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Bacteroides thetaiotaomicron carries dozens of gene clusters dedicated to breaking down dietary fibers your own body cannot digest, turning them into fuel for you and for other gut microbes.
Bacteroides thetaiotaomicron is a keystone fiber-degrading symbiont of the human gut and the model organism for polysaccharide utilization. Its many carbohydrate-processing gene clusters break down complex dietary fibers into short-chain fatty acids that feed the host and cross-feeding microbes, and it helps shape a stable, healthy gut community.
Microbiome-targeted interventions (MBTIs) are validated using a dual-evidence logical framework. First, the intervention must realign the condition’s microbiome signature by increasing beneficial taxa that are consistently depleted and reducing pathogenic taxa that are consistently enriched. Second, the intervention must demonstrate measurable clinical benefit. Concordance of these effects in the same context validates the intervention as an MBTI and supports the clinical relevance of the microbiome signature.
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreBacteroides thetaiotaomicron is a Gram-negative anaerobe and one of the most abundant and best-studied symbionts of the human gut. It is the model organism for the breakdown of complex dietary fiber: it encodes dozens of polysaccharide utilization loci that let it sense and digest glycans the host cannot, releasing sugars and short-chain fatty acids that feed both the host and neighboring microbes.[1] On this database it appears as a differentially abundant taxon across many human microbiome studies.
By turning fiber into fuel and adapting its gene expression to whatever carbohydrates the diet supplies, B. thetaiotaomicron stabilizes the gut ecosystem and supports barrier and metabolic health.[1] In this database's framework it is not a metal-weaponizing pathogen but a beneficial glycan specialist whose presence marks the healthy anaerobic gut in which nutritional immunity keeps opportunists suppressed.[2]
B. thetaiotaomicron is a Gram-negative, non-motile, rod-shaped, strictly anaerobic bacterium whose defining feature is an unusually large repertoire of carbohydrate-active enzymes packaged into starch and fiber utilization systems.[1][3]
B. thetaiotaomicron is a beneficial keystone commensal. Its fiber breakdown creates a critical nutrient source for the microbiota and host, produces short-chain fatty acids, and supports colonization resistance against pathogens.[1] Its starch-utilization machinery can even be selectively modulated with small molecules, illustrating how central its glycan metabolism is to the gut.[3]
Its useful features are metabolic.
| Factor | Description and role |
|---|---|
| Polysaccharide utilization loci | Dozens of gene clusters sense and digest complex dietary fibers the host cannot, a defining capability of gut Bacteroides.[1] |
| Starch utilization system (Sus) | The archetypal outer-membrane machinery, including the amylase SusG, that captures and breaks down starch.[3] |
| Short-chain fatty acid output | Fiber fermentation yields acids that feed colonocytes and cross-feeding microbes.[1] |
| Diet-responsive regulation | Switches its enzyme repertoire to match available carbohydrates, helping it persist through dietary change and stabilize the community.[1] |
B. thetaiotaomicron is a fiber-fermenting commensal, not a metal scavenger. Its glycan breakdown feeds cross-feeders and keeps the mucosa anaerobic, indexing a gut that resists the shift toward oxygen-tolerant, lipopolysaccharide-rich Enterobacteriaceae, the metal-weaponizing opportunists this database tracks.[2]
Its dependence on dietary fiber makes it diet-sensitive.
| Pressure | Effect |
|---|---|
| Low-fiber diet | Scarce fermentable fiber narrows its substrate and can push it toward foraging host mucus instead.[1] |
| Antibiotics and dysbiosis | Loss of anaerobic commensals accompanies the Enterobacteriaceae shift and a less protective gut.[2] |
The entries below are supportive strategies classified by our validation method and are not medical advice. The goal is to sustain this fiber-fermenting commensal.
| Intervention | Class | Status |
|---|---|---|
| Dietary fiber diversity | Diet | Validation In Progress |
| Resistant starch | Diet | Validation In Progress |
| Anaerobe-sparing antibiotic stewardship | Practice | Validation In Progress |
Where Bacteroides thetaiotaomicron (NCBI:txid818) appears as a differentially abundant taxon across the Microbiome Medicine corpus. Each row aggregates every experiment in which the organism moved in a given condition; direction is its change in the case/exposure group, and grade is the strongest single study's methodology weight (A·D·S·C·R), the same engine that grades every signature on this site.
Across 72 conditions and 75 studies, the signal is genuinely mixed: enriched in 24, depleted in 32, and direction-conflicting in 16 (directional agreement 0.55). Because B. thetaiotaomicron is a versatile core commensal that can bloom or recede with diet, its direction varies by context, so the aggregate evidence tier is Low.
How to read these. B. thetaiotaomicron is a highly adaptable fiber degrader, so its abundance responds strongly to diet and can move in either direction across cohorts. A differential signal is best read as a shift in the gut's carbohydrate ecology, which is why the aggregate tier stays Low.
Internal summaries of the 75 studies we reviewed in which B. thetaiotaomicron was a differential taxon across this corpus.
This pilot study applied an integrative multi-omics workflow to identify plasma metabolite, lipid, and gut-microbiome signatures associated with sarcopenia. Sarcopenia is the age-related decline in muscle mass and strength, and the researchers combined plasma metabolomics, lipidomics, and 16S rRNA gut-microbiome sequencing to look for markers linked to the condition. Participants were classified as sarcopenic or non-sarcopenic using EWGSOP2 criteria, which incorporate grip strength, chair rise time, psoas muscle cross-sectional area on CT, and the SARC-F screening score.
The cohort consisted of forty community-dwelling older adults, aged 60 to 87 years, from an Indian population. Of these, fifteen were classified as sarcopenic and twenty-five as non-sarcopenic based on EWGSOP2 criteria. This was a pilot study, so the sample size was small and intended to generate preliminary integrative findings rather than definitive population-level estimates.
Dominant hand grip strength was the strongest clinical predictor of sarcopenia, with an AUROC of 0.93. Sarcopenic subjects showed higher systemic inflammation, reflected in an elevated neutrophil-to-lymphocyte ratio, and elevated plasma arachidonic acid compared to non-sarcopenic subjects. Thirteen lipid species, primarily lysophosphatidylcholines, lysophosphatidylethanolamines, and hexosylceramides, were identified as discriminating between the two groups, and a support vector machine model with recursive feature elimination was used to identify these discriminative metabolites, with gut microbiome profiles correlated against the metabolite patterns. The abstract as provided does not mention Faecalibacterium prausnitzii, butyrate, or anti-inflammatory commensals specifically.
The findings suggest that sarcopenia in older adults is accompanied by a distinct signature of systemic inflammation, altered lipid metabolism, and arachidonic acid elevation that can be captured through integrative multi-omics profiling. Combining clinical measures like grip strength with plasma metabolomic, lipidomic, and gut-microbiome data may help identify biological markers of sarcopenia beyond physical function tests alone. Because this was a small pilot study within an Indian cohort, larger and more diverse studies would be needed before these metabolite, lipid, and microbiome signatures could be used as validated diagnostic or monitoring tools.
This randomized, double-blind, placebo-controlled trial tested whether daily supplementation with two specific probiotic strains, Bifidobacterium animalis subsp. lactis XLTG11 and Lactiplantibacillus plantarum CCFM8661, could reduce recurrent respiratory tract infections (RRTIs) in children. Over 180 days, the study tracked infection frequency and duration alongside changes in gut microbiota composition, functional metabolic pathways, and immune biomarkers. The design allowed the researchers to link clinical respiratory outcomes to underlying shifts in the gut microbial community and immune regulation.
The study enrolled 120 children who had been diagnosed with recurrent respiratory tract infections. Participants were randomly assigned to receive either the probiotic combination or a matched placebo daily for 180 days. The abstract does not provide further demographic details such as age range or sex distribution.
Children receiving the probiotics had significantly reduced duration and frequency of fever, cough, upper respiratory tract infections, trachea or bronchitis, pneumonia, and overall RRTI recurrence compared with placebo (all p < 0.05). Gut microbiota profiling at day 180 showed clear community differences between groups, with the probiotic group showing greater abundance of beneficial commensal taxa and the placebo group showing more opportunistic genera. Functional pathway analysis pointed to enhanced metabolic stability in the probiotic recipients, and immune biomarker patterns showed comparatively stable IgG, IgM, and complement C3 levels, suggesting a more regulated humoral immune response. Growth trajectories remained normal in both groups.
These findings support strain-defined probiotic supplementation as a viable adjunct strategy for reducing the burden of recurrent respiratory infections in children. The parallel shifts in gut microbial composition, metabolic function, and humoral immune stability suggest the respiratory benefit may be mediated through gut-immune axis modulation rather than a direct respiratory-tract effect. Because growth remained normal, the intervention appears well tolerated over a six-month period, supporting its potential for longer-term pediatric preventive use pending further confirmatory trials.
This study examined whether gut microbiome composition and microbial metabolite profiles differ between lean and obese youth with type 1 diabetes (T1D). Researchers used metagenomic shotgun sequencing of stool samples to characterize bacterial community structure and taxa abundance. They also measured short-chain fatty acids (SCFAs) as microbial metabolite outputs. The goal was to describe obesity-associated gut microbial changes in a T1D population, a group already at elevated risk for complications.
The pilot study included T1D youth divided into a lean group (BMI 5th to under 85th percentile, n = 27) and an obese group (BMI at or above the 95th percentile, n = 21). Participants had a mean age of 15.3 years, mean glycated hemoglobin A1c of 7.8%, and mean diabetes duration of 5.1 years. The combined sample was 42.0% female and 94.0% White.
Bacterial community composition (beta-diversity) differed significantly between BMI groups. The obese group showed a significantly higher ratio of Prevotella to Bacteroides and increased relative abundance of Prevotella copri, along with other taxa that differed between lean and obese groups. Functional profiling also revealed upregulation of branched-chain amino acid (BCAA) biosynthesis pathways in the obese group, pointing to a metabolic signature accompanying the taxonomic shifts.
These findings suggest that obesity in T1D youth is accompanied by measurable, structured changes in gut microbial ecology and function, not just body composition differences. The Prevotella to Bacteroides shift and BCAA biosynthesis upregulation echo patterns reported in obesity research more broadly, raising the possibility of shared microbial mechanisms across metabolic conditions. Because this was a pilot study, the findings support further investigation into the gut microbiome as a potential contributor to, or biomarker for, obesity-related complications in T1D.
Inflammation and innate immune activation are associated with chronic HIV infection, despite effective treatment. Although gut microbiota alterations are linked to systemic inflammation, the relationships between the gut microbiome, inflammation and HIV remain unclear.
The UPBEAT-CAD sub-study, examining cardiovascular disease (CVD) risk in HIV, enrolled participants matched on HIV status and traditional CVD risk factors. Subclinical CVD was assessed using coronary computed tomography angiography (CCTA). 34 biomarkers were measured using quantitative immunoassays. Microbiota composition was analysed by 16S rRNA sequencing of stool samples, with taxonomic assignment via the SPINGO pipeline. Differentially abundant species were identified by Analysis of Compositions of Microbiomes with Bias Correction (ANCOM-BC) and correlated to biomarkers, diet and CCTA outcomes using Spearman correlation.
Among 81 participants (median age 51 years, 73% male), people with HIV (n=44 , 54%) had a higher prevalence of hypercholesterolaemia (p <0.025) and statin use (p <0.001). A significant separation in gut microbiome β-diversity was observed between people with and without HIV. ANCOM-BC analysis identified 42 differentially abundant species and 10 genera in those with HIV. Enrichment of Bifidobacterium pseudocatenulatum, Megamonas hypermegale and Selenomonas ruminantium and depletion of Fusicatenenibacter correlated with lower plaque burden. Depletion of SCFA-producing Ruminococcus bromii correlated with higher plaque burden and fat intake, while depletion of Bacteroides spp and Alistepes spp correlated with elevated inflammatory biomarkers (D-dimer, CD40-ligand, CRP and IFN-γ).
Significant gut microbiota differences in people with HIV were linked to subclinical CVD, diet, and inflammation, suggesting a role for the microbiome in cardiovascular risk in HIV infection.
This study examined whether gut microbiota structure and function relate to outcomes of immune checkpoint inhibitor (ICI) therapy in non-melanoma skin cancers. The researchers performed 16S rRNA V1-V2 gene amplicon sequencing on fecal samples collected longitudinally, then ran tumor-dependent differential analyses of bacterial composition alongside untargeted fecal metabolomics. The goal was to identify bacterial genera, species, and metabolic pathways associated with response versus non-response to ICI treatment.
The analysis drew on 68 fecal samples collected longitudinally from individuals with basal cell carcinoma (n = 5), Merkel cell carcinoma (n = 5), or cutaneous squamous cell carcinoma (CSCC, n = 11). All participants were undergoing ICI therapy for a non-melanoma skin cancer. This is a small, exploratory cohort spanning three distinct tumor types rather than a single large patient population.
Across all tumor types combined, the researchers identified 10 differential bacterial genera between ICI responders and non-responders. Within the CSCC subgroup specifically, 10 genera and 20 species distinguished responders from non-responders, and predicted functional pathway analyses found 8 pathways enriched in non-responders and 12 enriched in responders. Untargeted fecal metabolomics further identified nine KEGG pathways associated with ICI efficacy in CSCC, pointing to microbial metabolic activity as a correlate of treatment response.
The findings suggest that gut microbiota composition and function are linked to ICI therapy outcomes in non-melanoma skin cancers, extending observations previously made mainly in melanoma to other skin cancer types. Because this is described as an exploratory study with a small sample size, the specific genera, species, and pathways identified should be viewed as hypothesis-generating rather than confirmed predictors. Larger studies are needed to validate these microbiome features before they could inform strategies to predict or improve ICI response in non-melanoma skin cancer.
The gut microbiome influences physiological responses to exercise by modulating inflammatory markers and metabolite production. Athletes typically exhibit greater microbial diversity, which may be associated with improved performance, but the mechanisms linking different exercise modalities to the gut microbiome are not fully understood. In this study, blood and stool samples were collected from endurance athletes, strength athletes, and non-athletic controls performing two maximal exercise tests (the anaerobic Wingate test and the aerobic Bruce Treadmill Test) to integrate serum biomarker data with gut bacterial metagenomic profiles. While most biochemical markers showed similar post-exercise trends across groups, SPARC (secreted protein acidic and rich in cysteine) and adiponectin levels showed modality-specific responses. Strength-trained participants showed unique microbiome-biomarker associations after the Wingate test. In addition, baseline enrichment of certain bacterial taxa, including Clostridium phoceensis and Catenibacterium spp., correlated with reduced Bruce Treadmill test response in strength-trained individuals. These findings, while requiring further validation, indicate the complex interplay between exercise type, training background, and the gut microbiome, and suggest that specific microbial species may help shape recovery and adaptation.
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.
This study investigated whether gut microbiota composition and plasma metabolic profiles are altered in lymph node tuberculosis (LNTB), a form of tuberculosis whose relationship with gut microbiota had not previously been explored. Researchers used metagenomic sequencing to characterize gut microbial diversity and composition, paired with plasma metabolomics to assess circulating metabolite changes. KEGG pathway analysis was applied to link microbial gene content to metabolic function, focusing especially on short-chain fatty acid (SCFA) biosynthesis. An integrated analysis then examined correlations between specific gut bacteria and plasma metabolites in LNTB.
The abstract does not report specific participant numbers, ages, or geographic setting. It indicates a comparison between individuals diagnosed with lymph node tuberculosis (the LNTB group) and healthy individuals serving as controls. Samples analyzed included gut microbiota (via metagenomic sequencing) and plasma (via metabolomics) from these two groups.
LNTB patients showed significantly altered gut microbial diversity, with notable reductions in SCFA-producing taxa including Ruminococcus, Faecalibacterium, Roseburia, and Blautia compared to healthy individuals. KEGG pathway analysis indicated that this gut dysbiosis negatively affected SCFA biosynthesis and metabolism. Plasma metabolomics revealed disruptions in metabolites tied to SCFA synthesis and inflammation pathways, and integrated analysis found significant correlations between taxa such as Blautia, Butyricicoccus, Coprococcus, Ruminococcus, Bacteroides, and Clostridium and plasma metabolites including alpha-benzylbutyric acid, acetic acid, and succinic acid.
The findings suggest that gut microbiota dysbiosis and consequent metabolic dysfunction, particularly reduced SCFA production, may play a role in LNTB pathophysiology. Because SCFAs and related anti-inflammatory commensal bacteria appear diminished in LNTB, restoring these microbial functions could represent a novel therapeutic target for disease management. This work opens a new avenue for considering the gut-immune axis in tuberculosis affecting lymph nodes, beyond the traditional focus on pulmonary disease.
This study examined whether rifaximin, a gut-specific non-absorbable antibiotic, could reduce gut-derived systemic inflammation in severe acute pancreatitis (SAP). The researchers combined murine experimental models with a single-center, open-label randomized controlled trial (ChiCTR2100049794). They assessed pancreatic injury, systemic inflammatory markers, and gut microbiota composition, and tested whether rifaximin's effects depended on modulating the microbiota by using antibiotic-treated and germ-free mice.
The animal component used murine models of severe acute pancreatitis, including antibiotic-treated and germ-free mice used to probe the mechanism. The clinical component enrolled 60 patients with predicted severe acute pancreatitis, randomized to receive rifaximin or standard control treatment. No further demographic details are given in the abstract.
In mice, rifaximin reduced pancreatic injury and systemic inflammation and decreased mucin-degrading gut genera such as Akkermansia, but its protective effects persisted even in antibiotic-treated and germ-free mice, indicating mechanisms beyond microbiota modulation. In patients, rifaximin significantly lowered systemic inflammation, with white blood cell count falling from a median of 11.50 x10^9/L to 8.49 x10^9/L and TNF-alpha falling from 15.05 pg/mL to 11.00 pg/mL. However, the rate of culture-confirmed infection was identical between rifaximin and control groups (13.3% vs 13.3%), and adverse events were comparable between groups.
The findings suggest rifaximin can dampen systemic inflammation in severe acute pancreatitis through mechanisms that are not solely dependent on reshaping the gut microbiota, pointing to a possible direct anti-inflammatory or barrier-protective effect. Because inflammation markers improved without any change in infection risk, rifaximin may offer a safe adjunct for controlling inflammatory injury in SAP without added infectious risk. This supports further investigation of rifaximin as a therapeutic strategy for gut-derived inflammation in acute pancreatitis, alongside continued study of its non-microbiota-dependent mechanisms.
This cross-sectional exploratory study examined associations between subjective sleep indices and gut microbiome features in adults with colorectal cancer (CRC). Researchers compared patients to their sleep-partner caregivers using sleep diaries, stool sampling, and dietary intake questionnaires. The design allowed comparison of microbiome and sleep characteristics within matched household pairs who shared similar diet and environment.
Forty participants were studied, consisting of 20 patient-caregiver dyads. Each dyad included an adult with colorectal cancer and their sleep-partner caregiver, and both members completed sleep diaries, stool sampling, and dietary questionnaires individually. Patients and caregivers had comparable demographics, dietary intake, and sleep indices at baseline.
Patients with CRC had significantly different gut microbiome beta diversity (p = .005) and alpha diversity (Inverse Simpson, p = .029) compared with their caregivers, along with 7 more and 6 less differentially abundant taxa. Among patients only, those with high sleep efficiency (at least 85%) had higher gut microbial diversity than those with lower sleep efficiency (Inverse Simpson p = .019, Shannon Index p = .035). Some oral and gut microbes were also differentially abundant between patients with high versus low sleep efficiency scores.
The findings highlight a link between sleep health and gut microbiome characteristics specifically in patients with colorectal cancer, distinct from their genetically unrelated but cohabiting caregivers. This suggests sleep quality may be associated with gut microbial diversity in cancer patients, though the abstract does not identify specific taxa driving this relationship. The authors note that further research with a larger sample is needed to replicate these findings and identify the pathways linking sleep to gut microbiome features.
Fermented milk products are part of the staple diet for many Mediterranean populations. Most of these traditional foods are enriched with lactobacilli and other lactic acid bacteria, as well as with metabolites resulting from lactose fermentation. Currently, there is very little scientific knowledge on how dietary supplementation with fermented milk affects the composition of the gut microbiota and its metabolic activities.
We integrated 16 S rRNA gene-based taxonomic profiling with metaproteomics-based functional analysis to investigate gut microbiota changes in rats exposed to an 8-week dietary supplementation with casu axedu, a traditional fermented milk produced within rural communities in Sardinia (Italy). Several microbial taxa showed a significantly increased abundance at the end of the dietary treatment, including Phascolarctobacterium, Prevotella, Blautia glucerasea, and Lactococcus lactis, while Bacteroides dorei and Helicobacter rodentium were decreased compared to the control rats. Metaproteomic analysis highlighted a striking reshaping of the Prevotella proteome in agreement with its blooming in casu axedu-fed animals, suggesting an increase of the glycolytic activity through the Embden-Meyerhof-Parnas pathway over the Entner-Doudoroff pathway. Moreover, an increased production of enzymes involved in succinate biosynthesis was observed, which in turn significantly boosted the abundance of Phascolarctobacterium and its production of propionate. Fermented milk consumption also promoted microbial synthesis of branched chain essential amino acids L-valine and L-leucine. Finally, metaproteomic data indicated a reduction of bacterial virulence factors and host inflammatory markers, suggesting that the consumption of casu axedu can have beneficial effects on the gut mucosa health.
Our integrated multi-omics approach reveals that dietary supplementation with the traditional Sardinian fermented milk, casu axedu, induces significant shifts in the rat gut microbiota composition and function, characterized by the enrichment of beneficial taxa and metabolic pathways associated with improved gut health and reduced inflammation.
This study examined whether the gut microbiome is related to brain structure in apparently healthy adults. The researchers used 16S ribosomal RNA gene sequencing of stool samples to characterize gut microbiome composition and diversity. They paired this with brain magnetic resonance imaging and automated voxel-based morphometry to measure brain volumes, including gray matter and white matter. Statistical methods included principal coordinate analysis, linear discriminant analysis, and multivariable linear regression to test associations between microbiome measures and brain volume.
The study population was 623 Japanese men drawn from the Shiga Epidemiological Study on Subclinical Atherosclerosis (SESSA), a population-based cross-sectional cohort. Stool samples were collected during the study's follow-up stage, and participants had a mean age of 68.0 years (SD 8.0), ranging from 46 to 83 years. All participants underwent brain MRI as part of the same assessment.
After adjusting for age and total intracranial volume, gray matter volume showed a positive association with alpha diversity, specifically the Shannon index richness, at a q-value below 0.01. However, this association was no longer significant once the analysis further adjusted for body mass index, physical activity, smoking, drinking, and hypertension. Beta diversity, measured using weighted UniFrac distances via principal coordinate analysis, showed differences related to white matter volume, though the abstract text describing this result is incomplete. This pattern of the abstract is not about Christensenellaceae, Christensenella, leanness, BMI-associated taxa, or heritability; the study centers instead on gut microbiome diversity and brain morphometry.
The findings suggest that in generally healthy older men, any apparent link between gut microbial diversity and gray matter volume may largely reflect shared lifestyle and metabolic factors such as body mass index, physical activity, smoking, drinking, and hypertension rather than a direct, independent relationship. This underscores the importance of adjusting for lifestyle and cardiometabolic confounders when studying gut-brain associations in human populations. The results also support continued investigation of beta diversity and white matter relationships as a potentially distinct avenue linking the gut microbiome to brain structure. Overall, the study adds population-based human evidence to a field previously dominated by animal models and specific patient populations.
Possible relationships between gut dysbiosis and breast cancer (BC) development and progression have been previously reported. However, the results of these metagenomics studies are inconsistent. Our study involved 88 patients diagnosed with breast cancer and 86 cancer-free control women. Participants were divided into groups based on their menopausal status. Fecal samples were collected from 47 and 41 pre- and postmenopausal newly diagnosed breast cancer patients and 51 and 35 pre- and postmenopausal controls, respectively. In this study, we performed shotgun metagenomic analyses to compare the gut microbial community between pre- and postmenopausal BC patients and the corresponding controls.
Firstly, we identified 12, 64, 158, and 455 bacterial taxa on the taxonomy level of phyla, families, genera, and species, respectively. Insignificant differences of the Shannon index and β-diversity were found at the genus and species levels between pre- and postmenopausal controls; the differences concerned only the Chao index at the species level. No differences in α-diversity indexes were found between pre- and postmenopausal BC patients, although β-diversity differed these subgroups at the genus and species levels. Consistently, only the abundance of single taxa differed between pre- and postmenopausal controls and cases, while the abundances of 14 and 23 taxa differed or tended to differ between premenopausal cases and controls, and between postmenopausal cases and controls, respectively. There were similar differences in the distribution of enterotypes. Of 460 bacterial MetaCyc pathways discovered, no pathways differentiated pre- and postmenopausal controls or BC patients, while two and one pathways differentiated cases from controls in the pre- and postmenopausal subgroups, respectively.
While our findings did not reveal an association of changes in the overall microbiota composition and selected taxa with the menopausal status in cases and controls, they confirmed differences of the gut microbiota between pre- and postmenopausal BC patients and the corresponding controls. However, these differences were less extensive than those described previously.
This study used species-level shotgun metagenomic sequencing to characterize the gut microbiota of men who have sex with men (MSM). It investigated why the MSM gut microbiome, previously shown to differ from that of non-MSM, so often resembles the microbial communities seen in non-Westernized populations. The researchers also used questionnaire data and machine learning to link specific sexual practices to variation in microbiota composition among MSM.
The study population was men who have sex with men of Western origin, compared against patterns typical of non-Westernized populations. The abstract does not give an exact sample size, but participants contributed both stool samples for shotgun metagenomics and questionnaire responses on sexual practices. This design allowed the authors to relate individual behavioral data to individual gut microbiome profiles within the MSM cohort.
Many MSM with Western origin had gut microbiomes resembling those of non-Westernized populations rather than typical Western gut profiles. These microbiomes were frequently dominated by Prevotellaceae family members, including co-colonization by species from the Segatella copri complex alongside unknown Prevotellaceae members. Questionnaire analysis and machine learning further identified specific sexual practices as microbial features associated with this altered, Prevotellaceae-rich composition.
The findings show that sexual activity itself can be a driver of major gut microbiome alterations, independent of the diet and lifestyle factors usually invoked to explain Westernized versus non-Westernized microbiota differences. Because MSM gut microbiomes can resemble non-Westernized profiles, sexual practice becomes an important variable that population-based microbiota studies may need to account for. This has implications for how researchers select and interpret control or reference populations in microbiome research and for disentangling behavioral from dietary or geographic influences on gut microbial composition.
This study examined the relationship between the gut microbiome and the host genome and transcriptome in colorectal cancer (CRC). Researchers profiled the fecal microbiome structure alongside genomic and transcriptomic data from matched tumor and normal mucosa tissue. Exome sequencing was used to identify somatic mutations, and gene expression patterns were annotated and clustered against microbial abundance data. Immune and stromal cell composition was also estimated from the transcriptomic profiles.
The cohort consisted of 41 patients with colorectal cancer. For each patient, matched tumor tissue and normal mucosa tissue were analyzed alongside fecal microbiome samples. The abstract does not provide further demographic details such as age, sex, or geographic origin of the participants.
The researchers identified 22 gut microbial species significantly associated with CRC and estimated relative abundance across functional (KEGG) pathway categories. Four significantly mutated genes, TP53, APC, KRAS, and SMAD4, were linked to specific cancer-associated microbes. Fusobacterium nucleatum in particular showed a positive correlation with multiple host metabolic pathways, tying a specific pathogen to altered tumor metabolism. The abstract text is truncated before further results are described.
The findings support a functional link between specific gut bacteria, such as Fusobacterium nucleatum, and the somatic mutation landscape and metabolic activity of colorectal tumors. This multi-omic approach suggests that microbial taxa may interact with host driver mutations like TP53, APC, KRAS, and SMAD4 rather than merely coexisting with the tumor. Such associations could inform future work on microbiome-informed risk stratification or targets in CRC, though the abstract does not describe therapeutic testing or outcomes.
UNLABELLED: The present study aimed to characterize the gut microbiota and serum metabolome changes associated with sleep deprivation (SD) as well as to explore the potential benefits of multi-probiotic supplementation in alleviating SD-related mental health disorders. Rats were subjected to 7 days of SD, followed by 14 days of multi-probiotics or saline administration. Open-field tests were conducted at baseline, end of SD (day 7), and after 14 days of saline or multi-probiotic gavage (day 21). Metagenomic sequencing was conducted on fecal samples, and serum metabolites were measured by untargeted liquid chromatography tandem-mass spectrometry. At day 7, anxiety-like behaviors, including significant decreases in total movement distance (P = 0.0002) and staying time in the central zone (P = 0.021), were observed. In addition, increased levels of lipopolysaccharide (LPS; P = 0.028) and decreased levels of uridine (P = 0.018) and tryptophan (P = 0.01) were detected in rats after 7 days of SD. After SD, the richness of the gut bacterial community increased, and the levels of Akkermansia muciniphila, Muribaculum intestinale, and Bacteroides caecimuris decreased. The changes in the host metabolism and gut microbiota composition were strongly associated with the anxiety-like behaviors caused by SD. In addition, multi-probiotic supplementation for 14 days modestly improved the anxiety-like behaviors in SD rats but significantly reduced the serum level of LPS (P = 0.045). In conclusion, SD induces changes in the gut microbiota and serum metabolites, which may contribute to the development of chronic inflammatory responses and affect the gut-brain axis, causing anxiety-like behaviors. Probiotic supplementation significantly reduces serum LPS, which may alleviate the influence of chronic inflammation. IMPORTANCE: The disturbance in the gut microbiome and serum metabolome induced by SD may be involved in anxiety-like behaviors. Probiotic supplementation decreases serum levels of LPS, but this reduction may be insufficient for alleviating SD-induced anxiety-like behaviors.
This study examined the microbial composition and temporal dynamics of the human microbiome at four body sites: stool, oral, skin, and nasal. The researchers tracked how these microbial communities changed over time and how they related to host multi-omics data, immune markers, and clinical features. The goal was to understand how the microbiome behaves dynamically during both health and disease.
The study followed 86 participants over a period of 6 years, sampling microbiomes from four body sites in each person. The abstract does not specify additional demographic details such as age range or sex distribution. Some participants in the cohort were insulin-resistant, allowing comparison between metabolically healthy and metabolically disrupted individuals.
Microbiome stability and individuality were found to be body-site specific and strongly shaped by the host, with the stool and oral microbiomes proving more stable than the skin and nasal microbiomes, likely due to differing levels of interaction with the host and external environment. The researchers identified both individual-specific and commonly shared bacterial taxa, and individualized taxa showed greater stability over time. Notably, microbiome dynamics were correlated across different body sites, pointing to systemic patterns driven by host-microbial-environment interactions. Insulin-resistant individuals showed altered microbial stability and disrupted associations among microbiome composition, molecular markers, and clinical features.
The findings suggest that microbiome stability is not uniform across the body and that host factors play a central role in shaping which microbial communities remain stable versus dynamic over time. The correlation of microbiome dynamics across separate body sites implies a systemic, whole-body relationship between host and microbiota rather than site-isolated behavior. The disrupted microbiome-host associations seen in insulin resistance suggest that metabolic disease may involve a breakdown in normal host-microbial coupling, offering a potential angle for understanding or monitoring metabolic disease through longitudinal microbiome tracking.
The study examined how peripheral neurons connected to the gastrointestinal tract influence the gut microbiome and gut physiology. Researchers activated choline acetyltransferase (ChAT)-expressing or tyrosine hydroxylase (TH)-expressing gut-associated neurons in mice. They then measured effects on intestinal microbial communities, microbial metabolites (including bile acid profiles), and host physiological responses using multi-omics approaches.
The subjects were mice in which ChAT+ or TH+ gut-associated neurons were experimentally activated. The abstract does not give a specific sample size or strain detail, so no cohort numbers can be stated. This was an animal model study, not a human cohort, and it generated multi-omics datasets from these mice rather than drawing on a public metagenomic dataset.
Activating either ChAT+ or TH+ neurons reshaped the structure of the intestinal microbiome, including changes to bile acid profiles and fungal colonization. Physiologically, activation of either neuron type increased fecal output, showing a shared downstream effect on gut transit. Only ChAT+ neuron activation additionally increased colonic contractility and produced diarrhea-like fluid secretion, indicating that these two neuronal subtypes act through distinct physiological pathways despite some overlapping effects.
The findings show that distinct subsets of peripheral, gut-associated neurons can independently shape microbiome composition and gastrointestinal physiology without requiring signals from the brain. This suggests the enteric and peripheral nervous system directly sculpts microbial ecology, including bacterial and fungal populations and bile acid metabolism, rather than the microbiome being shaped only by diet or host genetics. Because different neuron subtypes produce different physiological outcomes (fecal output alone versus contractility and diarrhea-like secretion), this points to neuron-specific pathways as potential targets for understanding or treating GI motility and secretory disorders.
The composition of the microbial community in the intestine may influence the functions of distant organs such as the brain, lung, and skin. These microbes can promote disease or have beneficial functions, leading to the hypothesis that microbes in the gut explain the co-occurrence of intestinal and skin diseases. Here, we show that the reverse can occur, and that skin directly alters the gut microbiome. Disruption of the dermis by skin wounding or the digestion of dermal hyaluronan results in increased expression in the colon of the host defense genes Reg3 and Muc2, and skin wounding changes the composition and behavior of intestinal bacteria. Enhanced expression Reg3 and Muc2 is induced in vitro by exposure to hyaluronan released by these skin interventions. The change in the colon microbiome after skin wounding is functionally important as these bacteria penetrate the intestinal epithelium and enhance colitis from dextran sodium sulfate (DSS) as seen by the ability to rescue skin associated DSS colitis with oral antibiotics, in germ-free mice, and fecal microbiome transplantation to unwounded mice from mice with skin wounds. These observations provide direct evidence of a skin-gut axis by demonstrating that damage to the skin disrupts homeostasis in intestinal host defense and alters the gut microbiome.
This study used shotgun metagenome sequencing to track the taxonomic and functional evolution of the faecal microbiota in piglets during the first two weeks after weaning. It compared three management strategies: in-feed antibiotics, therapeutic zinc oxide, and no medication, in the context of post weaning diarrhoea (PWD), a major driver of antimicrobial use. The goal was to understand how removing these interventions, as required by new EU regulations, affects the piglet gut microbiota and to inform alternative approaches to controlling PWD.
The subjects were post weaning piglets housed on commercial farms that routinely use antimicrobials during the post weaning period. Animals were divided into three experimental groups receiving in-feed antibiotics, therapeutic zinc oxide, or no medication. Faecal samples were collected and analyzed across multiple days post weaning and across multiple farms, though the abstract does not give an exact animal count.
Microbiota diversity was affected by day post weaning, treatment, and diarrhoea status, but not by which farm the pigs were on, and composition shifted toward dominance by groups such as Prevotella spp. by day 14. Zinc oxide inhibited E. coli overgrowth, increased abundance of the family Bacteroidaceae, and decreased Megasphaera spp. Pigs treated with antibiotics showed inconsistent taxonomic changes over time, with an overall rise in Limosilactobacillus reuteri and Megasphaera elsdenii. Non-medicated pigs showed virulence-related functions at day 7 post weaning.
The findings show that zinc oxide has a more consistent, taxonomically defined suppressive effect on E. coli overgrowth than in-feed antibiotics, which produced more variable microbiota changes over time. This distinction is relevant as the EU restricts both interventions and producers seek alternatives to control post weaning diarrhoea. The detection of virulence-related functions in non-medicated pigs early after weaning underscores the vulnerability of the unmedicated microbiota during this period and the need for new, function-informed strategies to manage it.
This study examined the gut microbiome's association with type 2 diabetes (T2D) by analyzing shotgun metagenomic sequencing data. Researchers looked beyond species-level associations to strain-level and phylogenetic diversity within species, aiming to identify specific microbial features and functional pathways linked to T2D. The analysis also explored community-level functional changes, such as perturbations in glucose metabolism, and mechanisms like horizontal gene transfer that could explain strain-specific effects on metabolic risk.
The study drew on 8,117 shotgun metagenomes pooled from 10 cohorts spanning the United States, Europe, Israel, and China. These cohorts included individuals with type 2 diabetes, prediabetes, and normoglycemic (non-diabetic) status. The abstract does not provide individual-level demographic details, but the analysis represents a large, multi-national, cross-cohort metagenomic dataset.
Dysbiosis in 19 phylogenetically diverse species was associated with T2D at a false discovery rate below 0.10, including enrichment of Clostridium bolteae and depletion of Butyrivibrio crossotus. These microorganisms contributed to community-level functional changes, such as perturbations in glucose metabolism, that may underlie T2D pathogenesis. The study further identified within-species phylogenetic diversity across 27 species, such as Eubacterium rectale, that explained inter-individual differences in T2D risk, with some effects attributable to strain-specific gene carriage involved in horizontal gene transfer and other novel biological processes.
By resolving microbial associations with T2D down to the strain level, this work helps explain why prior species-level findings have been inconsistent across studies. Identifying strain-specific gene carriage and functional pathways, including those affecting glucose metabolism, offers a clearer mechanistic basis for how gut microbes may contribute to T2D pathogenesis. This strain-resolved approach could inform future efforts to develop microbiome-based biomarkers or targeted interventions for metabolic disease risk.
Fecal microbiota transplantation (FMT) and fecal virome transplantation (FVT, sterile filtrated donor feces) have been effective in treating recurrent Clostridioides difficile infections, possibly through bacteriophage-mediated modulation of the gut microbiome. However, challenges like donor variability, costly screening, coupled with concerns over pathogen transfer (incl. eukaryotic viruses) with FMT or FVT hinder their wider clinical application in treating less acute diseases.
To overcome these challenges, we developed methods to broaden FVT's clinical application while maintaining efficacy and increasing safety. Specifically, we employed the following approaches: (1) chemostat-fermentation to reproduce the bacteriophage FVT donor component and remove eukaryotic viruses (FVT-ChP), (2) solvent-detergent treatment to inactivate enveloped viruses (FVT-SDT), and (3) pyronin-Y treatment to inhibit RNA virus replication (FVT-PyT). We assessed the efficacy of these processed FVTs in a C. difficile infection mouse model and compared them with untreated FVT (FVT-UnT), FMT, and saline.
FVT-SDT, FVT-UnT, and FVT-ChP reduced the incidence of mice reaching the humane endpoint (0/8, 2/7, and 3/8, respectively) compared to FMT, FVT-PyT, and saline (5/8, 7/8, and 5/7, respectively) and significantly reduced the load of colonizing C. difficile cells and associated toxin A/B levels. There was a potential elimination of C. difficile colonization, with seven out of eight mice treated with FVT-SDT testing negative with qPCR. In contrast, all other treatments exhibited the continued presence of C. difficile. Moreover, the results were supported by changes in the gut microbiome profiles, cecal cytokine levels, and histopathological findings. Assessment of viral engraftment following FMT/FVT treatment and host-phage correlations analysis suggested that transfer of phages likely were an important contributing factor associated with treatment efficacy.
This proof-of-concept study shows that specific modifications of FVT hold promise in addressing challenges related to donor variability and infection risks. Two strategies lead to treatments significantly limiting C. difficile colonization in mice, with solvent/detergent treatment and chemostat propagation of donor phages emerging as promising approaches. Video Abstract.
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.
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.
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.
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.
This study examined whether a history of repeated, but not recent, antibiotic use has lasting effects on the gut microbiota and on microbiota-mediated intestinal mucus barrier function. Researchers used human-to-mouse fecal microbiota transplantation to transfer gut microbial communities from previously antibiotic-exposed and healthy individuals into mice. They then measured mucus growth rate and mucus penetrability using ex vivo analyses of viable colonic tissue explants, and characterized the transplanted microbiota using shotgun metagenomic sequencing and metabolite profiling.
The human source population was drawn from the deeply phenotyped Estonian Microbiome Cohort (EstMB), from which individuals with a history of repeated antibiotic use and healthy controls were selected for fecal sampling. The functional experiments were then carried out in mice that received fecal microbiota transplants from these human donors, so the mucus and microbiota outcomes reported reflect this humanized mouse model rather than direct measurements in the human donors themselves.
Mice transplanted with microbiota from humans with a history of repeated antibiotic use showed a reduced mucus growth rate and increased mucus penetrability compared to mice given microbiota from healthy controls. Shotgun metagenomic sequencing showed the antibiotic-shaped microbial community had a significantly altered composition, with mucus-utilizing bacteria, including Akkermansia muciniphila and Bacteroides fragilis, dominating the gut. This altered microbiota was also marked by a distinct metabolite profile.
The findings suggest that repeated antibiotic use can leave a lasting, microbiota-encoded imprint on the gut that impairs the mucus barrier long after the antibiotics themselves are gone. Because a healthy mucus layer normally protects the intestinal epithelium against infection and inflammation, this microbiota-driven thinning and increased penetrability could plausibly raise vulnerability to gut infection or inflammatory conditions. The dominance of mucus-utilizing organisms such as Akkermansia muciniphila and Bacteroides fragilis points to microbial mucus consumption as a candidate mechanism linking antibiotic history to barrier dysfunction, warranting further mechanistic study.
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.
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.
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.
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.
The gut microbiota of infants in low- to middle-income countries is underrepresented in microbiome research. This study explored the faecal microbiota composition and faecal cytokine profiles in a cohort of infants in a rural province of Cambodia and investigated the impact of sample storage conditions and infant environment on microbiota composition. Faecal samples collected at three time points from 32 infants were analysed for microbiota composition using 16S rRNA amplicon sequencing and concentrations of faecal cytokines. Faecal bacterial isolates were subjected to whole genome sequencing and genomic analysis. We compared the effects of two sample collection methods due to the challenges of faecal sample collection in a rural location. Storage of faecal samples in a DNA preservation solution preserved Bacteroides abundance. Microbiota analysis of preserved samples showed that Bifidobacterium was the most abundant genus with Bifidobacterium longum the most abundant species, with higher abundance in breast-fed infants. Most infants had detectable pathogenic taxa, with Shigella and Klebsiella more abundant in infants with recent diarrhoeal illness. Neither antibiotics nor infant growth were associated with gut microbiota composition. Genomic analysis of isolates showed gene clusters encoding the ability to digest human milk oligosaccharides in B. longum and B. breve isolates. Antibiotic-resistant genes were present in both potentially pathogenic species and in Bifidobacterium. Faecal concentrations of Interlukin-1alpha and vascular endothelial growth factor were higher in breast-fed infants. This study provides insights into an underrepresented population of rural Cambodian infants, showing pathogen exposure and breastfeeding impact gut microbiota composition and faecal immune profiles.
This study examined how gut microbiota and their metabolites change during acute pancreatitis (AP), an inflammatory disease of the pancreas that currently lacks effective therapy. The researchers used metagenomic sequencing to profile gut bacterial communities and metabolomic sequencing to profile metabolites, then applied correlation analysis to clarify how the two systems interact. KEGG pathway analysis was used to connect differential bacteria and metabolites to specific metabolic functions.
The study was conducted using three distinct AP mouse models rather than human subjects. Each model was constructed specifically to allow comparison of gut microbiota and metabolite profiles across different disease conditions. No human cohort, sample size, or patient population is described in the abstract.
Each AP mouse model exhibited a unique flora and metabolite profile, with differential bacteria and metabolite-enriched pathways correlating with lipid metabolism and amino acid metabolism. Two bacterial species, Burkholderiales bacterium YL45 and Bifidobacterium pseudolongum, emerged as core differential species across the models. Eleven differential metabolites were also identified as appearing to exert effects during the course of AP.
By mapping the crosstalk between gut microbiota and their derived metabolites, the study suggests specific bacterial species and metabolites, especially those tied to lipid and amino acid metabolism, may play mechanistic roles in AP development. This integrated metagenomic-metabolomic approach could inform new diagnostic markers and treatment strategies for AP. Further exploration of this microbiota-metabolite relationship is proposed as a route to novel clinical insights.
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.
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.
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.
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.
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.
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.
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.
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.
Gut microbiota are associated with the pathological features and development of colorectal cancer (CRC); however, how gut microbiota changes in patients with CRC is unknown. This study investigated the role of gut microbiota in the development and progression of CRC by retrospectively comparing the structural differences between the gut microbiota of patients with CRC and healthy individuals.
Together with clinical data, we collected fecal samples from patients with CRC (n = 18) and healthy controls (n = 18) and performed 16S rRNA gene sequencing and alpha and beta diversity analysis to compare microbiota richness and diversity. Based on the differences in microbiota between the CRC and control groups, we identified disease-specific microbial communities after relevant factors. PICRUSt2 software was used to predict the differential microbial functions.
The CRC and control groups differed in both composition and abundance of intestinal microbiota. Firmicutes and Bacteroidetes were the most abundant phyla in both groups, while Verrucomicrobi was significantly more abundant in the CRC group. Megamonas, Lachnospira, and Romboutsia were more abundant in the control group; 18 genera differed significantly in abundance between the groups, which were found to involve 21 metabolic pathways. The distribution and abundance of gut microbiota differed significantly between patients with CRC with and without lymph node metastasis; at the genus level, the abundance of Rothia and Streptococcus was significantly higher and that of Bacteroides, Parabacteroides, and Oscillibacter was significantly lower in patients with lymph node metastasis.
The gut microbiota is altered in CRC patients compared with healthy individuals, with specific changes in the microbiota associated with clinical and pathological features such as tumor stage, lymph node involvement, and tumor differentiation. Our findings elaborate to some extent on the link between the gut microbiota and CRC.
This study examined whether appendectomy raises colorectal cancer (CRC) risk by disturbing the gut microbiome. The researchers combined a population-based longitudinal analysis with shotgun metagenomic sequencing of fecal samples to characterize microbial changes after appendectomy. They then tested whether appendectomy directly promotes colorectal tumorigenesis using a mouse model, and examined microbial network structure to identify which bacteria most strongly organize the post-appendectomy community.
Cohort 1 was a large population-based longitudinal group of 129,155 individuals followed for up to 20 years to assess CRC incidence after appendectomy. Cohort 2 consisted of 314 people whose fecal samples underwent shotgun metagenomic sequencing to compare gut microbial composition between appendectomy subjects and controls. The mouse tumorigenesis experiments used an animal model to test causality, as described in the abstract.
Appendectomy was associated with a 73.0 percent increase in CRC risk over 20 years of follow-up (adjusted SHR 1.73, 95% CI 1.49-2.01, P < 0.001). Metagenomic sequencing showed appendectomy subjects had enrichment of seven CRC-promoting bacteria, including Bacteroides fragilis (B. fragilis), Bacteroides vulgatus, Veillonella dispar, and several Prevotella species, alongside depletion of five beneficial commensals such as Collinsella aerofaciens and multiple Blautia species. Microbial network analysis revealed stronger correlations among the enriched, oncogenic-pathway-associated bacteria in appendectomy subjects, with B. fragilis occupying the central, most connected position in this network. Mouse experiments confirmed that appendectomy promoted colorectal tumorigenesis through its effects on the gut microbiome.
These findings suggest appendectomy is not a neutral procedure with respect to long-term colorectal cancer risk, and that this risk may be mediated by a shift toward a CRC-promoting, B. fragilis-centered microbial network. Because B. fragilis functioned as the hub of this altered network, it may represent a key node for monitoring or intervention in post-appendectomy patients. The mouse data support a causal, not merely correlational, link between appendectomy-driven dysbiosis and tumorigenesis, strengthening the rationale for microbiome surveillance in this population.
This study investigated the microbiome associated with ovarian cancer (OC) and its potential role in detection, disease progression, and prognosis. Researchers examined microbial taxa across multiple body sites in OC patients compared with a benign cohort. The aim was to identify microbial indicators that could aid early detection, track disease stage and grade, and predict treatment response.
The abstract does not give a specific cohort size or demographic description. It describes an OC patient cohort compared against a benign cohort, with sampling across several body sites; stool and omentum were sampled in the OC cohort but not in the benign cohort. Beyond this, the population can only be described in general terms as ovarian cancer patients versus patients with benign gynecological conditions.
The researchers identified a distinct OC microbiome with general enrichment of several microbial taxa, including Dialister, Corynebacterium, Prevotella, and Peptoniphilus, across body sites in the OC cohort. These same taxa were depleted in advanced-stage and high-grade OC patients compared with early-stage and low-grade patients, suggesting decreased accumulation as disease advances. The mainly pathogenic taxa were also more abundant in OC patients with adverse treatment outcomes compared to those without treatment-related events.
The enrichment and depletion patterns of these taxa suggest they could serve as potential indicators for early detection of ovarian cancer. Their accumulation in patients with adverse treatment outcomes suggests they could also help predict how patients will respond to treatment. Together these findings point to a possible diagnostic and prognostic role for the OC-associated microbiome, though the abstract does not describe validation in an independent cohort.
Research on the gut microbiota in irritable bowel syndrome (IBS) shows discordant results due to inconsistent study designs or small sample sizes. This study aimed to characterize how gut microbiota in IBS patients differs from that in healthy controls by performing a case-control study and cross- and mega-cohort analysis. Multiple publicly shared data sets were examined by using a unified analytical approach. We performed 16S rRNA gene (V3-4) sequencing and taxonomic profiling of the gut bacterial communities. Fecal samples from children with IBS (n = 19) and age-matched healthy controls (n = 24) were used. Next, we analyzed 10 separate data sets using a unified data-processing and analytical approach. In total, 567 IBS patients and 487 healthy controls were examined. In our data sets, no significant differences existed in stool α-diversity between IBS patients and healthy controls. After combining all the data sets using a unified data-processing method, we found significantly lower α-diversity in IBS patients than in healthy controls. In addition, the relative abundance of 21 bacterial species differed between the IBS patients and healthy participants. Although the causal relationship is uncertain, gut bacterial dysbiosis is associated with IBS. Further functional studies are needed to assess whether the change in gut microorganisms contributes to the development of IBS. IMPORTANCE Research on the gut bacteria in irritable bowel syndrome (IBS) shows discordant results due to inconsistent study designs or small sample sizes. To overcome these issues, we analyzed microbiota of 567 IBS patients and 487 healthy people from 10 shared data sets using a unified method. We demonstrated that gut bacteria are less diverse in IBS patients than in healthy people. In addition, the abundance of 21 bacterial species is different between the two groups. Altered bacterial balance, called dysbiosis, has been reported in several disease states. Although the causal relationship is uncertain, gut bacterial dysbiosis also seems to be associated with IBS.
Plant-based diets offer more beneficial microbes and can modulate gut microbiomes to improve human health. We evaluated the effects of the plant-based OsomeFood Clean Label meal range ('AWE' diet), on the human gut microbiome.
Over 21 days, ten healthy participants consumed OsomeFood meals for five consecutive weekday lunches and dinners and resumed their regular diets for other days/meals. On follow-up days, participants completed questionnaires to record satiety, energy and health, and provided stool samples. To document microbiome variations and identify associations, species and functional pathway annotations were analyzed by shotgun sequencing. Shannon diversity and regular diet calorie intake subsets were also assessed.
Overweight participants gained more species and functional pathway diversity than normal BMI participants. Nineteen disease-associated species were suppressed in moderate-responders without gaining diversity, and in strong-responders with diversity gains along with health-associated species. All participants reported improved short-chain fatty acids production, insulin and γ-aminobutyric acid signaling. Moreover, fullness correlated positively with Bacteroides eggerthii; energetic status with B. uniformis, B. longum, Phascolarctobacterium succinatutens, and Eubacterium eligens; healthy status with Faecalibacterium prausnitzii, Prevotella CAG 5226, Roseburia hominis, and Roseburia sp. CAG 182; and overall response with E. eligens and Corprococcus eutactus. Fiber consumption was negatively associated with pathogenic species.
Although the AWE diet was consumed for only five days a week, all participants, especially overweight ones, experienced improved fullness, health status, energy and overall responses. The AWE diet benefits all individuals, especially those of higher BMI or low-fiber consumption.
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.
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.
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.
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.
This study investigated the duodenal mucosa-associated microbiota and its surrounding microenvironment in relation to hyperglycemia, an area far less studied than stool microbiota in metabolic disease. The researchers compared paired stool and duodenal microbial samples between hyperglycemic and normoglycemic individuals. They also assessed the duodenal microenvironment directly by measuring tissue oxygen saturation, serum inflammatory markers, and zonulin as a marker of gut permeability. The goal was to determine whether duodenal, rather than stool, microbial changes track more closely with glycemic status.
The study population consisted of 33 subjects with hyperglycemia, defined as HbA1c of 5.7% or higher and fasting plasma glucose above 100 mg/dl, compared against 21 normoglycemic subjects. Both groups contributed paired stool and duodenal samples, allowing direct comparison of microbiota across two body sites within the same individuals. No further demographic details are given in the abstract.
Hyperglycemic subjects had a significantly higher duodenal bacterial count than normoglycemic subjects, along with increased pathobionts and reduced beneficial flora. This bacterial overload correlated with elevated serum zonulin and higher TNF-alpha, suggesting a link to increased gut permeability and inflammation. The hyperglycemic group also showed reduced duodenal oxygen saturation, higher total leukocyte count, and lower IL-10, indicating a systemic proinflammatory state. Notably, unlike stool flora, duodenal bacterial profile variability was specifically associated with glycemic status.
These findings suggest the duodenal microbiome and its local microenvironment, rather than stool alone, may play a distinct role in the pathogenesis of hyperglycemia and prediabetes. The association between bacterial overload, reduced oxygen saturation, and systemic inflammatory markers points to a possible mechanistic pathway linking small intestinal dysbiosis to metabolic dysfunction. This work highlights the duodenum as an underexplored but potentially important site for understanding and possibly intervening in early glycemic disturbances.
Antibiotic-induced gut microbiome dysbiosis (AID) is known to be influenced by host dietary composition. However, how and when diet modulates gut dysbiosis remains poorly characterized. Thus, here, we utilize a multi-omics approach to characterize how a diet supplemented with oats, a rich source of microbiota-accessible carbohydrates, or dextrose impacts amoxicillin-induced changes to gut microbiome structure and transcriptional activity. We demonstrate that oat administration during amoxicillin challenge provides greater protection from AID than the always oats or recovery oats diet groups. In particular, the group in which oats were provided at the time of antibiotic exposure induced the greatest protection against AID while the other oat diets saw greater effects after amoxicillin challenge. The oat diets likewise reduced amoxicillin-driven elimination of Firmicutes compared to the dextrose diet. Functionally, gut communities fed dextrose were carbohydrate starved and favored respiratory metabolism and consequent metabolic stress management while oat-fed communities shifted their transcriptomic profile and emphasized antibiotic stress management. The metabolic trends were exemplified when assessing transcriptional activity of the following two common gut commensal bacteria: Akkermansia muciniphila and Bacteroides thetaiotaomicron. These findings demonstrate that while host diet is important in shaping how antibiotics effect the gut microbiome composition and function, diet timing may play an even greater role in dietary intervention-based therapeutics. IMPORTANCE We utilize a multi-omics approach to demonstrate that diets supplemented with oats, a rich source of microbiota-accessible carbohydrates, are able to confer protection against antibiotic-induced dysbiosis (AID). Our findings affirm that not only is host diet important in shaping antibiotics effects on gut microbiome composition and function but also that the timing of these diets may play an even greater role in managing AID. This work provides a nuanced perspective on dietary intervention against AID and may be informative on preventing AID during routine antibiotic treatment.
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.
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.
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.
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.
This study examined whether the gut microbiome differs in young children with airway allergic disease compared with healthy children. Researchers used high-throughput metagenomic shotgun gene sequencing on fecal samples to characterize the gut microbiota at both the phylum and genus levels. The goal was to identify unique gut microbial features associated with allergic asthma and allergic rhinitis in children.
The study included three groups of children: those with allergic asthma (n = 23), those with allergic rhinitis (n = 18), and healthy controls (n = 19). Fecal samples were collected from each child for shotgun metagenomic analysis. No further demographic details, such as age range or geographic location, are given in the abstract.
Children with allergic asthma and allergic rhinitis showed increased gut microbial richness and diversity compared with healthy controls, with Simpson and Shannon diversity indices significantly elevated in the asthma group. Principal coordinates analysis showed that gut microbial community clustering in both allergic groups differed significantly from healthy controls, though asthma and rhinitis groups did not differ significantly from each other. At the phylum level, Firmicutes was enriched and Bacteroidetes was reduced in both allergic groups, while at the genus level Corynebacterium, Streptococcus, Dorea, Actinomyces, Bifidobacterium, Blautia, and Rothia were significantly enriched in the allergic children. The abstract does not mention Candida, fungi, yeast, or the mycobiome.
The findings support a link between gut microbiome composition and airway allergic disease in children, suggesting the gut-lung axis may play a role in asthma and rhinitis development. The shared microbial alterations across asthma and rhinitis groups suggest a common underlying gut dysbiosis pattern rather than disease-specific signatures. These bacterial taxa could serve as candidate biomarkers or targets for future microbiome-directed strategies in pediatric airway allergic disease, pending further mechanistic and validation studies.
This study examined the role of gut microbiome changes in mediating the effects of a dietary intervention on the frequency and severity of postmenopausal vasomotor symptoms
Postmenopausal women (n = 84) reporting ≥2 moderate-to-severe hot flashes daily were randomly assigned, in 2 successive cohorts, to an intervention including a low-fat, vegan diet and cooked soybeans (½ cup [86 g] daily) or to stay on their usual diet. Over a 12-week period, frequency and severity of hot flashes were recorded with a mobile application. In a subset of 11 women, gut microbiome was analyzed at baseline and after 12 weeks of the dietary intervention (low-fat vegan diet with soybeans), using deep shotgun metagenomic sequencing. Differences in the microbiome between baseline and 12 weeks were assessed by comparing alpha diversity with Wilcoxon signed rank tests, beta diversity with permanovaFL, and taxon abundance with Wilcoxon signed rank tests. Pearson correlations were used to assess the association between changes in hot flashes and gut bacteria.
In the subset for which microbiome testing was done, total hot flashes decreased by 95 % during the dietary intervention (p = 0.007); severe hot flashes disappeared (from 0.6 to 0.0/day; p = 0.06); and moderate-to-severe hot flashes decreased by 96 % (p = 0.01). Daytime and nighttime hot flashes were reduced by 96 % (p = 0.01) and 94 % (p = 0.004), respectively. Alpha and beta diversity did not significantly differ in the intervention group between baseline and 12 weeks. Two families (Enterobacteriaceae and Veillonellaceae), 5 genera (Erysipelatoclostridium, Fusicatenibacter, Holdemanella, Intestinimonas, and Porphyromonas), and 6 species (Clostridium asparagiforme, Clostridium innocuum, Bacteroides thetaiotaomicron, Fusicatenibacter saccharivorans, Intestinimonas butyriciproducens, Prevotella corporis, and Streptococcus sp.) were differentially abundant, but after correction for multiple comparisons, these differences were no longer significant. Changes in the relative abundance of Porphyromonas and Prevotella corporis were associated with the reduction in severe day hot flashes both unadjusted (r = 0.61; p = 0.047; and r = 0.69; p = 0.02), respectively), and after adjustment for changes in body mass index (r = 0.63; p = 0.049; and r = 0.73; p = 0.02), respectively). Changes in relative abundance of Clostridium asparagiforme were associated with the reduction in total severe hot flashes (r = 0.69; p = 0.019) and severe night hot flashes (r = 0.82; p = 0.002) and the latter association remained significant after adjustment for changes in body mass index (r = 0.75; p = 0.01).
This exploratory analysis revealed potential associations between changes in vasomotor symptoms in response to a diet change and changes in the gut microbiome. Larger randomized clinical trials are needed to investigate these findings.
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.
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.
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.
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.
This study used metagenomic shotgun sequencing to characterize the oral microbiota, antibiotic resistance genes (ARGs), and virulence genes (VirGs) associated with periodontitis. The researchers examined shifts in microbial community composition and functional pathways in periodontitis compared with controls. They also analyzed selection pressure on ARGs and VirGs using the Ka/Ks ratio to determine whether these genes were being positively selected in the oral microbiome.
The abstract describes periodontitis patients compared with control subjects, though it does not specify exact sample sizes or demographic details. The researchers combined their own metagenomic sequencing data with a previously published periodontitis dataset for the gene selection analysis. No cohort age range, geographic origin, or recruitment setting is given in the abstract.
Periodontitis patients showed a significant shift in oral microbiota composition along with several functional pathways that were more abundant than in controls. Several ARGs and VirGs showed evidence of positive selection (Ka/Ks ratio greater than 1) across both datasets analyzed. Notably, 5 of 12 positively selected ARGs and VirGs found in periodontitis patients were also present in the genomes of respiratory tract pathogens, and most background VirGs carried non-synonymous mutations consistent with natural selection.
The overlap between positively selected virulence and resistance genes in periodontal bacteria and respiratory pathogens suggests a possible mechanistic link between periodontitis and respiratory infection. This raises the possibility that oral microbial communities could act as a reservoir for genes that enhance virulence or antibiotic resistance in distant infection sites. The findings support closer surveillance of oral microbiota as a factor in respiratory disease risk and antibiotic resistance spread, though further studies are needed to establish causality.
This prospective, observational study examined whether gut microbiota composition is associated with immune responses and adverse events following COVID-19 vaccination. Researchers compared two vaccine types: the inactivated CoronaVac vaccine and the mRNA BNT162b2 vaccine. They performed shotgun metagenomic sequencing on stool samples collected at baseline and again one month after the second vaccine dose. Immune responses were assessed using a SARS-CoV-2 surrogate virus neutralisation test and a spike receptor-binding domain IgG ELISA.
The study included 138 adult COVID-19 vaccine recipients, of whom 37 received CoronaVac and 101 received BNT162b2. Stool samples from these vaccinees were collected at two time points, baseline and one month post second dose, for shotgun metagenomic analysis. The abstract does not specify additional demographic details such as age range, sex distribution, or geographic location.
Immune responses were significantly lower in CoronaVac recipients than in BNT162b2 recipients. Among CoronaVac vaccinees, higher persistent levels of Bifidobacterium adolescentis were associated with higher neutralising antibody responses, and their baseline gut microbiome was enriched in carbohydrate metabolism pathways. In BNT162b2 vaccinees, neutralising antibody levels correlated positively with the total abundance of flagellated and fimbriated bacteria, including Roseburia faecis. Prevotella copri and two Megamonas species were enriched in individuals who experienced fewer adverse events after vaccination.
These findings suggest that baseline gut microbiota composition and function may help explain individual variation in vaccine immunogenicity and tolerability. Specific taxa, such as Bifidobacterium adolescentis, Roseburia faecis, Prevotella copri, and Megamonas species, and microbial functional features like carbohydrate metabolism pathways and flagellar or fimbrial machinery, appear linked to stronger antibody responses or fewer adverse events. This raises the possibility that gut microbiome profiling or modulation could eventually inform strategies to improve vaccine efficacy or reduce adverse events. Further research is needed to determine whether these associations are causal and generalizable across vaccine platforms and populations.
Nonalcoholic fatty liver disease (NAFLD) is the most common form of liver disease and is often the precursor for more serious liver conditions such as nonalcoholic steatohepatitis and cirrhosis. Although the gut microbiome has been implicated in the development of NAFLD, the strong association of obesity with NAFLD and its effect on microbiome structure has made interpreting study outcomes difficult. In the present study, we examined the taxonomic and functional differences between the microbiomes of youth with obesity and with and without NAFLD. Shotgun metagenome sequencing was performed to profile the microbiomes of 36 subjects, half of whom were diagnosed with NAFLD using abdominal magnetic resonance imaging. Beta diversity analysis showed community-wide differences between the groups (p = 0.002). Specific taxonomic differences included increased relative abundances of the species Fusicatenibacter saccharivorans (p = 0.042), Romboutsia ilealis (p = 0.046), and Actinomyces sp. ICM47 (p = 0.0009), and a decrease of Bacteroides thetaiotamicron (p = 0.0002), in the NAFLD group as compared with the non-NAFLD group. At the phylum level, Bacteroidetes (p < 0.0001) was decreased in the NAFLD group. Functionally, branched-chain amino acid (p = 0.01343) and aromatic amino acid (p = 0.01343) synthesis pathways had increased relative abundances in the NAFLD group along with numerous energy use pathways, including pyruvate fermentation to acetate (p = 0.01318). Conclusion: Community-wide differences were noted based on NAFLD status, and individual bacterial species along with specific metabolic pathways were identified as potential drivers of these differences. The results of the present study support the idea that the NAFLD phenotype displays a differentiated microbial and functional signature from the obesity phenotype.
This study examined how pharmacologically induced weight loss affects the gut microbiome in obese rats. Researchers treated obese female Wistar rats for 42 days with a panel of weight-loss drugs, including sibutramine, bupropion, naltrexone, and tacrolimus (FK506), given alone or in combination. Using shotgun metagenomic sequencing, they measured taxonomic and functional changes in the faecal microbiome alongside physiological outcomes such as body weight, food intake, and glucose tolerance.
The subjects were obese female Wistar rats maintained on a high-fat diet, studied across two cohorts of about 10 to 12 animals each, for a total of 82 rats. This was an animal model of pharmacologically induced weight loss, not a human cohort. The rats' faecal microbiome was profiled before and after the 42-day drug treatment period.
Only sibutramine produced consistent weight loss and improved glycaemic control among the four drugs tested. Sibutramine-associated weight loss coincided with reduced food intake and distinct faecal microbiome shifts, including increased beta-diversity and increased relative abundance of multiple Bacteroides species. The Bacteroides-to-Firmicutes ratio rose, and genes and pathways linked to obesity-induced inflammation changed, particularly those encoding the bacterial flagellum and its assembly.
The findings suggest that effective pharmacological weight loss can reshape the gut microbiome in ways that parallel reduced obesity-associated inflammation. The shift toward higher Bacteroides abundance and altered flagellum-related bacterial genes points to specific microbial mechanisms that may accompany metabolic improvement. This dataset offers a foundation for exploring how weight-loss drugs and the gut microbiome interact to influence metabolic health, though findings from this rat model would need confirmation in humans.
This study examined how delivery mode shapes the early gut microbiota of newborns using high-resolution shotgun sequencing. Researchers tracked the composition and dynamics of the neonatal gut microbiome over the first month of life. The design specifically compared elective cesarean section against vaginal delivery to sidestep the confounding effect of emergency cesareans, which can muddy conclusions about delivery mode's true influence.
The cohort consisted of Tunisian newborns, with stool samples collected from 5 infants born by elective cesarean section and 5 born vaginally. Samples were taken longitudinally at Day 0, Day 15, and Day 30 after birth. This is a small, delivery-mode-stratified newborn cohort rather than a large population sample.
Bacterial richness and diversity were similar between the elective cesarean and vaginally delivered groups, and both showed a shift in microbiota community composition during the first two weeks regardless of delivery mode. Both groups were dominated by Proteobacteria, Actinobacteria, and Firmicutes. However, starting from the second week, cesarean-delivered infants showed an underrepresentation of Bacteroides alongside an enrichment of opportunistic pathogenic species belonging to the ESKAPE group.
The findings suggest that even elective, non-emergency cesarean delivery is associated with a distinct early gut microbiota signature marked by Bacteroides depletion and ESKAPE pathogen enrichment, not merely overall diversity differences. This points to delivery mode as an independent driver of neonatal microbiome composition beyond confounding clinical circumstances. The emergence of opportunistic ESKAPE species by two weeks of age raises questions about potential vulnerability to opportunistic infection in cesarean-born infants that merit further, larger-scale investigation.
Psoriasis is a chronic, inflammatory skin disease that affects 2‒3% of the global population. Besides skin manifestations, patients with psoriasis have increased susceptibility to a number of comorbidities, including psoriatic arthritis, cardiovascular disease, and inflammatory bowel disease. To understand the systemic component of psoriasis pathogenesis, we performed a pilot study to examine the fecal metagenome, host colonic transcriptome, and host peripheral blood immune profiles of patients with psoriasis and healthy controls. Our study showed increased functional diversity in the gut microbiome of patients with psoriasis. In addition, we identified microbial species that preferentially associate with patients with psoriasis and which have been previously found to associate with other autoimmune diseases. Intriguingly, our data revealed three psoriasis subgroups that have distinct microbial and host features. Integrating these features revealed host‒microbe associations that are specific to psoriasis or particular psoriasis subgroups. Our findings provide insight into the factors that may affect the development of comorbidities in patients with psoriasis and may hold diagnostic potential for early identification of patients with psoriasis at risk for these comorbidities.
This study investigated the connection between the oral and gut microbiome in Parkinson's disease (PD) using shotgun metagenomic sequencing. Researchers examined both the taxonomic composition and the functional gene content of these microbial communities. The aim was to determine whether oral microbiome changes relate to gut microbiome changes in PD, and whether these shifts produce functional alterations rather than just compositional differences.
The abstract does not report specific sample sizes, ages, or recruitment details. The study compared PD patients to healthy controls, using paired oral and gut microbiome samples analyzed by shotgun metagenomic sequencing. Beyond the PD-versus-control design, no further cohort characteristics are given in the abstract.
The taxonomic composition of both the oral and gut microbiome differed significantly between PD patients and healthy controls (P = 0.003 and 0.001, respectively). Oral Lactobacillus was more abundant in PD patients and was associated with opportunistic pathogens in the gut (FDR-adjusted P < 0.038). Functionally, microbial gene markers for glutamate and arginine biosynthesis were downregulated, while antimicrobial resistance gene markers were upregulated in PD patients compared to healthy controls (all P < 0.001).
The findings suggest a connection between the oral and gut microbiota in PD that may drive functional, not just compositional, alterations of the microbiome. The rise in oral Lactobacillus alongside opportunistic gut pathogens points to the oral cavity as a potential contributor to gut dysbiosis in PD. Reduced glutamate and arginine biosynthesis and increased antimicrobial resistance gene markers highlight functional microbial pathways that may warrant further investigation as they relate to PD pathophysiology.
This study examined whether non-nutritive sweeteners (NNS), long presumed to be metabolically inert, actually alter the human microbiome and glucose tolerance. The researchers ran a randomized-controlled trial testing four NNS, saccharin, sucralose, aspartame, and stevia, given as sachets for two weeks at doses below the acceptable daily intake. They compared outcomes against control groups receiving vehicle glucose or no supplement, and measured effects on stool and oral microbiome composition, plasma metabolome, and glycemic responses. They also used gnotobiotic mice conventionalized with human donor microbiomes to test whether the microbiome could causally transmit these effects.
The human arm of the study enrolled 120 healthy adults, randomized to receive saccharin, sucralose, aspartame, stevia, vehicle glucose, or no supplement for two weeks. In parallel, the researchers used gnotobiotic mice conventionalized with microbiomes drawn from multiple top and bottom glycemic responders within each of the four NNS-supplemented human groups. This combination allowed comparison of directly treated humans with mice whose only exposure to NNS effects came through transplanted human microbiomes.
Each of the four NNS distinctly altered the stool and oral microbiome and plasma metabolome as a group, even at doses below the acceptable daily intake. Saccharin and sucralose specifically caused significant impairment of glycemic responses in the human participants. When gnotobiotic mice were conventionalized with microbiomes from top and bottom human responders, their glycemic responses largely mirrored those of their respective human donors. Distinct microbial signals, exemplified in the sucralose group, preempted these glycemic outcomes, indicating the microbiome was mechanistically involved rather than merely correlated.
The findings challenge the assumption that non-nutritive sweeteners are metabolically inert, showing instead that they can alter the microbiome and glycemic control even at doses within currently accepted safety limits. Because effects were person-specific and transmissible via microbiome transplantation, individual microbiome composition may determine who experiences adverse glycemic responses to a given sweetener. The authors conclude that these person-specific, microbiome-dependent effects warrant further assessment of their clinical implications for human health.
Chronic kidney disease (CKD) is associated with gut microbiome dysbiosis, but the role of intestinal flora in CKD treatment remains to be elucidated. Fecal microbiota transplantation (FMT) can be utilized to re-establish healthy gut microbiota for a variety of diseases, which offers new insight for treating CKD. First, 5/6 nephrectomy rats (Donor CKD) and sham rats (Donor Sham) were used as donors for FMT, and fecal metagenome were analyzed to explore potential therapeutic targets. Then, to assess the effect of FMT on CKD, sterilized 1/2 nephrectomy rats were transplanted with fecal microbiota from Donor sham (CKD/Sham) or Donor CKD (CKD/CKD) rats, and 1/2 nephrectomy rats without FMT (CKD) or no nephrectomy (Sham) were used as model control or normal control. Results showed that Bacteroides uniformis and Anaerotruncus sp. 1XD22-93 were enriched in Donor CKD, while Lactobacillus johnsonii and Lactobacillus intestinalis were reduced. In addition, the increased abundance of microbial functions included tryptophan metabolism and lysine degradation contributing to the accumulation of protein-bound uremic toxins (PBUTs) in Donor CKD. Genome analysis indicated that FMT successfully differentiated groups of gut microbes and altered specific gut microbiota after 1 week of treatment, with Bacteroides uniformis and Anaerotruncus sp. 1XD22-93 increasing in CKD/CKD group as well as Lactobacillus johnsonii and Lactobacillus intestinalis being improved in CKD/Sham group. In comparison to CKD group, substantial PBUT buildup and renal damage were observed in CKD/CKD. Interestingly, compared to CKD or CKD/CKD group, tryptophan metabolism and lysine degradation were efficiently suppressed in CKD/Sham group, while lysine biosynthesis was promoted. Therefore, FMT considerably reduced PBUTs accumulation. After FMT, PBUTs and renal function in CKD/Sham rats remained the same as in Sham group throughout the experimental period. In summary, FMT could delay the malignant development of CKD by modifying microbial amino acid metabolism through altering the microenvironment of intestinal flora, thereby providing a novel potential approach for treating CKD.
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in children and adolescents. The gut microbiota plays an important role in the pathophysiology of NAFLD through the gut-liver axis. Therefore, we aimed to investigate the genus and species of gut microbiota and their functions in children and adolescents with NAFLD. From May 2017 to July 2018, a total of 58 children and adolescents, including 27 abnormal weight (AW) (obese) NAFLD patients, 16 AW non-NAFLD children, and 15 healthy children, were enrolled in this study at Shenzhen Children's Hospital. All of them underwent magnetic resonance spectroscopy (MRS) to quantify the liver fat fraction. Stool samples were collected and analysed with metagenomics. According to body mass index (BMI) and MRS proton density fat fraction (MRS-PDFF), we divided the participants into BMI groups, including the AW group (n = 43) and the Lean group (n = 15); MRS groups, including the NAFLD group (n = 27) and the Control group (n = 31); and BMI-MRS 3 groups, including NAFLD_AW (AW children with NAFLD) (n = 27), Ctrl_AW (n = 16) (AW children without NAFLD) and Ctrl_Lean (n = 15). There was no difference in sex or age among those groups (p > 0.05). In the BMI groups, at the genus level, Dialister, Akkermansia, Odoribacter, and Alistipes exhibited a significant decrease in AW children compared with the Lean group. At the species level, Megamonas hypermegale was increased in the AW group, while Akkermansia muciniphila, Dialister invisus, Alistipes putredinis, Bacteroides massiliensis, Odoribacter splanchnicus, and Bacteroides thetaiotaomicron were decreased in AW children, compared to the Lean group. Compared with the Control group, the genus Megamonas, the species of Megamonas hypermegale and Megamonas rupellensis, increased in the NAFLD group. Furthermore, the genus Megamonas was enriched in the NAFLD_AW group, while Odoribacter, Alistipes, Dialister, and Akkermansia were depleted compared with the Ctrl_Lean or Ctrl_AW group at the genus level. Megamonas hypermegale and Megamonas rupellensis exhibited a significant increase in NAFLD_AW children compared with the Ctrl_Lean or Ctrl_AW group at the species level. Compared with healthy children, the pathways of P461-PWY contributed by the genus Megamonas were significantly increased in NAFLD_AW. We found that compared to healthy children, the genus Megamonas was enriched, while Megamonas hypermegale and Megamonas rupellensis were enriched at the species level in children and adolescents with NAFLD. This indicates that the NAFLD status and/or diet associated with NAFLD patients might lead to the enrichment of the genus Megamonas or Megamonas species.
This study tracked the co-development of gut microbiomes and metabolomes in mothers and their infants, spanning late pregnancy through the infant's first year of life. Researchers used longitudinal multi-omics data to characterize how microbial communities and their metabolic outputs change and interact over this period. A central focus was mobile genetic elements, the segments of DNA that can move between bacterial species, and how they might transfer from mother to infant. The study also examined infant metabolomes and serum cytokine signatures in relation to feeding type.
The study followed a cohort of 70 mother-infant dyads, or pairs, sampled longitudinally from late pregnancy to the infant's first year. Both maternal and infant gut microbiomes and metabolomes were profiled across this timeframe. Infants were also grouped by feeding method, comparing those who received regular formula, extensively hydrolyzed formula, or exclusive breastfeeding. The abstract does not provide further demographic or geographic details about the cohort.
The researchers discovered large-scale interspecies transfer of mobile genetic elements from mothers to infants, many of which carried genes linked to diet-related adaptations. Infant gut metabolomes were less diverse overall than maternal metabolomes, yet they contained hundreds of unique metabolites and microbe-metabolite associations not seen in the mothers. Metabolomes and serum cytokine signatures differed between infants fed regular formula and those exclusively breastfed, while infants fed extensively hydrolyzed formula did not show this same distinction. These findings indicate that infant gut microbial and metabolic development follows its own distinct trajectory rather than simply mirroring the maternal state.
The findings expand the concept of vertical transmission of the gut microbiome beyond the transfer of whole microbial strains to include mobile genetic elements carrying functionally relevant, diet-related genes. This suggests maternal microbiomes can shape infant microbial capabilities through gene transfer even without direct strain colonization. The feeding-related differences in infant metabolomes and cytokine signatures also point to formula composition, particularly the degree of hydrolysis, as a factor that may influence early immune and metabolic development. Together, these insights could inform how maternal and infant gut ecosystems are considered in supporting healthy immune and cognitive development during the perinatal period.
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.
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.
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.
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.
This study examined the gut microbiota of patients with COVID-19 pneumonia using 16S rRNA gene sequencing performed on rectal swabs. Researchers compared microbial composition and diversity between patients treated in the intensive care unit (i-COVID19), patients treated in infectious disease wards (w-COVID19), and healthy controls (CTRL). The goal was to characterize how gut microbial communities differ across varying levels of COVID-19 disease severity.
The study population consisted of patients hospitalized with COVID-19 pneumonia, divided into two groups by care setting: those admitted to the intensive care unit and those managed in infectious disease wards. These two patient groups were compared against a control group without COVID-19. The abstract does not report exact sample sizes, ages, or other demographic details for these cohorts.
Patients in the ICU showed a decrease in the Chao1 index compared to both controls and ward patients, indicating lower microbial richness in the most severely ill patients, while the Shannon index showed no significant change. At the phylum level, ward patients showed an increase in Proteobacteria compared to controls. Fusobacteria and Spirochetes were both decreased relative to controls, with Spirochetes showing the greatest decrease in ICU patients specifically.
The findings indicate that gut microbial communities shift in composition and richness according to COVID-19 disease severity, with the most pronounced changes occurring in critically ill ICU patients. These preliminary results suggest the gut microbiota may hold promising biomarkers for diagnosing COVID-19 and gauging disease severity. The authors note that validation in larger cohorts could support using microbiota profiles to help stratify patients by severity.
This study examined 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.
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.
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.
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.
This study examined the fecal gut metagenomes of three common intestinal diseases: Crohn's disease, ulcerative colitis, and colorectal cancer. The researchers performed a meta-analysis across 13 separate fecal metagenome data sets spanning these three conditions. Their goal was to identify microbial species and metabolic pathways that change consistently across multiple data sets for each disease, and to compare these signatures across diseases. They also built multidisease diagnostic models based on the markers they identified.
The abstract does not describe a single new patient cohort but rather a meta-analysis pooling 13 existing fecal metagenome data sets covering Crohn's disease, ulcerative colitis, and colorectal cancer patients and controls. No specific sample sizes, ages, or geographic origins are given in the abstract. This can be honestly described as a secondary analysis of multiple public or previously published metagenomic cohorts rather than a single primary study population.
The analysis identified 87 marker species and 65 marker pathways that were consistently altered across multiple data sets of the same disease. These markers grouped into disease-specific and disease-common clusters with distinct phylogenetic relationships: species specific to Crohn's disease were phylogenetically closely related, while colorectal cancer-specific species were more phylogenetically distant from one another. Notably, ulcerative colitis-specific species were phylogenetically closer to colorectal cancer-associated species, consistent with the known elevated colorectal cancer risk in ulcerative colitis patients. Marker species within the same cluster shared metabolic preferences, and disease cases showed more tightly coordinated microbial changes than controls, suggesting a more stressed, selective gut environment in disease states, with a subset of markers also correlating with an indicator of gut barrier (leaky gut) dysfunction.
By mapping how disease-specific and disease-common microbial signatures relate phylogenetically and metabolically, this work supports the development of multidisease diagnostic models that could help distinguish between conditions with overlapping symptoms, such as Crohn's disease, ulcerative colitis, and colorectal cancer. The finding that ulcerative colitis markers resemble colorectal cancer markers phylogenetically offers a microbiome-based rationale for the elevated cancer risk seen in ulcerative colitis. The link between marker species and leaky gut indicators further ties gut dysbiosis to compromised intestinal barrier function. Overall, the study suggests cross-disease microbiome comparisons can sharpen diagnostic precision beyond single-disease marker panels.
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.
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.
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.
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.
This study examined whether gut microbiota composition is associated with fever in patients with moderate COVID-19. Researchers compared clinical features and laboratory results between patients with and without fever, and identified inflammatory markers linked to fever. They then conducted a gut metagenome-wide association study to characterize the microbes and microbial epitopes potentially involved in fever and hyperinflammation.
The cohort included 187 patients with moderate COVID-19, of whom 127 (67.9 percent) presented with fever and the remainder did not. A subset of 31 individuals from this group underwent gut metagenome-wide association analysis to identify microbial features linked to fever and hyperinflammation. The abstract does not provide further demographic details such as age or sex distribution.
Patients with fever showed significantly reduced lymphocytes, CD3+ T cells, CD4+ T cells, and CD4+ to CD8+ T cell ratios, alongside significantly elevated AST, LDH, CRP, IL-6, and IL-10. Gut microbiome composition differed significantly between patients with fever and those without. Opportunistic pathogens, including Enterococcus faecalis and Saccharomyces cerevisiae, were enriched in patients with fever, and E. faecalis abundance was positively correlated with LDH and D-dimer levels.
These findings suggest that gut microbiota dysbiosis, particularly enrichment of opportunistic pathogens such as Enterococcus faecalis, may be linked to the abnormal immune responses and inflammation seen in febrile moderate COVID-19 patients. This raises the possibility that gut microbes or their components contribute to fever and hyperinflammation in this population. The results point to gut microbiota as a potential area of interest for understanding COVID-19 severity and prognosis in moderate cases.
This study examined how gut microbiota composition changes after stroke and whether those changes relate to functional recovery. Researchers compared fecal microbial diversity, composition, and species cooccurrence between stroke patients and healthy controls. They used 16S rRNA gene sequencing (V3-V4 regions) on the Illumina MiSeq platform to characterize the bacterial communities. Random forest and receiver operating characteristic analyses were then applied to identify bacterial genera that might serve as diagnostic biomarkers linked to poststroke outcomes.
The cohort consisted of thirty-eight patients who had experienced a stroke and thirty-five healthy controls matched to the patients by demographics. Fecal DNA was extracted from all participants for microbial sequencing. This was a prospective cohort study comparing a clinical stroke population against a demographically similar healthy comparison group.
Poststroke patients showed significantly higher alpha diversity of gut microbiota than healthy controls. Beta diversity analysis confirmed that overall microbiota composition differed significantly between the two groups. At the genus level, nine genera increased significantly in abundance in poststroke patients, while eighty-two genera decreased significantly, indicating a broad and pronounced shift in the gut microbial community following stroke.
The findings support the existence of a distinct poststroke gut microbiota signature linked to the gut-microbiota-brain axis. Because specific bacterial genera were identified as potential discriminant markers with ties to functional outcomes, gut microbiota profiling may eventually help predict or monitor functional recovery after stroke. This adds to evidence that stroke does not just affect the brain but is accompanied by substantial, measurable disruption of the gut microbial ecosystem.
This study examined whether gut microbiome composition, measured before treatment, is associated with response to immune checkpoint inhibitors in metastatic melanoma. Researchers used metagenomic shotgun sequencing on stool samples collected prior to treatment. The analysis specifically corrected for known confounders of gut microbiome composition, including age, BMI, and antibiotic use, which prior studies had often overlooked. Both taxonomic abundance and survival outcomes were assessed in relation to checkpoint inhibitor response.
The study included 25 patients with unresectable metastatic melanoma who were treated with immune checkpoint inhibitors. Of these, 12 were classified as responders and 13 as non-responders. Pre-treatment stool samples were freshly frozen and analyzed from each of these patients.
Alpha-diversity and overall bacterial prevalence did not differ significantly between responders and non-responders. However, after correcting for confounders in a zero-inflated multivariate analysis, 68 taxa showed differential abundance between the two groups. Carriership of Streptococcus parasanguinis was associated with longer overall survival, and carriership of Bacteroides massiliensis was associated with longer progression-free survival. In contrast, carriership of an unclassified Peptostreptococcaceae species was associated with shorter overall survival.
The findings suggest that simple measures like overall diversity are insufficient to explain gut microbiome links to checkpoint inhibitor outcomes in melanoma, and that confounder-adjusted, species-level analysis reveals associations that broader measures miss. Identifying specific taxa tied to survival, such as Streptococcus parasanguinis and Bacteroides massiliensis, points to candidate biomarkers or mechanistic targets for future investigation. This approach, accounting for confounders like antibiotic use, age, and BMI, may help explain why prior studies lacked consensus on which taxa matter for treatment response.
This study examined whether gut microbiota composition in young children and their mothers is associated with different environmental exposures in a low-income, rural setting. Researchers analyzed faecal samples using 16S rRNA sequencing to characterize bacterial OTU and genus abundances, microbiota maturity, diversity, and UniFrac distances. Environmental exposure variables considered included socio-economic status, water source, sanitary facility, presence of domestic animals, maternal characteristics, season, antibiotic use, and delivery mode. The guiding hypothesis was that more adverse environmental exposures would correspond to lower microbiota maturity and diversity.
The study drew on faecal samples from up to 631 children and their mothers participating in a nutrition intervention trial in rural Malawi. Children were sampled longitudinally at 1, 6, 12, 18, and 30 months of age, while mothers were sampled at 1 month after their child's birth. This is a population from a low-income setting where childhood malnutrition is common, a context the authors note has been understudied for microbiota-environment relationships.
The abstract text describing the results is truncated, so specific quantitative findings on microbiota maturity and diversity in children cannot be reported here. What is stated is that measures of microbiota maturity and diversity in children were examined in relation to the listed environmental exposures using comparisons of OTU and genus abundances and UniFrac distances. No mention of Faecalibacterium prausnitzii, butyrate, or specific anti-inflammatory commensals appears in the provided abstract text.
By linking specific environmental exposures, such as water source, sanitation, domestic animal contact, and antibiotic use, to gut microbiota development in early childhood, this work supports the idea that environmental conditions shape microbiota maturation in low-income settings. Because childhood malnutrition is common in this population, understanding these environment-microbiota relationships could inform strategies to support healthier microbiota development during a critical early-life window. The longitudinal, multi-timepoint design in both children and mothers also provides a framework for tracking how exposures and microbiota composition evolve together over the first years of life.
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.
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.
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.
Healthy subjects of Chinese (n = 12), Malay (n = 12) and Indian (n = 10) ancestry, aged 21-37 years, were enrolled. They provided a baseline stool sample (Day 1) and were then given a course of omeprazole at therapeutic dose (20 mg daily) for seven days. Stool samples were collected again on Day 7 and 14 (one week after stopping omeprazole). Microbial DNA was extracted from the stool samples, followed by polymerase chain reaction, library construction, 16S rRNA sequencing using Illumina MiSeq, and statistical and bioinformatics analyses.
The findings showed an increase in species richness (p = 0.018) after omeprazole consumption on Day 7, which reverted to baseline on Day 14. There were significant increases in the relative abundance of Streptococcus vestibularis (p = 0.0001) and Veillonella dispar (p = 0.0001) on Day 7, which diminished on Day 14. Faecalibacterium prausnitzii, Sutterella stercoricanis and Bacteroides denticanum were characteristic of Chinese, Malays and Indians, respectively. Lactobacillaceae and Bacteroides xylanisolvens were the signature taxa of male and female subjects, respectively.
The study demonstrated alterations in the gut microbiome following omeprazole treatment. This may explain the underlying pathology of increased risk of Clostridium difficile infections associated with omeprazole therapy.
Schizophrenia (SCZ) is a devastating mental disorder with poorly defined underlying molecular mechanisms. The gut microbiome can modulate brain function and behaviors through the microbiota-gut-brain axis. Here, we found that unmedicated and medicated patients with SCZ had a decreased microbiome α-diversity index and marked disturbances of gut microbial composition versus healthy controls (HCs). Several unique bacterial taxa (e.g., Veillonellaceae and Lachnospiraceae) were associated with SCZ severity. A specific microbial panel (Aerococcaceae, Bifidobacteriaceae, Brucellaceae, Pasteurellaceae, and Rikenellaceae) enabled discriminating patients with SCZ from HCs with 0.769 area under the curve. Compared to HCs, germ-free mice receiving SCZ microbiome fecal transplants had lower glutamate and higher glutamine and GABA in the hippocampus and displayed SCZ-relevant behaviors similar to other mouse models of SCZ involving glutamatergic hypofunction. Together, our findings suggest that the SCZ microbiome itself can alter neurochemistry and neurologic function in ways that may be relevant to SCZ pathology.
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.
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.
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.
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.
The study investigated how fecal microbiota metabolize non-digestible oligo- and polysaccharides, using isothermal microcalorimetry to track fermentation in real time. Five substrates were tested: raffinose, melibiose, an oligo- and polysaccharide mixture produced from raffinose by levansucrase, levan synthesized from raffinose, and levan from timothy grass. Growth was assessed from heat evolution curves along with organic acid and gas production, and taxonomic shifts were profiled by 16S rDNA sequencing.
The work used pooled fecal samples as inocula rather than individual human subjects tested directly. Three fecal pools were compared: one from overweight children, one from normal-weight children, and one from healthy adult volunteers. A pure culture of Bacteroides thetaiotaomicron was included as a reference colon bacterium alongside these pooled samples.
Raffinose and melibiose promoted bifidobacteria growth across all three fecal pools, but each pool showed distinct additional responses. In the overweight children's pool, lactate-producing bacteria such as Streptococcus and Enterococcus became enriched, making lactic acid the dominant fermentation product from the short saccharides. In the normal-weight children's pool, acetic and butyric acids predominated instead, coinciding with enrichment of Catenibacterium, while in the adult pool the levans specifically promoted Bacteroides and Lachnospiraceae.
The findings indicate that fecal microbiota from overweight versus normal-weight children ferment the same prebiotic-type substrates into different metabolic end products, not just different taxa. Because overweight children's microbiota favored lactic acid production over the acetate and butyrate seen in normal-weight children, substrate choice and host metabolic status together shape fermentation outcomes. This suggests that prebiotic selection may need to be tailored by weight status or metabolic phenotype rather than applied uniformly across pediatric populations.
This study examined differences in intestinal flora structure between obese and normal-weight school-age children. Researchers used Illumina Miseq next-generation sequencing with 16S rDNA high-throughput sequencing technology to characterize gut bacterial communities. Gut bacteria were classified into Operational Taxonomic Units (OTUs) using the RDP 16S rRNA database and RDP classifier. Both alpha diversity (within-sample diversity) and beta diversity (between-sample dissimilarity) were calculated to compare the two groups.
The study included 39 obese school-age children and 38 normal-weight control children of the same age range. The abstract does not specify the children's exact ages, sex distribution, or geographic location beyond this case-control design. Comparisons were made strictly between these two defined groups based on obesity status.
Intestinal flora in obese children showed lower alpha diversity than in normal-weight controls. Significant differences in the relative abundance of intestinal flora were detected at multiple levels of taxonomic classification. Beta diversity comparisons further confirmed that the microbial community structure differed meaningfully between the obese and normal groups. The abstract does not name specific bacterial taxa or note Faecalibacterium prausnitzii, butyrate, or other anti-inflammatory commensals.
Identifying which specific intestinal bacteria differ between obese and normal-weight children may help clarify the role these organisms play in the development of childhood obesity. This case-control comparison suggests reduced gut microbial diversity could be a feature of pediatric obesity. The findings may support future work aimed at finding new approaches, such as microbiome-targeted strategies, for addressing childhood obesity. Because the abstract's findings section was truncated, further specific implications beyond this general direction cannot be confirmed.
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.
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.
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.
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.
This prospective study examined whether pretreatment gut microbiota and metabolites are associated with response to immune checkpoint inhibitor (ICT) therapy in metastatic melanoma. Patients were treated with ipilimumab, nivolumab, ipilimumab plus nivolumab (IN), or pembrolizumab (P), and response was assessed using Response Evaluation Criteria in Solid Tumors. The study combined metagenomic shotgun sequencing of gut microbiota with unbiased shotgun metabolomic profiling to identify features linked to therapy efficacy. It builds on preclinical work showing specific gut microbiota can promote melanoma regression in mice.
The study included 39 metastatic melanoma patients treated with ICT regimens (ipilimumab, nivolumab, ipilimumab plus nivolumab, or pembrolizumab). The abstract does not provide further demographic details such as age, sex distribution, or geographic site. IN yielded 67% responses and 8% stable disease, while pembrolizumab achieved 23% responses and 23% stable disease among these patients.
Across all therapy types, ICT responders were enriched for Bacteroides caccae in their gut microbiome. Among IN responders specifically, the microbiome was enriched for Faecalibacterium prausnitzii, Bacteroides thetaiotaomicron, and Holdemania filiformis, while pembrolizumab responders showed enrichment of Dorea formicogenerans. Unbiased shotgun metabolomics further revealed high levels of anacardic acid in ICT responders, linking a specific metabolite to treatment response.
The findings suggest that specific gut bacteria, including the anti-inflammatory commensal Faecalibacterium prausnitzii, and metabolites such as anacardic acid may serve as pretreatment indicators of ICT response in melanoma. As a pilot study, the authors state that both additional confirmatory clinical studies and preclinical testing of these bacterial and metabolite associations are needed. If validated, these microbiota and metabolite signatures could inform patient selection or adjunct strategies to improve ICT efficacy, particularly for patients failing standard therapy.
Dysbiosis may play a role in irritable bowel syndrome (IBS), hitherto an enigmatic disorder. We evaluated selected fecal microbes in IBS patients and healthy controls (HC).
Fecal 16S rRNA copy number of selected bacteria was studied using qPCR in 47 patients with IBS (Rome III) and 30 HC.
Of 47 patients, 20 had constipation (IBS-C), 20 diarrhea (IBS-D), and seven unclassified IBS (IBS-U). Relative difference in 16S rRNA copy number of Bifidobacterium (P = 0.042) was lower, while those of Ruminococcus productus-Clostridium coccoides (P = 0.016), Veillonella (P = 0.008), Bacteroides thetaiotamicron (P < 0.001), Pseudomonas aeruginosa (P < 0.001), and Gram-negative bacteria (GNB, P = 0.001) were higher among IBS patients than HC. Number of Lactobacillus (P = 0.002) was lower, while that of Bacteroides thetaiotamicron (P < 0.001) and segmented filamentous bacteria (SFB, P < 0.001) was higher among IBS-D than IBS-C. Numbers of Bacteroides thetaiotamicron (P < 0.001), P. aeruginosa (P < 0.001), and GNB (P < 0.01) were higher among IBS-C and IBS-D than HC. Quantity of SFB was higher among IBS-D (P = 0.011) and lower among IBS-C (P = 0.002) than HC. Number of Veillonella species was higher among IBS-C than HC (P = 0.002). P. aeruginosa was frequently detected among IBS than HC (46/47 [97.9 %] vs. 10/30 [33.3 %], P < 0.001). Abdominal distension (n = 34/47) was associated with higher number of Bacteroides thetaiotamicron, Clostridium coccoides, P. aeruginosa, SFB, and GNB; bloating (n = 22/47) was associated with Clostridium coccoides and GNB. Microbial flora was different among IBS than HC on principal component analysis.
Fecal microbiota was different among IBS than HC, and different sub-types were associated with different microbiota. P. aeruginosa was more frequent and higher in number among IBS patients.
Obesity has become one of the most serious social problems in developed countries, including Japan. The relationship between the gut microbiota and obesity has recently attracted the attention of many researchers. Although the gut microbiota was long thought to contribute to obesity, the exact association remains largely unknown. We examined the human gut microbiota composition in a Japanese population in order to determine its relationship to obesity.
Stool samples from 23 non-obese subjects (body mass index [BMI] <20 kg/m(2)) and 33 obese subjects (BMI ≥25 kg/m(2)) were collected and DNA was extracted prior to colonoscopy. After terminal restriction fragment length polymorphism (T-RFLP) analysis, samples from 10 subjects (4 non-obese and 6 obese) were selected and subjected to next-generation sequencing for species-level analysis.
T-RFLP analysis showed significantly reduced numbers of Bacteroidetes and a higher Firmicutes to Bacteroidetes ratio in obese subjects compared with non-obese subjects. Bacterial diversity was significantly greater in obese subjects compared with non-obese subjects. Next-generation sequencing revealed that obese and non-obese subjects had different gut microbiota compositions and that certain bacterial species were significantly associated with each group (obese: Blautia hydrogenotorophica, Coprococcus catus, Eubacterium ventriosum, Ruminococcus bromii, Ruminococcus obeum; non-obese: Bacteroides faecichinchillae, Bacteroides thetaiotaomicron, Blautia wexlerae, Clostridium bolteae, Flavonifractor plautii).
Gut microbial properties differ between obese and non-obese subjects in Japan, suggesting that gut microbiota composition is related to obesity.
This study examined whether the composition of the intestinal (fecal) microbiota differs in children who have developed beta-cell autoimmunity, marked by diabetes-associated autoantibodies, compared with children who have not. Fecal microbiota composition was profiled using pyrosequencing. The design specifically controlled for secondary effects of diabetes itself and of HLA risk genotype, since prior human data on this question were described as tentative and based on small numbers of subjects.
The study compared children with at least two diabetes-associated autoantibodies (n = 18) to autoantibody-negative children who did not have this autoimmunity. The comparison children were matched to the autoantibody-positive group for age, sex, early feeding history, and HLA risk genotype. The abstract does not give further demographic or geographic detail beyond these matching criteria.
Principal component analysis showed that a low abundance of lactate-producing and butyrate-producing bacterial species was associated with beta-cell autoimmunity. Children with beta-cell autoimmunity also had a dearth of the two most dominant Bifidobacterium species, Bifidobacterium adolescentis and Bifidobacterium pseudocatenulatum, along with an increased abundance of the Bacteroides genus. Despite these microbial differences, the study did not find increased fecal calprotectin or IgA, markers of intestinal inflammation, in the children with beta-cell autoimmunity.
The findings suggest that reduced levels of bifidobacteria and butyrate-producing species could adversely affect intestinal epithelial barrier function, even though no overt inflammatory markers were elevated. Because the design excluded confounding by diabetes onset or HLA genotype, the association between this altered microbiota pattern and beta-cell autoimmunity appears more likely to precede or accompany early autoimmune changes rather than simply result from established disease. The authors call for functional studies to clarify the mechanisms behind these microbiome alterations.
This study compared the diversity, composition, and temporal stability of the distal gut (fecal) microbiota between healthy children living in two very different settings. The researchers used molecular sequencing of the 16S rRNA gene, analyzing over 8,000 near full-length sequences plus more than 845,000 pyrosequencing reads of the V1-V3 region, to characterize which bacteria were present and how communities were structured. The goal was to fill a gap in knowledge, since prior gut microbiome research had focused mostly on infants and adults in developed countries rather than older children in developing countries.
The study compared healthy children ages 9 to 14 years living in an urban slum in Bangladesh with healthy children of the same age range living in an upper-middle class suburban community in the United States. Both groups were sampled for fecal bacterial community composition, and community structure was also tracked over time to assess stability. The abstract does not give an exact number of participants in each cohort.
The distal gut microbiota of Bangladeshi children showed significantly greater bacterial diversity than that of U.S. children, including novel lineages from several bacterial phyla. Bangladeshi and U.S. children also had distinct fecal bacterial community membership and structure overall. The Bangladeshi children's microbiota was enriched in Prevotella, Butyrivibrio, and Oscillospira and depleted in Bacteroides relative to U.S. children, a pattern that was similar to what has been seen in Bangladeshi adults.
These findings show that geography, diet, and living environment are associated with substantial differences in gut microbial diversity and composition even among healthy children of the same age. The presence of novel bacterial lineages and a distinct compositional pattern in Bangladeshi children suggests that microbiome reference data drawn mainly from developed-country populations may not generalize to children in developing countries. This underscores the need to study diverse populations and age groups, including older children and adolescents, when defining what constitutes a healthy gut microbiome.
This study examined whether human intestinal microbes play a role in the autoimmunity that often leads to type 1 diabetes (T1D), building on prior murine and rat models linking gut bacteria to diabetes onset. Researchers used high-throughput, culture-independent sequencing approaches to profile gut bacterial communities over time. They tracked how bacterial composition and diversity changed as autoimmunity developed, comparing children who progressed to T1D-associated autoimmunity with those who did not.
The subjects were young children at high genetic risk for type 1 diabetes. Autoimmune cases were compared over time against age-matched, genotype-matched, nonautoimmune control children. The abstract does not give an exact sample size, but the design followed this at-risk pediatric cohort longitudinally as they moved from infancy toward the toddler stage.
Bacterial diversity diminished over time in children who developed autoimmunity, relative to matched nonautoimmune controls. A single species, Bacteroides ovatus, accounted for nearly 24% of the total increase in the phylum Bacteroidetes in autoimmune cases compared with controls. Conversely, a human Firmicute strain (CO19) represented nearly 20% of the increase in Firmicutes seen in controls over the same period, a pattern opposite to what was seen in cases.
The findings support the idea that healthy infants develop increasingly stable, more diverse microbiomes as they approach toddlerhood, while children destined for autoimmunity show a different, less stable trajectory. This suggests specific microbial shifts, including loss of certain Firmicutes and expansion of Bacteroides ovatus, may be linked to the immune processes preceding type 1 diabetes. The results point toward the gut microbiome as a potential early marker or contributor to autoimmune risk in genetically susceptible children, warranting further work to define an autoimmune-associated microbiome signature.
This study examined how diet shapes gut microbial composition by comparing the fecal microbiota of children eating different diets. Researchers used high-throughput 16S rDNA sequencing together with biochemical analyses to characterize bacterial community composition and short-chain fatty acid output. The design set a fiber-rich, agrarian-style diet against a modern European diet to test whether microbiota differ along with dietary pattern.
The study compared fecal samples from European children (EU) with those from children living in a rural African village in Burkina Faso (BF). The BF children's diet was high in fiber content and described as similar to the diet of early human settlements around the birth of agriculture. Exact sample sizes are not given in the abstract, but the comparison was structured as two defined pediatric cohorts, one European and one rural Burkinabe.
BF children showed significant enrichment in Bacteroidetes and depletion in Firmicutes compared to EU children (P < 0.001). BF children also had a unique abundance of Prevotella and Xylanibacter, genera known to carry genes for cellulose and xylan hydrolysis, which were completely absent in EU children. BF children produced significantly more short-chain fatty acids than EU children (P < 0.001). Enterobacteriaceae, specifically Shigella and Escherichia, were significantly underrepresented in BF children relative to EU children (P < 0.05).
The findings support the idea that gut microbiota coevolved with a polysaccharide-rich diet, helping BF children extract more energy from fiber through bacterial fermentation to short-chain fatty acids. The reduced abundance of Enterobacteriaceae, including Shigella and Escherichia, in the high-fiber BF group suggests diet may also influence the balance between beneficial fiber-degrading bacteria and potentially pathogenic Enterobacteriaceae. Together these results indicate that dietary pattern is a major driver of gut microbial ecology in children, with possible downstream effects on metabolic energy harvest and gut colonization resistance.
2026-07-04
Bacteroides thetaiotaomicron majorTaxon page created: biology (morphology, health role, beneficial factors), its glycan-degrading metabolic role, what depletes it, supportive interventions, the data-derived Conditions table across 72 conditions, and the full research feed.
Schwalm ND, Townsend GE, Groisman EA.
Multiple signals govern utilization of a polysaccharide in the gut bacterium Bacteroides thetaiotaomicron.mBio. 2016
Hiippala K, Jouhten H, Ronkainen A, Hartikainen A, Kainulainen V, Jalanka J, Satokari R.
The potential of gut commensals in reinforcing intestinal barrier function and alleviating inflammation.Nutrients. 2018
Kwain S, Dominy BN, Whitehead KJ, Miller BA, Whitehead DC.
Exploring the interactive mechanism of acarbose with the amylase SusG in the starch utilization system of the human gut symbiont Bacteroides thetaiotaomicron through molecular modeling.Chem Biol Drug Des. 2023
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