (50% male, mean age 58.3 plus or minus 12.8 years) and 105 healthy controls (57% male, mean age 59.2 plus or minus 10.6 years), all participants in the TransplantLines Biobank and Cohort Study (NCT03272841). The median time since transplantation among RTRs was 6.0 years, with a range of 1.5 to 12.5 years. Fecal samples were collected from both groups for microbiome analysis.

What were the most important findings?

The gut microbiome composition of RTRs was significantly different from that of healthy controls, and RTRs had significantly lower gut microbiome diversity (p less than 0.01). Proton-pump inhibitors, mycophenolate mofetil, and estimated glomerular filtration rate (eGFR) were identified as significant determinants of the gut microbiome in RTRs (p less than 0.05). These findings point to specific medications and kidney function as key factors shaping post-transplant dysbiosis, rather than transplantation alone.

What are the greatest implications of this study?

The findings indicate that renal transplant recipients experience measurable intestinal dysbiosis linked to specific modifiable factors, particularly proton-pump inhibitor use and mycophenolate mofetil therapy. This suggests that clinicians managing RTRs might consider the gut microbiome impact of routine medication choices as part of post-transplant care. Further research could explore whether adjusting these determinants influences microbiome recovery or long-term transplant outcomes.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

Gut microbiome alterations are closely related to human health and linked to a variety of diseases. Although great efforts have been made to understand the risk factors for multiple myeloma (MM), little is known about the role of the gut microbiome and alterations of its metabolic functions in the development of MM.

What were the most important findings?

Here, in a cohort of newly diagnosed patients with MM and healthy controls (HCs), significant differences in metagenomic composition were discovered, for the first time, with higher bacterial diversity in MM. Specifically, nitrogen-recycling bacteria such as Klebsiella and Streptococcus were significantly enriched in MM. Also, the bacteria enriched in MM were significantly correlated with the host metabolome, suggesting strong metabolic interactions between microbes and the host. In addition, the MM-enriched bacteria likely result from the regulation of urea nitrogen accumulated during MM progression. Furthermore, by performing fecal microbiota transplantation (FMT) into 5TGM1 mice, we proposed a mechanistic explanation for the interaction between MM-enriched bacteria and MM progression via recycling urea nitrogen. Further experiments validated that Klebsiella pneumoniae promoted MM progression via de novo synthesis of glutamine in mice and that the mice fed with glutamine-deficient diet exhibited slower MM progression.

What are the greatest implications of this study?

Overall, our findings unveil a novel function of the altered gut microbiome in accelerating the malignant progression of MM and open new avenues for novel treatment strategies via manipulation of the intestinal microbiota of MM patients. Video abstract.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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).

What are the greatest implications of this study?

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.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study examined how mode of delivery affects the earliest colonization of the infant gut microbiota during the neonatal period (up to one month of age) and into infancy. The researchers used longitudinal sampling combined with whole-genome shotgun metagenomic analysis to track which microbial strains and species established themselves in newborns over time. They specifically compared babies born by caesarean section to those born vaginally, and also looked at the effects of maternal antibiotic prophylaxis and breastfeeding status during the neonatal window.

Who was studied?

The cohort comprised 596 full-term babies born in UK hospitals, from whom 1,679 gut microbiota samples were collected at multiple time points during the neonatal period and later in infancy. For a subset of these infant-mother pairs, matched maternal samples were also collected, totaling 175 mothers paired with 178 babies. This gave the study both a large infant sample size and a smaller nested set of mother-infant pairs for tracking strain transmission.

What were the most important findings?

Babies delivered by caesarean section showed disrupted transmission of maternal Bacteroides strains, meaning these commensal organisms were less successfully passed from mother to infant compared to vaginal delivery. Caesarean-born infants also showed high-level colonization by opportunistic pathogens associated with the hospital environment, including Enterococcus, Enterobacter, and Klebsiella species. These same disruptions, though to a lesser extent, were also observed in vaginally delivered babies whose mothers received antibiotic prophylaxis and in infants who were not breastfed during the neonatal period.

What are the greatest implications of this study?

The findings suggest that both caesarean delivery and antibiotic exposure around birth can independently disrupt the normal, low-risk colonization of the infant gut by maternal commensal strains. This disruption opens the door for opportunistic, hospital-associated pathogens to establish themselves early in life instead. Because early gut microbiota composition has been linked to later childhood and lifelong disease risk, these results point to birth mode, antibiotic use, and breastfeeding as modifiable factors that could be targeted to support healthier early microbiome establishment.

What was studied?

Anti-PD-1-based immunotherapy has had a major impact on cancer treatment but has only benefited a subset of patients. Among the variables that could contribute to interpatient heterogeneity is differential composition of the patients' microbiome, which has been shown to affect antitumor immunity and immunotherapy efficacy in preclinical mouse models. We analyzed baseline stool samples from metastatic melanoma patients before immunotherapy treatment, through an integration of 16S ribosomal RNA gene sequencing, metagenomic shotgun sequencing, and quantitative polymerase chain reaction for selected bacteria. A significant association was observed between commensal microbial composition and clinical response. Bacterial species more abundant in responders included Bifidobacterium longum, Collinsella aerofaciens, and Enterococcus faecium. Reconstitution of germ-free mice with fecal material from responding patients could lead to improved tumor control, augmented T cell responses, and greater efficacy of anti-PD-L1 therapy. Our results suggest that the commensal microbiome may have a mechanistic impact on antitumor immunity in human cancer patients.

What was studied?

This study evaluated whether faecal metagenomes could be used to diagnose colorectal cancer (CRC) non-invasively. Researchers performed metagenome-wide association studies on stool samples to identify microbial species and gene markers associated with CRC. They then tested whether a small set of these markers could reliably distinguish CRC patients from controls using both metagenomic sequencing and targeted quantitative PCR (qPCR) assays. The candidate biomarkers were validated across multiple independent cohorts from different countries.

Who was studied?

The primary cohort included 74 patients with CRC and 54 controls from China. Validation cohorts included 16 CRC patients and 24 controls from Denmark, plus two previously published cohorts from France and Austria. A further independent Chinese cohort of 47 patients with CRC and 109 controls was used for qPCR-based validation.

What were the most important findings?

The study confirmed known associations between CRC and Fusobacterium nucleatum and Peptostreptococcus stomatis, and identified new associations with species including Parvimonas micra and Solobacterium moorei. Researchers identified 20 microbial gene markers differentiating CRC and control microbiomes, of which 4 were validated in the Danish cohort. These four genes distinguished CRC from controls in the French and Austrian cohorts with AUCs of 0.72 and 0.77, and qPCR measurement of two of these genes classified CRC patients in an independent Chinese cohort with an AUC of 0.84 and an odds ratio of 23.

What are the greatest implications of this study?

These findings suggest that faecal microbial gene markers, including some detectable at early cancer stages, could serve as non-invasive biomarkers for CRC screening. Validation across cohorts from China, Denmark, France, and Austria supports the generalizability of a small panel of markers across different populations. Because qPCR is a simple, targeted assay, these markers may be practical to develop into a clinical diagnostic test for CRC.

What was studied?

This study examined how the gut microbiome and circulating serum metabolites differ between lean and obese individuals. Researchers used a metagenome-wide association study paired with serum metabolomics profiling to identify obesity-associated gut microbial species and link them to changes in blood metabolites. They further tested a specific microbial species, Bacteroides thetaiotaomicron, in mice to determine its direct effect on body weight and fat accumulation. The study also examined whether bariatric surgery could reverse the microbial and metabolic changes seen in obesity.

Who was studied?

The human portion of the study involved a cohort of lean and obese, young, Chinese individuals, though the abstract does not specify exact sample size. A subset of these obese individuals also underwent bariatric surgery as a weight-loss intervention, with pre- and post-surgery comparisons used to assess reversal of obesity-associated changes. In addition to the human cohort, the researchers used a mouse model to test the functional effects of B. thetaiotaomicron administration via gavage.

What were the most important findings?

The abundance of Bacteroides thetaiotaomicron, a glutamate-fermenting commensal, was markedly decreased in obese individuals and was inversely correlated with serum glutamate concentration. In mice, gavage with B. thetaiotaomicron reduced plasma glutamate concentration and alleviated diet-induced body-weight gain and adiposity. Weight-loss intervention by bariatric surgery partially reversed these obesity-associated microbial and metabolic alterations, including restoring B. thetaiotaomicron abundance and lowering elevated serum glutamate.

What are the greatest implications of this study?

These findings identify a previously unknown link between a specific gut commensal, circulating amino acid levels, and obesity. The inverse relationship between B. thetaiotaomicron and serum glutamate, confirmed functionally in mice, suggests this microbe helps regulate host metabolism through glutamate fermentation. The results suggest it may be possible to intervene in obesity by directly targeting the gut microbiota, offering a potential mechanistic target for future metabolic therapies.

What was studied?

This study examined how Roux-en-Y gastric bypass (RYGB) surgery changes the gut microbiota of morbidly obese patients over time. The researchers used shotgun metagenomic sequencing of fecal DNA to characterize microbial composition at both the species and gene level. They also performed functional annotation of the microbial genes to understand how the metabolic potential of the gut community shifted after surgery. The goal was to describe the taxonomic and functional changes that accompany the weight loss and metabolic improvements known to follow RYGB.

Who was studied?

The study recruited 13 morbidly obese patients scheduled to undergo RYGB surgery. Patients were phenotyped and had stool samples collected before surgery (n = 13), then again at 3 months (n = 12) and 12 months (n = 8) after surgery. This design allowed the same individuals to be followed longitudinally as their own before-and-after comparison.

What were the most important findings?

Gut microbial diversity increased within the first 3 months after RYGB and remained elevated a year later, tracking alongside the weight loss and metabolic improvements the patients experienced. RYGB altered the relative abundance of 31 bacterial species within the first 3 months after surgery. These shifts occurred rapidly and persisted through the 12-month follow-up, indicating the surgery induces a durable restructuring of the individual gut microbiota rather than a transient disturbance.

What are the greatest implications of this study?

The findings support the idea that major, lasting changes in gut microbial community structure accompany the metabolic benefits of RYGB, such as improved insulin sensitivity and glucose homeostasis. Because the diversity and compositional changes appear swiftly and persist for at least a year, the gut microbiota may be an active participant in, rather than a passive bystander to, post-surgical metabolic improvement. This raises the possibility that microbiome-targeted strategies could someday complement or mimic some of the benefits currently achieved only through bariatric surgery.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study examined the gut microbial community using 16S rRNA gene sequencing to compare obese and lean populations in Japan. Researchers sequenced the V3-V4 hypervariable regions of 16S rRNA from fecal samples using the Illumina MiSeq II platform. The goal was to characterize how gut microbiota composition differs with obesity status and to identify specific taxa associated with each phenotype.

Who was studied?

The study included 20 Japanese volunteers divided into two groups of 10 obese and 10 lean individuals. The average body mass index was 38.1 kg/m2 in the obese group and 16.6 kg/m2 in the lean group, a statistically significant difference. Fecal samples from these volunteers formed the basis of all microbial community comparisons.

What were the most important findings?

The lean group showed significantly higher Shannon diversity than the obese group, indicating greater microbial richness and evenness. Firmicutes and Fusobacteria were significantly more abundant in obese participants, while the Bacteroidetes abundance and Bacteroidetes/Firmicutes ratio did not differ between groups. At the genus level, Alistipes, Anaerococcus, Corpococcus, Fusobacterium, and Parvimonas were enriched in obese individuals, while Bacteroides, Desulfovibrio, Faecalibacterium, Lachnoanaerobaculum, and Olsenella were enriched in lean individuals. Notably, Faecalibacterium prausnitzii, a species known for anti-inflammatory properties, increased significantly in the lean group, whereas pro-inflammatory species increased in the obese group.

What are the greatest implications of this study?

These findings support a link between reduced gut microbial diversity, a shift toward pro-inflammatory taxa, and obesity in a Japanese population. The enrichment of anti-inflammatory commensals like Faecalibacterium prausnitzii in lean individuals suggests that gut microbial composition may influence inflammatory tone and metabolic health. This work adds population-specific evidence to the broader case that gut microbiota profiling could inform obesity risk assessment or targeted interventions, though causality cannot be established from this comparative design.

What was studied?

This study investigated how the composition of the human intestinal microbiota relates to intestinal permeability and both local and systemic inflammation in obesity. Researchers profiled fecal microbiota using a phylogenetic microarray and compared this to markers of gut and whole-body inflammation. They also assessed gastroduodenal, small intestinal, and colonic permeability using a multisaccharide test, alongside metabolic markers such as HbA1c, transaminases, and lipids.

Who was studied?

The study population consisted of 28 subjects spanning a wide BMI range of 18.6 to 60.3 kg/m2, covering both nonobese and obese individuals. Based on microbiota composition, these subjects segregated into two clusters: one made up predominantly of obese participants (15 of 19) and another made up exclusively of nonobese participants (9 of 9). This design allowed comparison of inflammatory and permeability measures across microbiota-defined groups rather than by BMI category alone.

What were the most important findings?

Intestinal permeability did not differ between the two microbiota clusters, but the obese-predominant cluster showed reduced bacterial diversity, a decreased Bacteroidetes to Firmicutes ratio, and an increased abundance of potentially proinflammatory Proteobacteria. Fecal calprotectin, a marker of intestinal inflammation, was only detectable in a subset of subjects within the obese microbiota cluster (8 of 19, P = 0.02). Plasma C-reactive protein, a marker of systemic inflammation, was also increased in these subjects, linking microbiota composition to both local and systemic inflammatory signals.

What are the greatest implications of this study?

The findings suggest that a distinct, less diverse microbiota profile enriched in Proteobacteria and depleted in Bacteroidetes relative to Firmicutes is associated with detectable gut and systemic inflammation in some obese individuals, independent of measured intestinal permeability. This points to microbiota composition, rather than barrier leakiness alone, as a candidate driver or marker of the inflammatory state seen in obesity. These results support further work on microbiota-targeted strategies to address obesity-associated inflammation.