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Bacteroides fragilis is a Jekyll-and-Hyde microbe: one of its molecules, polysaccharide A, trains your immune system and calms inflammation, yet toxin-producing strains of the same species are linked to colon cancer.
Bacteroides fragilis is a keystone gut commensal with a dual nature. Its polysaccharide A trains the immune system and protects against colitis, but it is also the most common anaerobic pathogen, and enterotoxigenic strains that make the B. fragilis toxin are linked to colorectal cancer.
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 fragilis is a Gram-negative, obligately anaerobic, bile-resistant rod and a keystone member of the human gut microbiota. Although it makes up only about 0.5 percent of the colonic flora, it is one of the most influential and best-studied gut symbionts, and also the anaerobe most often isolated from human infections.[1] On this database it appears as a differentially abundant taxon across many human microbiome studies, where its meaning depends on which side of its dual nature is in play.
What makes B. fragilis distinctive is that it is both a beneficial partner and a potential pathogen. As a commensal it educates the immune system through a single molecule, polysaccharide A, that induces regulatory T cells and protects against colitis.[2][3] But when it escapes the gut it causes abscesses and bloodstream infections,[1] and enterotoxigenic strains that secrete the B. fragilis toxin are linked to inflammation and colorectal cancer.[4] Reading its signal here means keeping that good-and-bad duality in mind.
B. fragilis is a Gram-negative, obligately anaerobic, non-spore-forming rod with a polysaccharide capsule and notable tolerance of bile, which helps it thrive in the gut.[1] It is saccharolytic, fermenting a wide range of sugars, and carries complex systems to sense and adapt to nutrient availability. Despite making up only about 0.5 percent of the colonic microbiota, its influence on host physiology is outsized.[1]
B. fragilis is the archetype of beneficial host-microbe symbiosis. A single capsular molecule, polysaccharide A (PSA), directs maturation of the host immune system: during colonization it corrects systemic T-cell deficiencies and T helper 1 / T helper 2 imbalances and guides lymphoid development.[2] PSA also protects against experimental colitis by inducing interleukin-10-producing regulatory T cells and suppressing pro-inflammatory interleukin-17, which is why PSA is studied as a candidate therapeutic for inflammatory bowel disease.[3]
B. fragilis has a Jekyll-and-Hyde relationship with the host. In the gut it is a beneficial commensal, but when it breaches the intestinal barrier it becomes the most common anaerobic pathogen, causing abscesses and bacteremia with significant mortality.[1] A distinct subset, enterotoxigenic B. fragilis (ETBF), secretes the B. fragilis toxin (BFT, a zinc metalloprotease also called fragilysin); ETBF drives interleukin-17 inflammation, DNA damage, and tumor formation, and is enriched in the colonic biofilms of colorectal cancer and familial adenomatous polyposis patients.[4] Non-toxigenic strains lack this toxin, and a differential-abundance signal cannot tell the two apart.
Among anaerobes, B. fragilis carries the most antibiotic-resistance mechanisms and the highest resistance rates, with rising resistance to agents including cefoxitin, clindamycin, carbapenems, and fluoroquinolones, plus multiple efflux systems that expel toxic compounds.[1] This makes anaerobic infections involving B. fragilis clinically challenging and susceptibility-guided; this page describes its biology and microbiome associations, not a treatment protocol.
B. fragilis's factors are notably context-dependent: the same capsule that drives abscesses carries the immunomodulatory molecule behind its benefits, and the toxin that defines the harmful ETBF strains is absent from the beneficial ones.
| Virulence factor | Description and role |
|---|---|
| Polysaccharide capsule / PSA | The capsule shields against complement and phagocytosis and is central to abscess formation; yet the same polysaccharide A is the immunomodulatory molecule behind the organism's beneficial effects, a striking case of context-dependent biology.[1][2] |
| B. fragilis toxin (BFT / fragilysin) | A secreted zinc metalloprotease made only by enterotoxigenic strains; it cleaves E-cadherin, triggers interleukin-17 inflammation and DNA damage, and promotes colorectal tumorigenesis.[4] |
| Efflux and resistance systems | Multiple drug-efflux pumps and a large repertoire of resistance genes make B. fragilis the most resistant anaerobic pathogen.[1] |
| Bile tolerance and nutrient sensing | Bile resistance and flexible nutrient sensing let it colonize the gut and, when displaced, survive at other body sites.[1] |
Because B. fragilis is mostly beneficial, the goal is less to attack it than to keep it on its good side. The levers act on its dual nature.
| Lever | Why it matters |
|---|---|
| Toxigenic vs non-toxigenic strain | The decisive distinction is strain-level: non-toxigenic B. fragilis is a beneficial commensal, while ETBF carrying the toxin gene drives inflammation and cancer. The real target is the toxin, not the species.[4] |
| Barrier integrity | B. fragilis turns harmful mainly when it escapes the gut (abscess, bacteremia) or when a leaky, biofilm-laden mucosa lets ETBF act, so supporting barrier integrity keeps it beneficial.[1][4] |
| PSA as a therapeutic | Its beneficial molecule, polysaccharide A, is itself a candidate immunotherapy for inflammatory bowel disease, so B. fragilis is as much a source of interventions as a target.[3] |
For a mostly beneficial commensal, an intervention is anything that keeps B. fragilis on its helpful side or blunts the harm of its enterotoxigenic strains. Everything below is research-stage and is not medical advice; each is classified by our validation method. The through-line is the good-and-bad duality: nurture the commensal, contain the toxin.
| Intervention | Class | Status |
|---|---|---|
| Polysaccharide A (PSA) immunotherapy | Concept | Validation In Progress |
| Support the non-toxigenic commensal | Concept | Validation In Progress |
| Contain enterotoxigenic ETBF / BFT | Concept | Validation In Progress |
| Intervention | Mechanism |
| Polysaccharide A immunotherapy | Purified PSA induces interleukin-10 regulatory T cells and suppresses interleukin-17, protecting against colitis in models, a candidate approach for inflammatory bowel disease.[3] |
| Support the non-toxigenic commensal | A stable non-toxigenic B. fragilis provides the immune education attributed to PSA and competes with harmful strains.[2] |
| Contain enterotoxigenic ETBF / BFT | The colorectal-cancer risk is tied specifically to the toxin-producing strains and their biofilms, so the target is BFT and mucosal biofilm, not the species overall.[4] |
Treating B. fragilis as uniformly good or uniformly bad. The species includes both a beneficial, immune-educating commensal and enterotoxigenic strains linked to colorectal cancer, and standard abundance measures do not separate them.[4]
Where B. fragilis (NCBI:txid817) 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 83 conditions and 109 studies, the signal is genuinely mixed: enriched in 28, depleted in 34, and direction-conflicting in 21 (directional agreement 0.5). Because B. fragilis has a dual beneficial-and-harmful nature and standard profiling cannot separate its strains, its direction in any one condition is hard to interpret in isolation, so the aggregate evidence tier is Low.
How to read these. B. fragilis is a genuine, influential gut resident, so these signals are ecologically real. Two caveats apply. 16S profiling often cannot separate B. fragilis from close relatives in the Bacteroides fragilis group, and it cannot distinguish the beneficial non-toxigenic strains from the enterotoxigenic ETBF strains that carry the toxin. So an enrichment says little on its own about whether the beneficial or the harmful side is at play. This is why direction can conflict between cohorts and the aggregate tier stays Low.
Internal summaries of the 111 studies we reviewed in which B. fragilis was a differential taxon across this corpus.
This pilot study applied an integrative multi-omics workflow to sarcopenia, the age-related loss of muscle mass and strength. Researchers combined plasma metabolomics, lipidomics, and gut microbiome profiling to identify biological signatures linked to the condition. Plasma metabolites and lipids were measured using LC-MS/MS, and a machine-learning model was used to pinpoint the most discriminative metabolites. Gut microbiome composition was assessed via 16S rRNA sequencing and correlated with the metabolite patterns.
The study included forty community-dwelling older adults between 60 and 87 years of age. Participants were classified as sarcopenic (15 people) or non-sarcopenic (25 people) according to EWGSOP2 criteria. Classification relied on dominant hand grip strength, chair rise time, psoas muscle cross-sectional area measured by CT, and the SARC-F questionnaire score.
Dominant hand grip strength was the strongest clinical predictor of sarcopenia, achieving an AUROC of 0.93. Sarcopenic participants showed higher systemic inflammation, reflected in an elevated neutrophil-to-lymphocyte ratio, and higher plasma arachidonic acid levels. Thirteen lipid species, mainly lysophosphatidylcholines, lysophosphatidylethanolamines, and hexosylceramides, differed between groups, pointing to a distinct circulating lipid profile associated with the condition.
These findings suggest that combining simple functional measures like grip strength with plasma lipid and inflammatory markers could improve early detection of sarcopenia. The inflammatory and lipidomic signatures point to specific metabolic pathways, such as arachidonic acid and sphingolipid metabolism, as possible targets for further investigation. Linking microbiome data to these metabolite patterns raises the possibility that gut-derived factors contribute to the metabolic changes seen in sarcopenia. As a pilot study, these results need confirmation in larger cohorts before they can guide clinical practice.
This randomized, double-blind, placebo-controlled trial studied whether a two-strain probiotic combination, Bifidobacterium animalis subsp. lactis XLTG11 and Lactiplantibacillus plantarum CCFM8661, could reduce recurrent respiratory tract infections (RRTIs) in children over 180 days of daily supplementation. Alongside clinical outcomes, the study examined gut microbiota community composition, functional metabolic pathways, and immune biomarkers to understand how the probiotics might be working. The design compared probiotic recipients against a matched placebo group across the same intervention period.
The trial 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, taken daily for 180 days. The abstract does not specify exact age range, sex distribution, or geographic setting beyond this pediatric RRTI cohort.
Children receiving the probiotic combination had significantly reduced duration and frequency of fever, cough, upper respiratory tract infections, trachea/bronchitis, pneumonia, and overall RRTI recurrence compared with placebo (all p < 0.05). Gut microbiota profiling at day 180 showed clear compositional differences between groups, with probiotic recipients showing more beneficial commensal taxa and placebo recipients showing more opportunistic genera. Functional pathway analysis pointed to enhanced metabolic stability in the probiotic group, and immune biomarkers showed comparatively stable IgG, IgM, and complement C3 levels over the intervention period. Growth trajectories remained normal in both groups.
These findings support strain-defined probiotic supplementation, specifically Bifidobacterium animalis subsp. lactis XLTG11 and Lactiplantibacillus plantarum CCFM8661, as a potential preventive strategy for reducing RRTI burden in children. The parallel shifts in gut microbial composition, metabolic pathway activity, and humoral immune stability suggest a plausible gut-immune axis mechanism linking microbiota modulation to fewer respiratory infections. Because growth remained normal, the intervention appears safe over a 180-day period, though the abstract does not address longer-term durability or generalizability beyond this cohort.
This study examined whether gut microbiome composition and microbial metabolite (short-chain fatty acid) profiles differ between youth with type 1 diabetes (T1D) who are lean versus those with obesity. Researchers analyzed stool samples using metagenomic shotgun sequencing to characterize bacterial community differences by body mass index (BMI) group. The work was designed to test the hypothesis that statistically significant gut microbial and metabolite differences exist between lean and obese T1D youth.
The pilot study included 48 youth with type 1 diabetes, 27 classified as lean (BMI 5th to under 85th percentile) and 21 classified as obese (BMI at or above the 95th percentile). Participants had a mean age of 15.3 years, a mean glycated hemoglobin A1c of 7.8%, and a mean diabetes duration of 5.1 years. The group was 42.0% female and 94.0% White.
Bacterial community composition differed significantly between BMI groups, with measurable differences in between-sample diversity (beta-diversity). The obese group showed a significantly higher ratio of Prevotella to Bacteroides compared to the lean group. There was also a differential distribution of significantly abundant taxa between groups, including an increased relative abundance of Prevotella copri, among other taxa, in the obese group. Functional profiling additionally showed differences, though the abstract text describing these functional results is incomplete.
These findings suggest that obesity in youth with T1D is associated with distinct shifts in gut microbial community composition, not just metabolic or clinical differences. The higher Prevotella to Bacteroides ratio and increased Prevotella copri abundance point to specific taxa that may warrant further investigation as markers or contributors to obesity in this population. Because obesity raises the risk of diabetes complications in T1D, understanding these microbial associations could inform future research into microbiome-related risk stratification or intervention strategies in this group.
This study examined how Moderate Acute Malnutrition (MAM) in early childhood relates to the gut microbiome, plasma lipid levels, brain electrical activity, and early language development. Using multi-system SHAP-interpreted random forest models and network analysis, the researchers looked for interconnected biological pathways linking these systems. The goal was to build a mechanistic picture of how malnutrition might give rise to lasting neurocognitive consequences.
The study population was a cohort of one-year-old children in Dhaka, Bangladesh. The abstract does not report an exact sample size. Children were assessed for fecal microbiome composition, plasma lipid profiles, electroencephalogram (EEG) activity, and vocalization as part of the analysis.
MAM was associated with enrichment of fecal Rothia mucilaginosa and Streptococcus salivarius, both oral commensal species, alongside depletion of Bacteroides fragilis. These microbiome shifts formed interconnected pathways linked to reduced plasma odd-chain fatty acid levels, decreased gamma and beta EEG power in temporal and frontal brain regions, and reduced vocalization. The pattern suggests that prolonged colonization of the gut by oral bacteria may coincide with delayed gut microbiome and brain development.
The findings support the hypothesis that oral commensal overgrowth in the gut, alongside loss of species such as Bacteroides fragilis, may delay both microbiome maturation and brain development in malnourished children. Because the fecal microbiome, plasma lipids, and brain activity appear connected through shared pathways, interventions might need to address multiple systems at once rather than gut bacteria alone. The authors note that causal links still require empirical validation, but this work offers a foundation for designing interventions targeting MAM-associated neurodevelopmental deficits.
The study examined how consumption of fermented foods, specifically fermented milk and soybean products, relates to seasonal changes in gut microbiota structure and metabolite composition. Researchers sampled gut microbiota across three seasons: hot-humid summer, autumn, and dry winter. They tracked shifts between two microbial community states, one driven by Prevotella and another driven by Bifidobacterium and Ruminococcus, along with associated fatty acid derivatives. They also examined bimodal changes in Bacteroidota community structure that appeared most pronounced during summer.
The study population was 78 healthy Indian agrarian individuals living in a rural setting. Participants differed in how much fermented milk and soybean products they consumed, and this variation was used to compare microbiota outcomes. Sampling occurred repeatedly across the three seasons to capture within-person seasonal fluctuation rather than a single cross-sectional snapshot.
Gut microbiota shifted seasonally between two ecological states, a Prevotella-driven type and a Bifidobacterium/Ruminococcus-driven type, each linked to distinct fatty acid derivative profiles. Bacteroidota community structure showed a bimodal change during summer, an effect that was particularly evident in people who consumed fermented milk. Long-term consumption of fermented foods was associated with reduced gut microbiota diversity and lower bacterial load overall. The researchers also identified specific taxonomic groups that appeared to drive these seasonal fluctuations and the transitions between the two ecological states.
The findings suggest that habitual fermented food intake can shape how stable or resilient a person's gut microbiota is across seasons, rather than only affecting its composition at one point in time. Identifying the taxa that drive seasonal shifts and ecological-state transitions offers concrete targets for future dietary interventions. The authors frame this as a step toward strategies that could help sustain a healthy and resilient gut microbiota through diet.
This study examined how juicing affects the composition of the gut and oral microbiome. Researchers compared three short-term dietary patterns: an exclusive juice diet, a juice-plus-food diet, and a plant-based food diet, each followed for three days. The work addresses a gap in knowledge about how removing insoluble fiber through juicing might alter microbiota linked to metabolism, immunity, and mental health. Stool, saliva, and inner cheek swab samples were analyzed using 16S rRNA gene amplicon sequencing.
Fourteen participants took part in this intervention study, each assigned to one of the three diet arms (exclusive juice, juice plus food, or plant-based food). Microbiota samples were collected from each participant at multiple timepoints: baseline, after a pre-intervention elimination diet, immediately after the juice intervention, and 14 days later. The abstract does not provide further demographic details such as age range, sex distribution, or health status of the participants.
The saliva microbiome changed significantly in response to the pre-intervention elimination diet, as shown by both unweighted UniFrac (F = 1.72, R = 0.06, p < 0.005) and weighted UniFrac (F = 7.62, R = 0.23, p = 0.0025) analyses. This shift included a significant reduction in Firmicutes abundance. These results indicate that oral microbiota composition responded measurably to dietary changes even before the juice intervention itself began.
The findings suggest that short-term dietary interventions, including elimination diets that precede juicing protocols, can produce measurable and rapid shifts in the oral microbiome. Because the saliva microbiome showed a significant response, oral samples may serve as a sensitive, non-invasive readout for detecting early microbiota changes tied to diet. This raises questions about whether marketed juicing or cleanse diets meaningfully affect microbial communities relevant to health, independent of any fiber loss. Further research is needed to clarify how these oral shifts relate to gut microbiome changes and downstream health outcomes.
This study examined whether balanced energy-protein (BEP) supplementation given to mothers during pregnancy and the first six months of lactation changes the maternal and infant gut microbiome. It was nested within the MISAME-III randomized controlled trial, which originally tested BEP supplementation's effect on small-for-gestational-age prevalence and infant length-for-age Z-scores. The sub-study used metagenomic sequencing of maternal and infant stool to assess microbiome diversity, composition, and function. It also explored whether microbiome changes mediate the trial's effects on birth outcomes and infant growth.
The sub-study included 152 mother-infant dyads from the MISAME-III trial conducted in rural Burkina Faso, with 71 dyads in the BEP intervention group and 81 in the control group. Stool samples were collected from mothers at the second and third trimesters of pregnancy, and from infants at 1 to 2 months and 5 to 6 months postpartum. This design allowed comparison of microbiome trajectories across pregnancy and early infancy between supplemented and non-supplemented mother-infant pairs.
BEP supplementation significantly altered the diversity, composition, and functional pathways of the maternal gut microbiome, particularly pathways with immune-modulatory properties. Lipopolysaccharide biosynthesis pathways were depleted in the gut microbiomes of BEP-supplemented mothers, while the species Bacteroides fragilis was enriched. Maternal BEP supplementation also accelerated changes in the infant gut microbiome and enhanced infant carbohydrate metabolism.
The findings suggest that maternal nutritional supplementation during pregnancy and lactation can shape the maternal gut microbiome in ways that may reduce inflammatory potential, evidenced by depleted lipopolysaccharide biosynthesis pathways and enriched Bacteroides fragilis. Because BEP supplementation also influenced infant microbiome development and carbohydrate metabolism, the maternal gut microbiome may serve as a mediating pathway linking prenatal nutrition to infant growth outcomes. This supports the gut microbiome as a plausible mechanistic target for nutritional interventions aimed at improving birth and early-life outcomes in undernourished populations.
This study pooled gut metagenomic data to identify microbial biomarkers of colorectal cancer (CRC) that hold up across different cancer stages and at the strain level. Researchers combined 12 existing metagenomic datasets with 6 new cohorts that added detailed information on cancer stage and tumor location. The analysis examined whether gut microbiome composition could predict CRC, distinguish tumor location, and track disease progression.
The pooled analysis drew on 3,741 stool metagenomes from 18 cohorts in total. This included 930 patients with CRC, 210 with adenomas, and 976 healthy control individuals from the 12 original datasets (2,116 total), expanded with 6 new cohorts contributing 1,625 additional samples. The new cohorts specifically provided granular data on cancer stage and the anatomic location of tumors.
Combining the larger, more diverse dataset improved CRC prediction accuracy based solely on gut metagenomics, reaching an average area under the curve of 0.85. The analysis identified 19 newly profiled species and distinct Fusobacterium nucleatum clades that contributed to this signal. Specific gut species could also distinguish left-sided from right-sided CRC (area under the curve of 0.66), with right-sided tumors showing enrichment of oral-typical microbes. Strain-level analysis further revealed that subclades of the commensal species Ruminococcus bicirculans and Faecalibacterium prausnitzii were associated with late-stage CRC.
The findings confirm that the gut microbiome can serve as a clinical target for CRC screening, supporting its use as a non-invasive biomarker. Because specific species and strains track with tumor location and cancer stage, the microbiome may also function as a biomarker for CRC progression, not just detection. This suggests future screening tools could be refined using strain-level and location-specific microbial signals rather than broad taxonomic markers alone.
This study examined the relationship between peripheral blood cytokine profiles and gut microbiota composition in Graves' disease (GD), the most common autoimmune thyroid disorder. Researchers used 16S rRNA gene sequencing of fecal samples alongside multiplex cytokine array analysis of blood immune markers. Electrochemiluminescence immunoassay was used to quantify thyroid function parameters, and Spearman correlation analysis linked cytokines, thyroid function indices, and microbial taxa. The goal was to clarify how cellular immunity and gut microbial community dynamics interact in GD pathogenesis.
The study enrolled 30 untreated GD patients consecutively admitted to the Department of Endocrinology at the Third Affiliated Hospital of Qiqihar Medical University between January and July 2023. These patients were compared against 30 age- and sex-matched healthy controls. This case-control design allowed direct comparison of microbiota and cytokine profiles between diseased and healthy individuals.
Alpha diversity analysis showed that the abundance and diversity of certain gut microbiota decreased in the GD group compared to healthy controls. Beta diversity analysis also indicated compositional differences between the two groups, though the abstract's full details on which specific taxa and cytokines correlated were not provided. The study framed gut microbiome alterations as linked to immune marker changes in GD patients, consistent with bidirectional communication between the gut microbiome and host immunity.
These findings support the idea that gut microbiota may act as a modulator of autoimmune pathogenesis in Graves' disease through interaction with cellular immune pathways. Identifying correlations between specific cytokines and microbial taxa could eventually help explain mechanisms driving thyroid autoimmunity. This work lays groundwork for future research into whether modifying the gut microbiome could influence immune dysregulation in GD.
This study examined whether chronic stress in adolescents is linked to changes in gut microbiota composition and microbiota-derived metabolites. Researchers used 16S rRNA gene sequencing across the full sample, then applied metagenomic sequencing and untargeted metabolomics to a subset for deeper multi-omics profiling. The design was cross-sectional, comparing microbial diversity, network structure, and metabolite patterns across stress-level groups.
The study included 124 adolescents aged 12 to 16 years, whose chronic stress was assessed with the Adolescent Life Events Scale and the Study Stress Scale. Participants were stratified into low stress (n = 42), medium stress (n = 41), and high stress (n = 41) groups based on these measures. A subset of this cohort, 30 high-stress and 29 low-stress adolescents, underwent additional metagenomic sequencing and metabolomic analysis. Fecal samples were collected from all participants for microbiota analysis.
Adolescents with high chronic stress showed lower alpha diversity, distinct beta diversity, and a more complex microbial network compared to those with lower stress. Statistical analysis identified five bacterial genera with decreased abundance in the high-stress group, including Faecalibacterium, Bacteroides, Akkermansia, and unclassified Lachnospiraceae. These findings indicate that chronic stress in adolescents corresponds to measurable shifts in gut microbial community structure and depletion of several commonly beneficial genera.
The findings support a link between chronic psychological stress and altered gut microbial ecology during adolescence, a developmentally sensitive period. Because genera such as Faecalibacterium and Akkermansia are often associated with gut health, their depletion under high stress suggests the microbiome could be a biological correlate, and potentially a modifiable target, in stress-related conditions in youth. The multi-omics approach also demonstrates a framework for future work connecting microbial and metabolomic signatures to adolescent mental health.
This study examined whether the gut microbiota influences functional recovery from acute ischemic stroke (IS) at three months. Researchers used shotgun metagenomic sequencing to characterize the gut microbial communities of stroke patients treated at a tertiary stroke centre between January 2020 and March 2022. They compared microbial diversity and taxonomic and functional profiles between patients with favorable versus unfavorable recovery. Two-sample Mendelian randomization using GWAS summary statistics was also applied to explore whether specific bacteria have a causal relationship with post-stroke outcomes.
The study population consisted of 128 patients with acute ischemic stroke treated at a single tertiary stroke centre. Functional outcomes were assessed three months after the stroke using the modified Rankin Scale (mRS), with scores of 0 to 2 classified as favorable and 3 to 6 as unfavorable. Patients were grouped for comparison based on this favorable versus unfavorable outcome split, and their gut microbiomes were profiled using shotgun metagenomic sequencing.
Beta-diversity analysis showed a clear separation in gut microbial community structure between patients with favorable and unfavorable outcomes. Alpha-diversity measures revealed greater bacterial richness in the favorable outcomes group. Taxonomic profiling showed that a greater abundance of pathogenic bacteria, including Pseudomonas, Finegoldia, and Porphyromonas, was associated with unfavorable outcomes. Functional profiling identified differences between the groups in the ethylbenzene degradation pathway and in 16S rRNA (uracil1498-N3)-methyltransferase activity.
These findings suggest that gut microbial richness and composition may help explain some of the unexplained variability in recovery after ischemic stroke. The association of specific pathogenic taxa with worse outcomes, supported by Mendelian randomization analysis exploring causality, points to the gut microbiome as a potential contributor to post-stroke prognosis rather than merely a bystander. This raises the possibility that gut microbiota profiling could eventually inform risk stratification or that microbiome-targeted strategies might be explored to support stroke recovery. Further research is needed to confirm causal mechanisms and clinical applicability.
This study examined the origins and early developmental dynamics of the infant gut microbiota, focusing on how much maternal gut versus maternal vaginal microbiota contributes to colonization after vaginal delivery. Researchers used 16S rDNA sequencing paired with Source Tracker analysis to trace microbial sources into meconium and day-14 infant stool. The design also compared vaginally delivered infants to cesarean-delivered infants and examined the role of placental microbiota and breast milk.
The study followed 26 mother-infant pairs, with sampling spanning the third trimester of pregnancy through 14 days postpartum. Both vaginally delivered and cesarean-delivered infants were included for comparison. Maternal gut, maternal vaginal, placental, and breast milk samples were collected alongside infant meconium and day-14 stool samples from this cohort.
Maternal gut microbiota at 32 weeks of gestation was identified as the primary source of meconium microbiota in vaginally delivered infants, and it continued to shape day-14 gut microbiota regardless of bacterial presence in breast milk. Maternal vaginal microbiota contributed minimally, less than 1 percent, to infant gut colonization. Placental microbiota was also an important contributor to meconium microbiota across both delivery modes. Cesarean-delivered infants showed more complex, transient bacterial signatures in meconium, but by day 14 their gut microbiota had become similar to that of vaginally delivered infants following breastfeeding.
These findings challenge the assumption that vaginal microbial exposure during birth is the main seeding source for the infant gut, pointing instead to the mother's own gut community as the dominant influence. This reframes how clinicians and researchers think about early microbiome establishment, since maternal gut health during late pregnancy may matter more than mode of delivery for gut colonization. The convergence of vaginal and cesarean infant microbiota by day 14 after breastfeeding also underscores breast milk as a powerful equalizing factor in early gut development.
Only the title of this study was available, so this summary is based on the title alone. The title indicates the study examined microbial sharing between siblings and whether shared microbes support metabolic functions that protect against allergy. No abstract details on methods, specific microbes, or metabolic pathways can be confirmed.
The title indicates the population consisted of siblings, implying a study comparing gut or other microbiomes within sibling pairs or sibling groups. No sample size, age range, geographic location, or health status is stated in the available material. These specifics cannot be inferred beyond the fact that siblings were the subjects.
The title suggests that siblings share microbes with one another, and that this shared microbiota is associated with metabolic functions considered protective against allergy. No quantitative results, statistical values, or specific taxa are available to describe further. The core finding implied by the title is a link between sibling microbial sharing and allergy-protective metabolism.
If sibling microbial sharing supports allergy-protective metabolic functions, this would reinforce the idea that household and family exposures shape a child's microbiome in ways relevant to allergic disease risk. This could support interest in strategies that encourage beneficial microbial transmission within families. Because only the title was available, these implications remain general and should be confirmed against the full study once its abstract or text can be reviewed.
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 models of SAP with a single-center, open-label randomized controlled trial. They assessed pancreatic injury, systemic inflammatory markers, and gut microbiota composition, and tested whether rifaximin's effects depended on modulating the gut 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 microbiota-independent mechanisms. The clinical component enrolled 60 patients with predicted severe acute pancreatitis in a randomized controlled trial registered with the Chinese Clinical Trial Registry (ChiCTR2100049794). Patients were assigned to rifaximin treatment or a control group.
In mice, rifaximin reduced pancreatic injury and systemic inflammation and decreased mucin-degrading gut genera such as Akkermansia (P < 0.05), and these protective effects persisted in antibiotic-treated and germ-free mice, suggesting a mechanism not solely dependent on gut microbiota modulation. In patients, rifaximin significantly lowered systemic inflammation, with white blood cell counts falling from a median of 11.50 x10^9/L to 8.49 x10^9/L (P = 0.04) and TNF-alpha falling from 15.05 pg/mL to 11.00 pg/mL (P = 0.009). However, the incidence of culture-confirmed infection did not differ between the rifaximin and control groups (13.3% vs. 13.3%; RR, 1.00; 95% CI, 0.28-3.63), and adverse events were comparable between groups.
The findings suggest rifaximin can dampen the systemic inflammatory response in severe acute pancreatitis through mechanisms that extend beyond simple gut microbiota modulation, since benefits persisted even in germ-free mice. Clinically, rifaximin appears to lower inflammatory markers without increasing infection risk or adverse events, supporting its safety profile in this setting. Because culture-confirmed infection rates were unchanged, rifaximin may be best understood as an anti-inflammatory adjunct rather than an infection-prevention strategy in SAP, warranting further mechanistic and larger clinical study.
This study examined the fecal microbiota of Tibeto-Burman-speaking hill-tribe populations in Northern Thailand using quantitative PCR to quantify microbial composition. The researchers investigated how ethnicity and geographic location each relate to gut microbiota composition and to dietary habits. Multivariate statistical methods, including multiple factor analysis and partial least squares discriminant analysis, were used to explore associations among microbiota, ethnicity, geography, diet, and other host characteristics. The overarching question was whether ethnic identity or geographic residence, or both, better explain variation in gut microbiota among these populations.
The study included 102 individuals from three Tibeto-Burman hill-tribe ethnic groups, the Akha, Lahu, and Lisu. Participants resided in two provinces of Northern Thailand, Chiang Mai and Chiang Rai. This design allowed the researchers to compare people of the same ethnicity living in different locations, as well as people of different ethnicities living in the same location.
Both ethnicity and geography were associated with gut microbiota composition and with dietary patterns, but geography showed a stronger association with microbiota variation than ethnicity did. Ethnicity, by contrast, was primarily linked to differences in dietary habits rather than to microbiota composition directly. Notably, fecal microbiota profiles were more similar among different ethnic groups sharing the same location than among the same ethnic group split across different regions. The relationship between diet and gut microbiota also varied depending on ethnic and geographic grouping, while other host factors had a comparatively minor influence.
The findings suggest that shared environment and geography can shape the gut microbiota more powerfully than shared ethnic or genetic background. This implies that local diet, water sources, sanitation, and other place-based exposures may be more influential drivers of microbiome variation than ethnic heritage alone. For microbiome research in understudied regions like Thailand, these results highlight the importance of accounting for geographic residence, not just ethnicity, when interpreting microbiota differences across populations.
The study built curatedMetagenomicData (cMD) 3, a uniformly processed collection of over 22,000 human microbiome shotgun metagenomic samples with manually curated metadata. Using this resource, the researchers performed a large-scale meta-analysis to identify microbial species and functions associated with host traits and disease status. They also developed a new metric, the oral enrichment score (OES), which quantifies the relative abundance of bacteria typically found in the oral cavity but not normally in the gut. The goal was to find broadly reproducible, cross-study patterns linking the microbiome to human health.
The dataset combined more than 22,000 human microbiome samples curated from 94 separate studies conducted across 42 countries. The abstract does not specify individual demographic breakdowns, but the pooled samples include variation in sex, age, body mass index, and disease status. This is a meta-analysis of existing public metagenomic datasets rather than a newly recruited cohort.
The meta-analysis identified hundreds of microbial species and thousands of microbial functions that were significantly associated with sex, age, body mass index, and disease status. The newly defined oral enrichment score (OES) captured the relative abundance of oral-associated bacteria present in the gut. Higher OES in the gut was found to be a consistent feature across individuals with disease, suggesting this signal reflects altered microbiome health regardless of the specific condition. The abstract does not mention Bacteroides fragilis, polysaccharide A, or the B. fragilis toxin in relation to these findings.
The oral enrichment score offers a simple, quantifiable, and reproducible signal of microbiome disruption that could serve as a general marker of disease across many conditions. The curatedMetagenomicData 3 resource itself provides a standardized, readily updatable reference for future microbiome research, reducing the burden of reconciling disparate datasets. Together, these findings support the value of large-scale, cross-study meta-analysis in revealing modest but broadly shared patterns in human microbiome-health relationships.
This study examined whether gut microbiota composition differs in men with asthenozoospermia (AS), a condition marked by reduced sperm progressive motility below 32%. Researchers used 16S rRNA gene high-throughput sequencing on fecal samples to characterize the intestinal flora. They compared alpha- and beta-diversity, dominant phyla and genera, and predicted functional pathways between AS patients and healthy men. LEfSe analysis was used to identify key microbial taxa distinguishing the two groups.
A total of 580 men were initially recruited from the outpatient department of Tianjin Medical University General Hospital between September 2021 and March 2023. After rigorous screening, 60 men with isolated asthenozoospermia (AS group) and 48 healthy men (NC group) were enrolled in the final analysis. The two groups did not differ significantly in demographic characteristics, semen volume, sperm concentration, or total sperm count.
AS patients had significantly lower alpha diversity (Chao1, observed OTUs, and PD Whole-tree indices) and a distinct beta-diversity profile compared to healthy men. Firmicutes, Bacteroidota, Proteobacteria, and Actinobacteria were the dominant phyla, with Bacteroides, Prevotella, and Blautia as leading genera; the abstract does not report findings specific to Bacteroides fragilis, polysaccharide A, or the B. fragilis toxin. Eleven key genera, including Escherichia_Shigella and Prevotellaceae_UCG_001, were identified as differentially abundant and mostly correlated negatively with sperm motility. Eighty-eight KEGG pathways, including steroid biosynthesis and meiosis, were significantly enriched between groups.
The findings suggest that gut microbiota dysbiosis may be associated with the development of asthenozoospermia, supporting the concept of a gut-testis axis linking intestinal flora to sperm motility. Identification of specific depleted or enriched genera could point toward microbial biomarkers or mechanistic targets for male infertility related to reduced sperm motility. Because this is a pilot study from a single Chinese hospital, the findings would need validation in larger, more diverse cohorts before microbiota-based diagnostics or interventions could be considered.
This study investigated how the gut microbiota of piglets relates to differential resistance against porcine epidemic diarrhea virus (PEDV) infection. Researchers combined single-cell transcriptomics, 16S amplicon sequencing, metagenomics, and untargeted metabolomics to trace this relationship. The work examined how fecal microbiota transplantation and specific gut bacteria and their metabolites influence disease outcome after PEDV infection.
The study used two pig breeds, Landrace pigs and Min pigs, comparing their differing resistance to PEDV infection. Fecal microbiota from Min pigs was transplanted into Landrace pigs to test whether this altered infection outcomes. Animal protection models were also used to test the effects of specific bacterial strains and metabolites on PEDV infection.
PEDV infection caused significant shifts in the gut microbiota of piglets, and Landrace pigs lost their resistance to infection quickly, while transplanting fecal microbiota from more resistant Min pigs alleviated infection status in Landrace pigs. Metagenomic and animal protection analyses identified Lactobacillus reuteri and Lactobacillus amylovorus as playing an anti-infective role. Metabolomic screening linked these bacteria to the secondary bile acids deoxycholic acid (DCA) and lithocholic acid (LCA), but only LCA showed a protective effect in the animal model, and LCA supplementation altered intestinal T-cell populations, including enrichment of CD8+ cells.
The findings point to specific gut Lactobacillus species and their bile acid metabolite LCA as mediators of host resistance to PEDV infection in piglets. This suggests that manipulating the gut microbiota, or supplementing with LCA directly, could be explored as a strategy to protect against PEDV infection. The results also highlight secondary bile acid metabolism and T-cell modulation as a mechanistic link between gut microbes and antiviral defense in the intestine.
This study examined how gut microbial composition differs among colorectal cancer (CRC) patients grouped by body mass index (BMI) status. Researchers used 16S rRNA gene sequencing on stool samples to characterize the intestinal flora, while paired tumor tissue samples underwent transcriptome sequencing to assess immune-related gene expression and tumor microenvironment characteristics. By integrating these two data types, the study sought to connect BMI-associated microbial patterns with tumor biology in CRC.
The subjects were colorectal cancer patients whose stool and tumor tissue samples were collected and stratified into different BMI groups, such as overweight versus non-overweight categories. The abstract does not give an exact cohort size, geographic setting, or additional demographic detail. What can be stated honestly is that the population consisted of diagnosed CRC patients undergoing paired microbiome and tumor transcriptome analysis.
The study was designed to identify differences in intestinal microbial composition between CRC patients with varying BMI status, using 16S rRNA sequencing of stool samples. It also aimed to link these microbial differences to immune-related gene expression and tumor microenvironment features detected through tumor transcriptome sequencing. The provided abstract text is truncated before specific results are reported, so no particular taxa, genes, or statistical outcomes can be stated here. The overarching aim was to elucidate how BMI, gut microbiota, and CRC pathogenesis relate to one another.
By integrating microbiome and tumor transcriptomic data, this approach could clarify how BMI-associated microbial alterations contribute to CRC development and progression. Such findings may support the idea that gut microbiota imbalance, together with body weight status, plays a role in immune regulation and tumor microenvironment shaping in colorectal cancer. This integrated framework could inform future strategies that consider BMI and gut microbiota jointly when assessing CRC risk or progression. No specific therapeutic or diagnostic claims can be drawn beyond this general direction, since the abstract's results section was not provided in full.
This study used species-level shotgun metagenomic analysis to characterize the gut microbiota of men who have sex with men (MSM) of Western origin. The researchers compared these profiles to the gut microbial communities typically seen in non-Westernized populations. They also used questionnaire data to examine how specific sexual practices relate to differences in microbiota composition among MSM.
The study population consisted of men who have sex with men (MSM) with Western origin. The abstract does not give an exact sample size, but participants contributed both metagenomic sequencing data and questionnaire responses on sexual activities. No non-MSM comparison cohort details beyond prior studies are specified in this abstract.
Many MSM gut microbiomes resembled those of non-Westernized populations rather than typical Western gut profiles. These microbiomes were frequently dominated by members of the Prevotellaceae family, including co-colonization by species from the Segatella copri complex alongside unknown Prevotellaceae members. Questionnaire-based analysis linked specific sexual practices to variation in microbiota composition, and machine learning identified microbial features associated with particular sexual activities.
The findings indicate that sexual activity itself can meaningfully alter gut microbiome composition, independent of the usual health and environmental factors. Because this effect can make Western MSM microbiomes resemble non-Westernized profiles, it may confound or bias population-based microbiome studies that do not account for sexual practices. This suggests future microbiome research should consider sexual behavior as a relevant variable when interpreting inter-individual and cross-population differences.
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 investigate correlations between CRC-associated bacterial taxa and somatic mutated genes, and differentially expressed genes were clustered with differentially abundant microbial species. Immune and stromal cell composition in the tissue was also characterized using the XCELL tool.
The study population consisted of 41 patients with colorectal cancer. For each patient, both fecal microbiome samples and matched tumor and normal mucosa tissue samples were analyzed. The abstract does not provide further demographic details such as age, sex, or geographic origin of the cohort.
The researchers identified 22 gut microbial species associated with colorectal cancer and estimated the relative abundance of related KEGG functional ontology categories. Four significantly mutated genes, TP53, APC, KRAS, and SMAD4, were identified and linked to associations with cancer-related microbes. Notably, Fusobacterium nucleatum was found to positively correlate with several host metabolic pathways, highlighting a functional link between this microbe and tumor biology. The abstract is truncated before further results are described.
By connecting specific gut microbial taxa to somatic mutations in well-established CRC driver genes, this work supports a model in which the microbiome and host genome interact during colorectal cancer development. The correlation between Fusobacterium nucleatum and host metabolic pathway activity reinforces this organism's relevance to CRC biology on a functional, not just compositional, level. Multi-omic integration of microbiome, genomic, and transcriptomic data may help identify microbial markers or mechanisms relevant to CRC pathogenesis, though the abstract does not report clinical or therapeutic outcomes.
This study examined the human microbiome across four body sites: stool, oral, skin, and nasal. Researchers analyzed microbial composition and temporal dynamics over a 6-year period. They also examined how microbiome patterns relate to host multi-omics, immune, and clinical markers, comparing stability and individuality across the four sampled sites.
The study followed 86 participants over 6 years, with microbiome samples collected from four body sites per person. The abstract does not specify additional demographic details about the cohort. Among these participants, a subset identified as insulin-resistant was analyzed separately for differences in microbial stability and host associations.
Microbiome stability and individuality varied by body site and were strongly shaped by the host, with stool and oral microbiomes remaining more stable than skin and nasal microbiomes. The researchers identified both individual-specific and commonly shared bacterial taxa, and taxa unique to individuals tended to be more stable over time. Microbiome dynamics were correlated across different body sites, pointing to systemic patterns driven by host-microbe-environment interactions. Insulin-resistant individuals showed altered microbial stability and disrupted associations among microbiome, molecular markers, and clinical features.
The findings suggest that microbiome stability is not uniform across the body but instead depends on site-specific interactions with the host and environment, which has implications for how and where microbiome sampling is interpreted. The correlation of dynamics across body sites suggests a systemic, host-driven layer of regulation rather than fully independent site-level microbial communities. The altered stability and disrupted associations seen in insulin-resistant individuals suggest that metabolic disease may involve a breakdown in normal host-microbiome-molecular coordination, offering a potential angle for future work on metabolic disease and the microbiome.
The study examined how peripheral neurons connected to the gastrointestinal tract influence the gut microbiome and gut physiology. Researchers activated choline acetyltransferase (ChAT)-expressing or tyrosine hydroxylase (TH)-expressing gut-associated neurons in mice. They then measured effects on intestinal microbial communities, microbial metabolites (including bile acid profiles), and host physiological responses using multi-omics approaches.
The subjects were mice in which ChAT+ or TH+ gut-associated neurons were experimentally activated. The abstract does not give a specific sample size or strain detail, so no cohort numbers can be stated. This was an animal model study, not a human cohort, and it generated multi-omics datasets from these mice rather than drawing on a public metagenomic dataset.
Activating either ChAT+ or TH+ neurons reshaped the structure of the intestinal microbiome, including changes to bile acid profiles and fungal colonization. Physiologically, activation of either neuron type increased fecal output, showing a shared downstream effect on gut transit. Only ChAT+ neuron activation additionally increased colonic contractility and produced diarrhea-like fluid secretion, indicating that these two neuronal subtypes act through distinct physiological pathways despite some overlapping effects.
The findings show that distinct subsets of peripheral, gut-associated neurons can independently shape microbiome composition and gastrointestinal physiology without requiring signals from the brain. This suggests the enteric and peripheral nervous system directly sculpts microbial ecology, including bacterial and fungal populations and bile acid metabolism, rather than the microbiome being shaped only by diet or host genetics. Because different neuron subtypes produce different physiological outcomes (fecal output alone versus contractility and diarrhea-like secretion), this points to neuron-specific pathways as potential targets for understanding or treating GI motility and secretory disorders.
This study tested whether Parkinson's disease alters the oral microbiome in people with periodontitis. Researchers compared clinical, periodontal, and neurological parameters across groups, and measured the severity of Parkinson's motor dysfunction. They collected unstimulated saliva and stool samples and used next-generation sequencing of the 16S ribosomal RNA gene (V1-V3 regions) to profile oral and gut bacterial communities.
Three groups were enrolled: patients with periodontitis and Parkinson's disease (PA+P), patients with periodontitis but without Parkinson's disease (P), and systemically and periodontally healthy individuals (HC). The abstract does not give exact sample sizes for each group. Saliva samples were collected from all participants, with stool samples also gathered as part of the protocol.
Patients with Parkinson's disease had mild to moderate motor dysfunction but plaque scores comparable to those without Parkinson's, indicating oral hygiene was effectively maintained in the PA+P group. Saliva beta diversity differed significantly between HC and PA+P, between HC and P, and between P and PA+P, and the microbial profiles of saliva and fecal samples were distinct from each other. Mycoplasma faucium, Tannerella forsythia, Parvimonas micra, and Saccharibacteria (TM7) were increased in the P group, while Prevotella pallens, Prevotella melaninogenica, and Neisseria multispecies were more abundant in the PA+P group. In fecal samples from the P group, Ruthenibacterium lactatiformans, Dialister succinatiphilus, Butyrivibrio crossotus, and Alloprevotella tannerae were detected.
The findings suggest that Parkinson's disease is associated with a distinct oral microbial signature in periodontitis patients, separate from oral hygiene status. Because saliva and fecal microbial profiles diverged, oral and gut compartments may need to be assessed separately when studying Parkinson's disease and periodontitis together. These shifts in specific taxa point to the oral cavity as a potential site of interest for understanding links between periodontal disease and neurological status in Parkinson's disease.
This study investigated whether the gut microbiome is altered in acute myeloid leukemia (AML) at diagnosis, and whether such alterations are associated with hallmarks of cachexia such as muscle weakness and anorexia. Researchers analyzed the composition and functional potential of the fecal microbiota using shotgun metagenomics, alongside fecal, blood, and urinary metabolomics. The goal was to link microbiome changes to altered gut function, redox status, and glycemic disorders observed in AML patients.
The study included 30 antibiotic-free AML patients evaluated at diagnosis, matched 1:1 with healthy volunteers, in a multicenter, cross-sectional, prospective design. Biological samples and clinical data were collected from both groups for comparison. No further demographic details are given in the abstract.
AML patients showed muscle weakness, anorexia, signs of altered gut function, and glycemic disorders compared to controls. The fecal microbiota composition differed between AML patients and controls, marked by an increase in oral bacteria, and functional and metabolomic alterations pointed to an altered redox status in the gut. Eubacterium eligens was reduced threefold in AML patients and was strongly correlated with muscle strength and with citrulline, a marker of enterocyte mass and function, while Blautia and Parabacteroides were increased in patients with AML.
The findings suggest that gut microbiome alterations in AML are linked to cachexia-related features such as muscle weakness and anorexia, rather than being incidental. The strong correlation between reduced Eubacterium eligens and both muscle strength and citrulline points to a possible gut-muscle axis worth further investigation in AML. These results may support future research into the gut microbiota as a marker or target related to nutritional and muscular decline in AML patients.
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 investigated the gut microbiome's association with type 2 diabetes (T2D) by analyzing shotgun metagenomic sequencing data. The researchers looked beyond species-level associations to examine strain-specific and within-species phylogenetic diversity, since prior species-level findings had been inconsistent and lacked mechanistic explanations. They also assessed community-level functional changes, such as perturbations in glucose metabolism, that might underlie T2D pathogenesis. The analysis drew on strain-specific gene carriage, including genes involved in horizontal gene transfer, to explain inter-individual variation in disease risk.
The study analyzed 8,117 shotgun metagenomes pooled from 10 separate cohorts. These cohorts included individuals with type 2 diabetes, prediabetes, and normoglycemic (normal blood sugar) status. The pooled cohorts spanned the United States, Europe, Israel, and China, making this a large, geographically diverse, multi-population dataset rather than a single new patient recruitment.
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 species also appeared to contribute to community-level functional shifts, such as changes in glucose metabolism pathways, that could plausibly underlie T2D pathogenesis. Beyond the species level, the study identified within-species phylogenetic diversity across strains of 27 species, such as Eubacterium rectale, that explained differences in T2D risk between individuals. In some cases these strain-level differences were tied to specific gene carriage, including loci involved in horizontal gene transfer and other biological processes linked to metabolic risk.
By resolving associations down to the strain level rather than stopping at species, the study offers a path toward mechanistic explanations for why gut microbes relate to T2D risk, rather than only correlational associations. The identification of specific genes and horizontal gene transfer loci tied to metabolic risk suggests concrete molecular mechanisms that future functional studies could test. Because the analysis pooled cohorts across four world regions, the findings point to microbial signatures that may generalize across diverse populations rather than being artifacts of a single study design. This strain-resolved approach could inform more precise microbiome-based biomarkers or targets for T2D risk stratification going forward.
This study examined how environmental, socioeconomic, and health factors relate to gut microbiome composition at both the species and strain levels. The researchers used deeply sequenced metagenomic data to identify associations between bacterial species and a range of host phenotypes and situational factors. They also incorporated strain-level phylogenetic information to see whether it changed the picture drawn from species-level analysis alone. The work also included a meta-analysis comparing species-level profiles across multiple datasets.
The cohort consisted of 1,871 people living in 19 isolated villages in the Mesoamerican highlands of western Honduras. This is described as a community-based cohort from a non-industrialized setting, a population the authors note is underrepresented in deeply sequenced microbiome research linked to detailed host phenotypes. No further demographic breakdown is given in the abstract.
Socioeconomic factors accounted for 51.44% of the total associations found between gut bacterial species and human phenotypes, making them the largest contributor identified. Meta-analysis across datasets confirmed several species associated with body mass index, consistent with prior research. Adding strain-level phylogenetic information changed the overall picture of the gut microbiome's relationship to phenotypes, particularly for household wealth: wealthier individuals were found to harbor different strains of Eubacterium rectale than less wealthy individuals, a distinction invisible at the species level alone.
The findings suggest that socioeconomic circumstances are a dominant force shaping the gut microbiome, at least as strong as or stronger than many biological or environmental factors measured. Strain-level analysis can reveal microbiome-phenotype relationships, such as with household wealth, that species-level analysis alone would miss. The authors conclude that gut microbiome surveillance in non-industrialized, understudied 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 examined gut microbial and metabolic profiles across seven different malignancies to identify taxonomic and metabolomic signatures common to cancer patients. Researchers used whole-genome shotgun sequencing (WGS) to characterize the fecal microbiome and gas chromatography/mass spectrometry (GC/MS) to measure short-chain fatty acids and amino acids. They compared taxonomic configurations, microbial diversity, and metabolite levels between cancer patients and matched healthy controls, then built a gut microbiome cancer index from the combined data.
The cohort included patients with seven malignancy types: 40 with colorectal cancer, 45 with stomach cancer, 71 with breast cancer, 34 with lung cancer, 50 with melanoma, 60 with lymphoid neoplasms, and 40 with acute myeloid leukemia (AML). Each patient group was compared against sex- and age-matched healthy controls (HC). The abstract does not specify additional demographic details such as country recruitment sites beyond the cohort composition itself.
Beta-diversity differed between every cancer group and its matched healthy controls, while alpha-diversity differed only for the lymphoid neoplasm and AML groups. Of 203 unique species identified, 179 were under-represented and 24 were over-represented in cancer patients relative to controls, and Faecalibacillus intestinalis was under-represented in all seven malignancy groups studied. Fecal formic acid was significantly higher in every case group than in healthy controls, and the newly developed gut microbiome cancer index showed a marked reduction in all groups except AML. The abundance of several species correlated negatively with amino acids and formic acid, and positively with acetic, propanoic, and butanoic acid.
The findings suggest that despite considerable variation in microbial and metabolomic profiles across different cancer types, a shared signature involving depleted Faecalibacillus intestinalis and elevated formic acid may mark general gut dysbiosis in cancer patients. The gut microbiome cancer index distinguished most cancer cases from healthy controls, pointing toward its potential use as a diagnostic or predictive tool for intestinal dysbiosis in oncology. The authors frame this as an early step toward new non-invasive tests rather than a finalized diagnostic, since differences across malignancies outweighed similarities overall.
This study examined whether fecal microbiota transplantation (FMT) changes gut microbiota composition and function in patients with irritable bowel syndrome (IBS), and whether those changes relate to symptom improvement. The researchers used 16S rRNA gene amplicon sequencing and shotgun metagenomics to track microbiota shifts after FMT. The study was part of a randomized, placebo controlled FMT trial, allowing comparison between active treatment and placebo. It specifically probed prior inconsistent findings on the link between post-FMT microbiota change and clinical outcome.
The study population consisted of 49 IBS patients enrolled in a randomized, placebo controlled FMT trial. Patients received either FMT from a healthy donor or a placebo procedure. Fecal samples from these patients were analyzed for microbiota composition and function before and after treatment. The abstract does not specify additional demographic details such as age range or sex distribution.
FMT from a healthy donor successfully modulated microbiota composition and functional profiles in IBS patients, confirming the transplant altered the gut ecosystem as intended. However, this successful microbiota modulation was not associated with resolution of IBS symptoms. Notably, a donor derived strain of Prevotella copri came to dominate the microbiota specifically in FMT group patients who had low relative abundance of P. copri before treatment. This suggests that a recipient's pre-existing microbiota state influences how well donor strains colonize.
The findings indicate that changing gut microbiota composition through FMT is not sufficient on its own to relieve IBS symptoms, pointing to a disconnect between microbial engraftment and clinical benefit. This highlights the multifactorial nature of IBS, meaning symptoms likely depend on more than microbiota composition alone. The study also shows that a recipient's baseline microbiota, such as pre-FMT Prevotella copri levels, shapes whether donor strains successfully colonize. These results suggest future FMT research should look beyond simple compositional shifts to understand what actually drives symptom relief in IBS.
This case-control study examined whether fecal gut microbiota composition differs between children with diarrhea and non-diarrheal controls, and whether these differences relate to how long the diarrhea lasts. The researchers compared microbiota patterns in children with acute diarrhea (under 7 days) versus prolonged or persistent diarrhea (7 days or more). The goal was to determine if compositional shifts in the gut microbiota are linked to diarrheal duration and etiology.
The study included Ethiopian children under five years of age. Cases comprised 554 children with acute diarrhea and 95 children with prolonged or persistent diarrhea, compared against 663 frequency-matched non-diarrheal controls. This case-control design allowed direct comparison of fecal microbiota across the different diarrhea duration categories.
Diarrhea cases showed lower bacterial diversity overall and were enriched in Escherichia spp., Campylobacter spp., and Streptococcus spp. compared to controls. Cases were also depleted in beneficial gut commensals, including Prevotella copri, Faecalibacterium prausnitzii, and Dialister succinatiphilus. This depletion of commensals was most pronounced in the prolonged and persistent diarrhea cases, suggesting a link between the severity of commensal loss and duration of illness.
The findings suggest that prolonged diarrhea duration is accompanied by progressive depletion of key gut commensal bacteria. The authors propose that re-establishing these depleted commensals, for example through microbiota-directed food supplements, offers a potential treatment strategy. This points toward microbiota-targeted interventions as a promising approach for addressing prolonged and persistent childhood diarrhea in low- and middle-income countries.
This study investigated periodontitis in pregnant women using an integrative, multi-omics approach that combined microbiome and metabolome profiling. Researchers analyzed subgingival plaque, saliva, serum, and stool samples through 16S rRNA sequencing, untargeted metabolomics, and clinical trait data. The goal was to characterize the oral-gut microbial and metabolic connections arising from periodontitis during early pregnancy, and to explore the translational potential of this oral-gut axis.
The cohort consisted of 54 Chinese pregnant women in their first trimester. Of these, 31 women had maternal periodontitis (the Perio group) and 23 women served as Non-Perio controls. Samples were collected directly from each participant across four body sites: subgingival plaque, saliva, serum, and stool.
The study identified Coprococcus as a novel fecal bacterial distinguisher of periodontitis subjects, and this genus was associated with subgingival periodontopathogens, setting it apart from other fecal genera within the Lachnospiraceae family. The researchers further found that the ratio of fecal Coprococcus to Lachnoclostridium could discriminate between the Perio and Non-Perio groups. The abstract text provided is truncated before the full quantitative result for this ratio is given, so the precise discriminatory value is not stated here.
These findings support the existence of an oral-gut axis linking periodontitis to distal microbial and metabolic changes in pregnant women. Identifying a fecal marker such as the Coprococcus to Lachnoclostridium ratio suggests gut microbiome signatures could have translational potential for detecting or monitoring periodontitis-related risk during pregnancy. This integrative microbiome-metabolome approach may help clarify how oral dysbiosis contributes to systemic and pregnancy-related outcomes, though further research is needed to confirm clinical utility.
This study examined how the gut microbiome and serum metabolome differ between people with lactose intolerance (LI) and controls. Researchers combined a paired-sample analysis of American Gut Project (AGP) data with metagenomic and untargeted metabolomic analyses in a separate Chinese cohort. They also conducted fecal microbiota transplantation (FMT) experiments to test whether the LI-associated gut microbiome directly affects inflammatory outcomes. The overall aim was to clarify the interaction between gut microbes and circulating metabolites in lactose intolerance.
The abstract describes two human data sources: a paired-sample subset drawn from the American Gut Project, a large public metagenomic dataset, and a separately recruited Chinese cohort analyzed with metagenomics and untargeted metabolomics. No specific sample sizes are given in the abstract. In addition to the human data, the researchers performed FMT experiments, which are typically done in animal models, to further probe how the LI-associated microbiome influences inflammation.
Fourteen microbial genera differed significantly between LI and control groups in the AGP data. In the Chinese cohort, a machine learning approach distinguished the two groups using seven bacterial species and nine serum metabolites. Notably, Escherichia coli was elevated in the LI group and was negatively correlated with several metabolites, including PC (22:6/0:0), indole, and Lyso PC, while reduced levels of Faecalibacterium prausnitzii and Eubacterium rectale were positively associated with other metabolic changes. The abstract text is cut off before further details on the FMT-based inflammatory results are given.
The findings suggest that lactose intolerance is associated with a distinct, identifiable gut microbial and metabolomic signature rather than being solely a matter of lactase deficiency. The reciprocal shifts, increased E. coli alongside reduced short-chain-fatty-acid-associated species like F. prausnitzii and E. rectale, point to a potential role for microbiome alterations in the symptoms or downstream inflammation seen in LI. This raises the possibility that microbiome-based markers or interventions could eventually help identify or manage lactose intolerance, though the abstract does not specify how the FMT results support this beyond the study's stated aim of examining inflammatory outcomes.
This study examined how exclusive enteral nutrition (EEN), a first-line therapy for pediatric Crohn's disease, achieves remission through changes in the fecal microbiome and its metabolites. The researchers used integrated multi-omics analysis to track functional and metagenomic changes in the gut microbiota of treatment-naive patients before and during EEN. They also used bioorthogonal non-canonical amino acid tagging to identify which bacterial species responded to medium-chain fatty acids. Functional findings were further tested in gut chemostat cultures and by transferring patient microbiota into germ-free mice.
The study population was a prospective pediatric cohort of treatment-naive Crohn's disease patients enrolled under a registered clinical trial (German Clinical Trials DRKS00013306). Fecal samples from these pediatric patients were profiled for microbiome and metabolite changes in response to EEN therapy. The abstract does not give an exact number of patients enrolled. Complementary experimental models included gut chemostat cultures and germ-free Il10-deficient mice colonized with patient-derived microbiota.
Multi-omics analysis revealed network clusters within individually variable microbiome profiles, identifying Lachnospiraceae and medium-chain fatty acids as protective features associated with EEN response. Metagenomic analysis showed high strain-level dynamics in the gut microbiota during EEN treatment. When patient-derived, diet-exposed fecal microbiota were transferred into germ-free Il10-deficient mice, individual patient-specific strain signatures either prevented or caused inflammatory bowel disease-like inflammation. This demonstrates that the functional consequences of EEN-driven microbiome changes vary by patient and can be reproduced in a gnotobiotic model system.
The findings suggest that EEN works through specific, measurable functional changes in the gut microbiome rather than through a single uniform mechanism. Because protective effects were tied to individually variable strain-level signatures, microbiome profiling could eventually help predict or explain why some pediatric Crohn's patients respond to EEN and others do not. The identification of Lachnospiraceae and medium-chain fatty acids as protective features points to specific microbial and metabolic targets that could inform future dietary or microbiome-based therapies for pediatric Crohn's disease.
This study investigated the neonatal gut bacterial and viral microbiome in infants exposed to HIV but not infected themselves, comparing them to unexposed infants. The researchers also examined how HIV exposure affects antibody (IgA) binding to gut microbiota in these neonates. Finally, they tested whether antibodies present in breast milk influence the growth of commensal gut bacteria, linking these maternal antibody functions to infant inflammatory outcomes.
The study population consisted of neonates exposed to HIV but uninfected (nHEU) and unexposed neonates (nHU), compared for gut bacteriome, virome, and plasma inflammatory markers. Mothers living with HIV were also studied, specifically their breast milk IgA and its ability to inhibit bacterial growth. The abstract does not report a specific cohort size, so exact sample numbers cannot be stated.
Neonates exposed to HIV but uninfected showed altered gut bacteriome composition and a milder shift in the enteric DNA virome compared to unexposed neonates. HIV exposure also changed how IgA bound to gut microbiota in these infants. The relative abundance of Blautia spp., whether in whole stool or in the IgA-bound microbiota fraction, was positively associated with plasma C-reactive protein, a marker of inflammation. Breast milk IgA from mothers living with HIV had 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 impaired breast milk antibody function in mothers living with HIV may contribute to altered gut microbiota and heightened inflammation in their HIV-exposed but uninfected infants. This points to a potential mechanism, reduced IgA control of specific commensals like Blautia coccoides, underlying the known immune alterations seen in this population. The results highlight breast milk antibody quality as a factor that may warrant attention in the care of infants born to mothers living with HIV.
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 examined the microbiome associated with ovarian cancer (OC) to determine its potential role in detection, disease progression, and prognosis. Researchers compared microbial taxa across multiple body sites in OC patients versus a benign comparison cohort. The goal was to identify microbial indicators that could aid earlier diagnosis, since OC is typically caught late and carries high mortality among gynecological cancers.
The study population consisted of an ovarian cancer (OC) cohort and a benign cohort, sampled across multiple body sites. The abstract notes that stool and omentum sites were sampled in the OC cohort but not in the benign cohort, indicating an asymmetry in site coverage between groups. No specific sample sizes or demographic details are given in the abstract, so a precise cohort size cannot be stated.
The researchers identified a distinct OC-associated microbiome, with general enrichment of taxa including Dialister, Corynebacterium, Prevotella, and Peptoniphilus in the OC cohort across sampled body sites. These same taxa were depleted in advanced-stage and high-grade OC patients compared to those with early-stage, low-grade disease, suggesting reduced accumulation as disease advances. The mainly pathogenic taxa were also more abundant in OC patients who had adverse treatment outcomes compared to those without such events.
These findings suggest the OC-associated microbiome could serve as a potential indicator for earlier detection of ovarian cancer, since taxa enrichment patterns differ by stage and grade. The association between taxa accumulation and adverse treatment outcomes also suggests a possible role for microbiome profiling in predicting patient response to treatment. Together, this points toward the microbiome as a candidate tool for both diagnostic and prognostic purposes in ovarian cancer care.
This study examined whether the gut microbiota differs between people with irritable bowel syndrome (IBS) and healthy controls, since earlier work on gut dysbacteriosis in IBS had been inconclusive. The researchers retrieved original multicenter 16S rRNA amplicon sequencing data from the GMrepo database and applied propensity score matching to reduce confounding bias between groups. They performed differential analysis of microbiota composition at multiple taxonomic levels, built a co-occurrence network, and ran subgroup analyses to look for microbial patterns specific to different IBS subtypes.
The dataset began with 1,522 amplicon samples pooled from multiple original studies in the GMrepo database. After propensity score matching to control for confounding factors, 708 individuals remained for analysis, consisting of 354 IBS patients and 354 matched healthy controls. This is therefore a secondary, integrated reanalysis of existing multicenter human 16S rRNA sequencing data rather than a newly recruited cohort.
Across the matched samples, the analysis identified 1,160 genera and found significant taxonomic differences between IBS and healthy controls. IBS samples were enriched for the families Enterobacteriaceae, Moraxellaceae, and Sphingobacteriaceae, and for the genera Streptococcus, Bacillus, Enterocloster, Sphingobacterium, Holdemania, and Acinetobacter. IBS samples were depleted in the phyla Firmicutes, Euryarchaeota, Cyanobacteria, Acidobacteria, and Lentisphaerae, and in the families Bifidobacteriaceae, Ruminococcaceae, and Methanobacteriaceae, among others noted in the abstract.
By using propensity score matching on pooled multicenter data, the study strengthens the case that specific, reproducible shifts in gut microbiota composition, rather than inconsistent or center-specific noise, are associated with IBS. The consistent depletion of Firmicutes-associated and beneficial taxa alongside enrichment of Enterobacteriaceae and related groups points to candidate microbial signatures that could inform future diagnostic or mechanistic research. Because this is a secondary analysis of existing sequencing data, these associations should be viewed as hypothesis-generating and would need confirmation in prospective, mechanistic studies before clinical application.
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 examined the gut microbiota landscape of patients with diffuse large B-cell lymphoma (DLBCL) and its relationship to peripheral blood immune cell subtypes. Researchers used metagenomic sequencing to characterize gut bacterial composition and full-spectral flow cytometry to profile immune cell subsets. The goal was to identify microbiota and immune features that differ across NCCN-International Prognostic Index (NCCN-IPI) risk categories, since the gut microbe landscape in DLBCL and its link to immunity had remained largely unknown.
A total of 87 newly diagnosed adult DLBCL patients were enrolled and had peripheral blood samples collected for immune cell subtyping. Of these, 69 of the 87 patients also had stool or tumor-associated samples submitted for metagenomic sequencing to assess microbiota composition. Patients were grouped according to NCCN-IPI risk categories: low-risk, low-intermediate-risk, intermediate-high-risk, and high-risk.
Metagenomic sequencing identified 10 bacterial phyla, 31 orders, and 455 bacterial species across the 69 profiled DLBCL patients. Six bacteria showed abundance differences of note, including Blautia sp. CAG 257, Actinomyces sp. S6 Spd3, Streptococcus parasanguinis, Bacteroides salyersiae, and Enterococcus faecalis. The abstract does not mention Bacteroides fragilis, polysaccharide A, or the B. fragilis toxin, so this study's findings center on other bacterial taxa and their association with NCCN-IPI risk groups and peripheral immune cell subsets.
By linking specific gut bacterial abundances to NCCN-IPI prognostic risk groups and peripheral immune cell subtypes, this work suggests the gut microbiome may play a role in shaping immune status and disease risk stratification in DLBCL. These integrated microbiome-immune signatures could eventually inform prognostic tools or risk-adapted monitoring for newly diagnosed patients. Further validation would be needed before such microbiota features could guide clinical decision-making in lymphoma care.
This study examined how the gut microbiota changes with age in people with colorectal cancer (CRC) and in healthy individuals, using eleven metagenomic data sets pooled from the curatedMetagenomicData R package. After batch effect correction, samples were split into three age groups, and species composition was visualized and compared using ggplot2 and Microbiota Process (PCA and LEfSe analysis by age within the healthy and CRC groups). Spearman correlation was then used to identify bacteria whose abundance tracked with age in each group, and these age-differentiated species were used to build an age prediction model and a CRC risk prediction model.
The analysis was based on eleven previously published metagenomic data sets related to colorectal cancer, pooled through the curatedMetagenomicData R package rather than a newly recruited cohort. Both healthy individuals and CRC patients from these combined data sets were divided into three age groups for comparison. Specific sample sizes for each age group are not given in the abstract.
Gut microbiota structure and composition differed significantly across the three age groups in both healthy individuals and CRC samples. Bacteroides vulgatus was lower in abundance in the oldest group compared to the other two, while Bacteroides fragilis abundance increased with aging. The analysis also identified seven bacterial species whose abundance rose with age, alongside an increase in pathogenic bacteria such as Escherichia coli.
By identifying specific age-differentiated gut bacteria, including the aging-associated rise in Bacteroides fragilis, the study supports building microbiota-based models that can predict biological age and estimate colorectal cancer risk. This suggests gut microbiota shifts across the lifespan may be a usable signal for stratifying CRC risk alongside chronological age. It also points to the aging gut environment, with declining beneficial taxa like Bacteroides vulgatus and rising pathogenic bacteria, as a potential contributor to CRC development.
This study used metagenomic sequencing to characterize the gut microbiota of people with non-segmental vitiligo. The researchers compared microbial diversity and species-level composition between patients and matched healthy controls. They also used the KEGG and MetaCyc databases to predict gene functions and gut metabolic modules, aiming to identify functional as well as compositional differences in the gut microbiome.
Twenty-five patients with non-segmental vitiligo were enrolled along with 25 matched healthy controls. Matching between the two groups is stated in the abstract, though the specific matching criteria (such as age or sex) are not detailed. The population size represents a modest, case-control cohort rather than a large-scale population study.
Alpha diversity of the gut microbiome was significantly reduced in vitiligo patients compared with healthy controls. At the species level, Staphylococcus thermophiles was decreased while Bacteroides fragilis was increased in patients with vitiligo. LEfSe analysis identified several representative microbial markers for vitiligo, including Lachnospiraceae_bacterium_BX3, Massilioclostridium_coli, TM7_phylum_sp_oral_taxon_348, and Bacteroides fragilis.
The findings support a link between altered gut microbial composition, including elevated Bacteroides fragilis, and non-segmental vitiligo. Identification of specific microbial markers such as Bacteroides fragilis raises the possibility that gut microbiota profiling could eventually help characterize or differentiate vitiligo. Further work on the predicted gene functions and metabolic modules may help clarify mechanistic pathways linking gut microbiota to vitiligo pathophysiology.
This study examined whether the COVID-19 mRNA vaccine BNT162b2 changes the composition of human breast milk microbiota during a two-dose vaccination regimen. It also examined how any such changes relate to the levels of SARS-CoV-2 spike-specific antibodies present in breast milk. The researchers tracked antibody levels and microbiota composition across several time points relative to vaccination, motivated by concerns that maternal mRNA vaccination could affect the breast milk microbiome that helps shape the early-life infant microbiome.
The study enrolled 49 lactating mothers from Hong Kong who received two doses of the BNT162b2 mRNA vaccine between June 2021 and August 2021. Each participant self-collected breast milk samples at four time points: before vaccination, one week after the first dose, one week after the second dose, and one month after the second dose. The abstract does not report additional demographic details about the cohort.
Levels of SARS-CoV-2 spike-specific IgA and IgG in breast milk peaked one week after the second vaccine dose, then rapidly waned, with IgA returning to baseline by one month post-second dose. The richness and overall composition of breast milk microbiota changed dynamically across the vaccination timeline. However, the abundance of beneficial microbes such as Bifidobacterium species did not significantly change following vaccination. The abstract does not mention Bacteroides fragilis, polysaccharide A, or the B. fragilis toxin, so these are not part of this study's findings.
The findings suggest that maternal BNT162b2 vaccination generates a transient but measurable antibody response in breast milk that could offer newborns temporary passive immunity to SARS-CoV-2. The preservation of beneficial Bifidobacterium abundance despite shifts in overall microbiota composition suggests the vaccine does not compromise a key beneficial component of the breast milk microbiome. These results may help reassure lactating mothers and clinicians about the microbiome safety of mRNA vaccination during lactation, while the observed waning of antibodies points to a limited window of passive protection for infants.
This study examined the gut microbiome of captive Asian elephants (Elephas maximus) using full-length 16S rRNA gene nanopore sequencing to achieve species-level resolution. The researchers aimed to characterize how the microbiome varies with age class and diet in this culturally significant Thai species. Nanopore sequencing allowed for higher-resolution taxonomic profiling than typically achieved with shorter-read approaches. The work was framed around supporting elephant welfare as part of sustainable captive management.
The subjects were 32 captive Asian elephants housed in Thailand. The animals were grouped into three age classes: baby (0 to 2 years), juvenile (2 to 10 years), and adult (over 10 years). Some adult elephants were also fed a local palm, Caryota urens, as a dietary supplement, allowing comparison of diet-associated microbiome differences within the adult group.
Eleven common uncultured bacterial species, including Rikenellaceae RC9 gut group, Kiritimatiellae WCHB1-41, Phascolarctobacterium, Oscillospiraceae NK4A214 group, Christensenellaceae R-7 group, Oribacterium, Oscillospirales UCG-010, Lachnospiraceae, Bacteroidales F082, uncultured rumen Rikenellaceae RC9 gut group, and Lachnospiraceae AC2044 group, were found across elephants fed solid food. Microbiome composition shifted progressively across the baby, juvenile, and adult age classes. Adult elephants supplemented with Caryota urens palm showed a distinct microbiome profile compared with other adults. Potential beneficial microbes were identified as varying according to both age class and feed diet.
The high-resolution, species-level microbiome data generated here could serve as a reference for monitoring elephant gut health in captivity. Understanding how age and diet shape the elephant microbiome may inform feeding and husbandry practices aimed at improving welfare. Identifying diet-associated shifts, such as those linked to Caryota urens supplementation, suggests specific dietary components could be leveraged to support beneficial microbial populations. This approach may contribute to more evidence-based, sustainable management of captive elephant populations.
This study examined whether gut microbiota composition influences the return of estrus in post-weaning sows by regulating the metabolism of sex steroid hormones. The researchers used 16S rRNA gene sequencing, metagenomic sequencing, and fecal metabolome analysis to link microbial community changes to hormone-related outcomes. They specifically looked at how shifts in gut bacterial species affect the functional capacity for steroid hormone biosynthesis within the gut microbiome.
The study analyzed 207 fecal samples from well-phenotyped sows using 16S rRNA gene sequencing to find associations between gut microbes and estrus return. A subset of 85 fecal samples underwent metagenomic sequencing to identify specific bacterial species tied to estrus return status. The findings were then confirmed in a separate validation cohort of sows.
Metagenomic analysis identified 37 bacterial species significantly associated with estrus return after weaning. Sows that returned to normal estrus had increased abundances of L. reuteri and P. copri, and decreased abundances of B. fragilis, S. suis, and B. pseudolongum, compared to non-returning sows. These microbial shifts significantly altered the gut microbiome's functional capacity for steroid hormone biosynthesis, and metabolome analysis found significant differences in sex steroid hormones and related compounds between normal and non-return sows.
By integrating differential bacterial species, metagenomic function, and fecal metabolome data, the study provides evidence that gut microbiota, including reduced B. fragilis abundance, is linked to normal post-weaning estrus return through effects on sex steroid hormone metabolism. This suggests that specific gut bacteria could serve as biomarkers or targets for improving reproductive efficiency in sows. The findings point toward potential microbiome-based strategies to address delayed or absent estrus return, a costly problem in swine production.
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 study investigated whether gut dysbiosis triggers brain inflammation that contributes to Alzheimer's disease (AD) pathogenesis. Researchers analyzed the gut microbiota composition of 3xTg mice (a transgenic AD mouse model) across different ages. They then generated germ-free 3xTg mice and recolonized them with fecal samples from either AD patients or age-matched healthy donors. Hippocampal RNA sequencing and metabolomic analysis were used to examine downstream inflammatory and metabolic pathways in the brain.
The subjects were 3xTg transgenic mice, a rodent model engineered to develop Alzheimer's-like amyloid-beta and tau pathology. Human involvement was limited to fecal donor samples, drawn from patients with AD and from age-matched healthy donors, used to recolonize germ-free mice. The abstract does not give a specific number of human donors or mice, so no sample size can be stated.
16S rRNA sequencing showed enrichment of Bacteroides in the gut microbiota of the mice. Germ-free 3xTg mice had markedly reduced cerebral amyloid-beta plaques and neurofibrillary tangle pathology compared with specific-pathogen-free mice. In the absence of gut microbiota, hippocampal inflammatory pathways and insulin/IGF-1 signaling were abnormally altered, and elevated poly-unsaturated fatty acid (PUFA) metabolites and their oxidative enzymes corresponded with microglia activation and inflammation. Transplanting AD patients' gut microbiota into mice worsened AD pathology and cognitive dysfunction, compared with healthy donor transplants, and was associated with activation of the C/EBPbeta/asparagine endopeptidase pathway.
The findings support that a complex gut microbiome is required for full expression of AD-related brain pathology and cognitive decline in this mouse model. They point to PUFA metabolism and associated neuroinflammation as a mechanistic link between gut dysbiosis and Alzheimer's disease progression. This suggests the gut microbiome could be a target for future interventions aimed at slowing AD-related neuroinflammation and cognitive impairment.
This prospective observational study examined whether gut microbiota composition is associated with immune responses and adverse events following SARS-CoV-2 vaccination. Researchers compared recipients of the inactivated CoronaVac vaccine with recipients of the mRNA BNT162b2 vaccine. They performed shotgun metagenomic sequencing on stool samples and measured immune markers using a surrogate virus neutralization test and a spike receptor-binding domain IgG ELISA.
The study included 138 adult COVID-19 vaccinees, comprising 37 recipients of CoronaVac and 101 recipients of BNT162b2. Stool samples were collected from each participant at baseline and again one month after the second vaccine dose. The abstract does not specify additional demographic details such as age range or geographic location.
CoronaVac recipients showed a significantly lower immune response than BNT162b2 recipients. Among CoronaVac vaccinees, higher neutralizing antibody levels were persistently associated with greater abundance of Bifidobacterium adolescentis, and their baseline gut microbiome was enriched in carbohydrate metabolism pathways. In BNT162b2 vaccinees, neutralizing antibody levels correlated positively with the total abundance of bacteria bearing flagella and fimbriae, including Roseburia faecis.
The findings suggest that baseline and post-vaccination gut microbiota composition may help explain individual variation in vaccine-induced immune responses. Specific taxa such as Bifidobacterium adolescentis and Roseburia faecis, along with related metabolic pathways, could serve as candidate biomarkers or targets for improving vaccine immunogenicity. These associations may differ by vaccine platform, since inactivated and mRNA vaccines showed distinct microbial correlates of response.
This study examined how the gut microbiota of Nigerian infants develops over the first year of life, a population underrepresented in existing microbiome research. Researchers characterized bacterial composition using 16S rRNA gene sequencing (V1-V2 region) and measured short chain fatty acids and lactate in faecal samples using gas chromatography. The goal was to track how delivery mode, feeding practices, and weaning shape the developing infant gut microbiota over time.
The cohort consisted of 28 Nigerian infants followed monthly from birth through one year of age, with faecal samples collected at each timepoint. Infants were born by a mix of natural (vaginal) birth and caesarean section, and were either exclusively breast-fed or mixed fed. This represents one of the relatively few longitudinal microbiome datasets from a non-Western infant population.
Microbial differences between vaginally delivered and caesarean-delivered infants were evident only in samples collected within the first 7 days of life, and these differences disappeared in later samples. Exclusively breast-fed infants showed predominance of Ruminococcus gnavus, Collinsella, and Sutterella species, and different Bifidobacterium species dominated in breast-fed compared to mixed-fed infants. Once infants began weaning, Clostridium, Enterococcus, Roseburia, and Coprococcus species emerged, and butyrate was first detected around this transition.
The findings suggest that delivery mode has only a short-lived influence on the early infant gut microbiota, while feeding practices exert a more sustained effect on which bacterial taxa, including specific Bifidobacterium species, come to dominate. The emergence of butyrate-producing genera at weaning highlights diet transition as a key driver of functional microbiota maturation. These results extend infant microbiome knowledge beyond Western cohorts and can inform feeding and care guidance in similarly underrepresented populations.
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 whether changes in the gut microbiome over time are linked to improvement in liver stiffness in people with nonalcoholic steatohepatitis (NASH). Researchers used 16S rRNA gene sequencing to profile gut microbial communities at baseline and again after 24 weeks of study participation. Liver stiffness was measured using magnetic resonance (MR) elastography, and the investigators compared microbial shifts in participants whose liver stiffness measurement (LSM) improved against those whose did not. They also looked at whether microbial changes tracked with secondary outcomes, including reduction in MRI-derived liver fat (MRI-PDFF) and regression of fibrosis on biopsy.
The cohort consisted of 69 adults with biopsy-confirmed NASH and significant fibrosis (stages 2 to 3), enrolled in a multi-center randomized controlled trial evaluating the drug selonsertib alone or combined with simtuzumab. For comparison, fecal samples were also collected from 32 healthy adults. Genus-level multidimensional scaling was used to see whether microbial changes in the NASH participants who improved resembled the composition seen in this healthy comparison group.
The abundance of 36 bacterial taxa shifted differently between participants with and without longitudinal improvement in liver stiffness. Lactobacillus showed a notably large decrease in participants with LSM improvement (log2 fold change of about -4.51, false discovery rate under 0.001), and Enterococcus was also among the taxa with altered abundance. These findings indicate that specific, identifiable shifts in gut bacterial composition accompany improvement in liver stiffness in NASH, rather than liver stiffness changing independently of the microbiome.
By pairing longitudinal microbiome sampling with an objective, imaging-based measure of liver stiffness, this study strengthens the case for a mechanistic link between gut bacteria and NASH fibrosis trajectory. Identifying taxa such as Lactobacillus and Enterococcus as markers of improvement points toward candidate microbial signatures that could eventually help monitor or stratify NASH patients undergoing treatment. Because the design also compared shifts against a healthy reference cohort, the work lays groundwork for testing whether restoring a more typical gut microbial profile could be a therapeutic target in NASH, though this abstract does not itself establish causation.
This pilot study investigated the gut bacteriome in colorectal cancer (CRC) using 16S rRNA gene sequencing of fecal samples. The researchers aimed to identify microbial markers characteristic of CRC and to determine whether CRC-associated changes in bacterial composition persist after surgical treatment. They also examined functional pathway predictions derived from the 16S rRNA gene data to compare CRC and non-cancer samples.
The study included 49 fecal samples collected from 25 non-cancer (NC) individuals and 12 CRC patients. The CRC patients were sampled both before surgery and again six months after surgery, allowing pre-op and post-op comparisons within the same patients.
CRC patients showed reduced bacterial richness and diversity compared to the non-cancer group, along with increased abundance of pro-carcinogenic bacteria such as Bacteroides fragilis and Odoribacter splanchnicus. These differences between CRC and non-cancer groups were no longer observed after surgery. However, comparing pre-op to post-op CRC samples revealed that while probiotic bacteria increased after surgery, bacteria associated with CRC progression also increased, suggesting persistent dysbiosis. Functional pathway predictions further showed differential enrichment of various pathways between CRC and non-cancer samples.
The findings suggest that CRC is associated with a distinct microbiome signature, including elevated Bacteroides fragilis, that is not fully resolved by surgical removal of the tumor. The persistence of dysbiotic elements after surgery implies a possible field-change effect in the remnant colon, meaning surgery alone may not restore a healthy microbial community. This raises the possibility that residual dysbiosis could contribute to disease recurrence and that post-surgical microbiome monitoring or intervention may warrant further investigation.
This study investigated how diet relates to gut microbiota diversity and composition in patients with colorectal cancer (CRC). Researchers used a nutrition-wide association approach, systematically correlating 216 dietary features with measures of gut microbial diversity and the abundance of 439 gut microbial taxa. They examined alpha-diversity indices, the Firmicutes/Bacteroidetes ratio, and enterotypes derived from beta-diversity, then applied linear regression and LEfSe to link dietary intake to specific microbiome features.
The study population consisted of 115 patients with colorectal cancer who underwent CRC surgery at the Department of Surgery, Seoul National University Hospital. This was a hospital-based cohort, meaning all participants were drawn from a single clinical surgical setting rather than the general population. No further demographic details are given in the abstract.
Several bacteria were found to be enriched in patients who consumed more mature pumpkin or pumpkin juice, with correlation coefficients ranging from about 0.31 to 0.41. Principal coordinate analysis based on the beta-diversity index identified main gut microbiome enterotypes among the CRC patients. Linear discriminant analysis effect size (LEfSe) further distinguished bacterial taxa that were phylogenetically enriched between groups with low versus high consumption of specific dietary items.
The findings suggest that specific dietary components, such as pumpkin and pumpkin juice, may be associated with shifts in the gut microbial community in people with colorectal cancer. This nutrition-wide association approach offers a systematic way to map diet-microbiome relationships in a clinical CRC population rather than relying on single-nutrient analyses. These associations may help inform future research into dietary strategies that could influence the gut microbiota in CRC patients, though the abstract does not report outcome or causal data to confirm clinical benefit.
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.
This study examined whether alterations in the gut microbiota and their metabolic byproducts are linked to glaucoma, a neurodegenerative eye disease marked by progressive loss of retinal ganglion cells (RGCs). Researchers used 16S rRNA (V1-V9 region) sequencing to profile cecal bacterial communities and untargeted metabolomics to characterize circulating metabolites. They then examined how microbial composition and metabolite levels related to RGC status. The overall aim was to determine whether gut-derived signals interact with the neurodegenerative process occurring in glaucoma.
The study population was a glaucomatous rat model compared against a control group of rats, rather than a human cohort. Cecal bacterial samples and metabolomic profiles were obtained from these two groups of animals. Specific numbers of animals per group are not stated in the abstract, so no sample size can be reported beyond the two-group comparison.
Glaucomatous rats showed markedly reduced diversity of cecal bacteria compared with controls, along with a significantly different overall microbial composition. The Firmicutes/Bacteroidetes ratio, the phylum Verrucomicrobia, and the genera Romboutsia, Akkermansia, and Bacteroides were all substantially elevated in glaucomatous animals, and each of these showed a negative correlation with RGC measures. Untargeted metabolomic analysis identified 284 differentially expressed metabolites, with pathway enrichment analysis pointing strongly to alterations in bile secretion pathways.
The findings suggest that gut microbial dysbiosis and disrupted bile-acid-related metabolism may be mechanistically connected to retinal ganglion cell loss in glaucoma. Because several dysbiosis markers correlated negatively with RGC status, the gut-retina axis may represent a contributing factor in glaucoma progression rather than a bystander phenomenon. These results position the gut microbiota and its bile secretion-related metabolites as potential targets for further mechanistic investigation in neurodegenerative eye disease.
This study examined the early-life gut microbiota of term small for gestational age (SGA) infants compared with appropriate for gestational age (AGA) infants. Fecal samples were collected on days 1, 3, 5, and 7 of life and analyzed using 16S ribosomal DNA amplicon sequencing. The researchers then followed the SGA infants for 6 months to assess whether early gut microbiota characteristics related to neurodevelopmental outcomes. The work was motivated by prior evidence that gut microbiota in early life can influence later neurodevelopment, a relationship that had been little studied in SGA populations specifically.
A total of 162 term neonates born at Peking University First Hospital between June 2020 and June 2021 were enrolled. Of these, 41 infants (25.3%) were classified as SGA and made up the study group, while 121 infants (74.7%) were classified as AGA and served as the control group. Neurodevelopmental outcomes at 6 months were assessed among the SGA infants using the Ages and Stages Questionnaires-3 (ASQ-3).
Gut microbial diversity was consistently lower in the SGA group than in the AGA group on days 1, 3, 5, and 7 after birth. Non-metric multidimensional scaling and analysis of similarities showed significant differences in the overall composition of the gut microbiota between the two groups. These findings indicate that being born small for gestational age is associated with a distinct and less diverse early gut microbial community from the first days of life.
The findings support the idea that SGA status shapes the gut microbiota from the earliest days of life, in a pattern distinguishable from AGA infants. Because the study also tracked neurodevelopment at 6 months using the ASQ-3, it points toward the gut microbiota as a possible early biological marker linked to the neurodevelopmental risks already known to affect SGA infants. This underscores the value of monitoring gut microbiota composition in SGA newborns as a potential avenue for identifying infants who may benefit from closer developmental follow-up.
This study analyzed the gut microbiome signatures of members of the Adi, Apatani, and Nyshi tribal communities of Arunachal Pradesh. Researchers sequenced the V3 and V4 regions of the 16S rRNA gene on the Illumina MiSeq platform to characterize bacterial community composition. The aim was to understand how traditional lifestyle and food habits shape the gut microbiome in these ethnic populations.
Thirty individuals were studied in total, drawn from three tribal groups of Arunachal Pradesh: the Adi, Apatani, and Nyshi. Each tribal cohort contributed ten individuals, all residing in remote areas and following traditional lifestyles. No further demographic details such as age or sex distribution are given in the abstract.
Across all three tribes, the gut microbiome was dominated by the phyla Firmicutes, Actinobacteria, Proteobacteria, and Bacteroidates. At the genus level, taxa including Bifidobacterium, Collinsella, Bacteroides, Prevotella, Lactobacillus, Streptococcus, and several others were commonly observed. The Adi and Nyshi tribes showed a high prevalence of Prevotella and Collinsella, while the Apatani tribe showed a high prevalence of Bifidobacterium and Catenibacterium, with the more traditional, remote-dwelling communities showing higher overall gut microbiome diversity.
The findings suggest that traditional lifestyle and dietary food factors are linked to distinct, tribe-specific gut microbiome profiles and greater microbial diversity. This work adds to the broader knowledge base connecting gut microbial communities, ethnicity, and diet, which can inform the identification of microbial biomarkers. Such biomarkers may eventually support therapeutic strategies and disease-state detection in understudied populations.
This study profiled the gut mucosa-associated microbiome of colorectal cancer (CRC) patients in Kenya, where CRC incidence has risen sharply, particularly among younger patients. The researchers used 16S rRNA sequencing to compare microbial community composition between CRC patients and healthy controls. They examined alpha and beta diversity, differential abundance of specific taxa, and predicted microbial metabolic pathways, including bacterial glutamate degradation. The goal was to better understand how gut microbiome dysbiosis may relate to CRC in an understudied Kenyan population.
The study included 18 CRC patients and 18 healthy controls recruited at a single center, the Moi Teaching and Referral Hospital at Moi University in Kenya. Gut mucosa-associated microbiome samples were collected from both groups for 16S rRNA sequencing analysis. The study also evaluated associations between microbiome profiles and the age of the CRC patients, reflecting the hospital's observed rise in younger CRC cases.
Alpha diversity did not differ significantly between CRC patients and healthy controls, but beta diversity showed clear dissimilarities in overall microbial community composition between the two groups. The most notably underrepresented species in the CRC group were Prevotella copri and Faecalibacterium prausnitzii. The depletion of these taxa was linked to microbial metabolic profiling findings involving bacterial glutamate degradation, suggesting a functional as well as compositional shift in the CRC gut microbiome.
These findings suggest that depletion of Prevotella copri and Faecalibacterium prausnitzii, alongside altered bacterial glutamate metabolism, may be part of the microbial dysbiosis pattern associated with CRC in Kenyan patients. Because microbiome data from Sub-Saharan African CRC populations are rare, this study helps fill a geographic and population gap in understanding CRC-associated dysbiosis. The results support further investigation into whether these microbial signatures contribute to, or result from, CRC pathobiology in this rapidly growing patient population, including its younger patients.
This study examined how the maternal and infant gut microbiomes and metabolomes co-develop from late pregnancy through the first year of infant life. The researchers used longitudinal multi-omics data to track microbial community changes alongside metabolite profiles over this perinatal window. A central focus was the transfer of mobile genetic elements from mothers to infants and how this transfer relates to infant gut microbial assembly and metabolism. The study also compared metabolome and immune signatures between infants fed different types of formula and those who were exclusively breastfed.
The study followed a cohort of 70 mother-infant dyads, with sampling spanning from late pregnancy to the infant's first year of life. Within this cohort, a subset of infants received regular formula, others received extensively hydrolyzed formula, and others were exclusively breastfed, allowing comparisons across feeding groups. The abstract does not specify additional demographic details such as geographic location or delivery mode.
The researchers discovered large-scale interspecies transfer of mobile genetic elements from mothers to infants, and these elements frequently carried genes tied 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 that were not present in the mothers. Infants fed regular, non-extensively-hydrolyzed formula showed distinct metabolome and serum cytokine signatures compared with exclusively breastfed infants. These findings indicate that early-life microbiome and metabolome development follows infant-specific trajectories rather than simply mirroring the maternal state.
The findings broaden the concept of vertical transmission of the gut microbiome beyond strain-level transfer to include mobile genetic elements that carry diet-adaptive genes. This suggests that maternal microbes contribute functional genetic material that helps shape how an infant's microbiome adapts to its own diet. The link between formula type and distinct metabolome and cytokine signatures points to feeding practices as a modifiable factor in early immune and metabolic development. Together, these insights provide a foundation for understanding how maternal and infant gut ecosystems co-evolve during a critical developmental window.
This study examined the interaction between the gut microbiota and colorectal cancer (CRC) using metagenomic sequencing data. The researchers analyzed species-level differences in gut microbial composition between CRC cases and controls, built a co-occurrence network to assess microbial interactions with environmental factors, and applied random forest models to identify biomarkers that could distinguish CRC samples from control samples. The overall goal was to build a more precise microbiota panel for CRC diagnosis.
The data came from the GMrepo database, a repository of original metagenomic samples. In total, 709 metagenomic samples from six projects were identified, and after matching, 86 CRC patients and 86 matched healthy controls from six countries were enrolled. Across these paired samples, 484 microbial species and 166 related genera were analyzed.
The analysis confirmed previously recognized associations between Fusobacterium nucleatum and species belonging to Peptostreptococcus, Porphyromonas, and Prevotella with CRC. It also identified new associations involving the novel species Parvimonas micra and Collinsella. These findings emerged from species-level comparisons across the paired CRC and control samples using the co-occurrence network and random forest modeling approach.
By combining paired-sample comparisons, co-occurrence network analysis, and machine learning across a multinational dataset, this study strengthens the case for specific gut bacterial species as CRC-associated biomarkers. The identification of new candidate taxa alongside established ones such as Fusobacterium nucleatum suggests the microbiota panel for CRC diagnosis could be refined and expanded. These results support further validation of species-level microbial signatures as tools for non-invasive CRC detection.
This study used whole-genome sequencing (WGS) to characterize the gut microbiota associated with colorectal cancer (CRC) across populations from different geographic regions. Researchers annotated species-level and genus-level composition with MetaPhlAn2, then compared community structure between regions using PCA and LEfSe analysis. Spearman correlation analysis was applied to CRC-associated differential species, and the findings were used to build CRC risk prediction models. The overall goal was to clarify how regional differences shape the CRC-related microbiome and to translate that into predictive tools.
The analysis drew on a metagenomic dataset of 601 samples from six countries, compiled from the GMrepo and NCBI databases. This represents a secondary, multi-population analysis of existing whole-genome sequencing data rather than a newly recruited clinical cohort. The abstract does not specify age, sex, or individual-level clinical details for the sample population.
The composition of the intestinal bacterial community varied by region, and the specific bacteria that distinguished CRC cases from controls were inconsistent from one region to another. Despite this regional variability, a common set of bacteria appeared across all six countries, including Peptostreptococcus. This pattern suggests both a shared core of CRC-associated taxa and substantial geography-driven variation layered on top of it.
The findings indicate that a single, universal microbial signature is unlikely to capture CRC risk across all populations, since regional differences must be accounted for in any predictive model. Building and validating CRC risk prediction models separately within each regional dataset, as this study did, may be necessary for accuracy across diverse populations. This work supports incorporating geography as a variable in future microbiome-based CRC screening and risk-stratification efforts.
This study examined the gut microbiome composition of patients newly diagnosed with Alzheimer's disease (AD) or mild cognitive impairment (MCI), before any medications or interventions were started. Researchers used 16S ribosomal RNA sequencing of fecal samples to characterize microbial community structure and compare it across diagnostic groups. The goal was to determine whether gut microbiome alterations were present at diagnosis and whether these alterations were more severe in AD than in MCI.
The study included 18 patients newly diagnosed with AD, 20 patients newly diagnosed with MCI, and 18 age-matched healthy controls. Fecal samples were collected in the morning from all participants. None of the AD or MCI patients had received medications or other interventions for their condition before sample collection, distinguishing this cohort from prior studies of already-treated patients.
Microbial alpha-diversity did not differ among the AD, MCI, and healthy control groups, but both AD and MCI patients showed increased beta-diversity compared with healthy controls. At the genus level, AD patients had decreased Bacteroides, Lachnospira, and Ruminiclostridium_9 along with increased Prevotella relative to healthy controls. MCI patients showed the same direction of change in these genera as AD patients, suggesting overlapping microbial alterations across the two conditions.
Because these findings were observed in newly diagnosed, medication-naive patients, they suggest gut microbiome alterations may be present early in cognitive decline rather than resulting from treatment. The similarity in genus-level shifts between MCI and AD patients raises the possibility that microbiome changes track with the progression from mild impairment toward dementia. These results support further investigation of the gut microbiome as an early biomarker or contributing factor in Alzheimer's disease and its prodromal stages.
This study used 16S rRNA gene sequencing of rectal swabs to characterize the gut microbiota of patients with COVID-19 pneumonia. Researchers compared microbial community composition and diversity across different levels of disease severity. The goal was to determine whether gut microbiota alterations accompany COVID-19 pneumonia and differ by clinical setting.
The abstract describes three groups: patients with COVID-19 pneumonia admitted to an intensive care unit (i-COVID19), patients with COVID-19 admitted to infectious disease wards (w-COVID19), and a control group (CTRL). Exact sample sizes and demographic details are not given in the abstract. The comparison design indicates the population was hospitalized adults with confirmed COVID-19 pneumonia of varying severity, alongside non-COVID-19 controls.
ICU patients (i-COVID19) showed a decreased Chao1 index compared to both controls and ward patients, indicating lower microbial richness in the most severe cases, while Shannon Index diversity did not differ. At the phylum level, Proteobacteria increased in ward patients compared to controls, and Fusobacteria and Spirochetes decreased, with Spirochetes reduced specifically in ICU patients relative to controls. These results show significant, severity-associated shifts in gut microbial community composition among COVID-19 pneumonia patients.
The findings suggest gut microbiota composition changes track with COVID-19 pneumonia severity, distinguishing ICU patients, ward patients, and controls. The authors describe these results as preliminary but propose that specific microbial features could serve as biomarkers for diagnosis. If validated in larger cohorts, such biomarkers could help stratify COVID-19 patients by severity or clinical trajectory.
This study examined gut microbiota composition and predicted functional profiles in diarrhea-predominant irritable bowel syndrome (IBS-D). Researchers used 16S ribosomal gene sequencing on fecal samples to characterize dominant bacterial taxa at multiple taxonomic levels. They also applied PICRUSt, a computational tool that infers likely metabolic functions of a microbial community from its 16S profile. The goal was to clarify how gut microbiota differ in IBS-D patients compared to healthy people, since regional variation in microbiota has made the mechanism of IBS hard to pin down.
The study included 30 patients with diarrhea-predominant IBS and 30 healthy controls, all recruited in Nanchang, China. Fecal samples were collected from each participant for 16S sequencing analysis. The abstract does not report age, sex distribution, or other demographic details, so no further inference about the cohort can be made beyond this case-control design in a Chinese population.
Gut microbiota richness, but not overall diversity, was reduced in IBS-D patients compared to healthy controls. At the phylum level, Firmicutes, Fusobacteria, and Actinobacteria were significantly decreased in IBS-D patients, while Proteobacteria was significantly increased. PICRUSt-based functional prediction indicated that IBS-D patients showed up-regulation of pathways related to metabolism of cofactors and vitamins and to xenobiotics biodegradation and metabolism, alongside down-regulation of pathways related to environmental adaptation and cell growth.
The findings suggest that IBS-D is associated with a distinct pattern of reduced microbial richness and a shifted phylum-level composition, marked by loss of Firmicutes, Fusobacteria, and Actinobacteria and gain of Proteobacteria. The predicted functional changes point to altered microbial metabolic capacity, including cofactor and vitamin metabolism and xenobiotic handling, as potentially relevant to IBS-D pathogenesis. Because gut microbiota composition varies by region, these results may help define a population-specific microbial signature for IBS-D in Chinese patients, though the predicted (not directly measured) nature of the functional data warrants cautious interpretation.
This study investigated 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 examine bacterial community structure, relative abundance, functional prediction, differentially abundant bacteria, and co-occurrence networks. The goal was to clarify how the intestinal microbiome differs among these three groups, since prior reports on the microbiome's role in IBD and CRC had not been fully explained.
The analysis drew on fecal metagenomic data from 290 healthy subjects, 512 IBD patients, and 285 CRC patients. Healthy and CRC samples were obtained from the European Nucleotide Archive under accession numbers PRJEB6070, PRJEB7774, PRJEB27928, PRJEB12449, and PRJEB10878. IBD patient data came from the Integrated Human Microbiome Project via the Human Microbiome Project Data Portal, meaning this was a study of previously collected, publicly deposited sequencing datasets rather than a newly recruited cohort.
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, indicating that these two diseases are associated with opposite diversity patterns. The abstract does not mention Bacteroides fragilis, polysaccharide A, or the B. fragilis toxin in the results provided.
These findings suggest that IBD and CRC are marked by distinct, disease-specific patterns of intestinal bacterial diversity and community structure rather than a single shared microbial signature. This distinction could help refine how microbiome-based markers are used to differentiate IBD from CRC in future diagnostic or research contexts. Because the analysis relied on reanalysis of existing public metagenomic datasets, the results also point to the value of large-scale public sequencing repositories for comparative gut microbiome research.
This study examined the composition of the gut microbiota in diffuse large B cell lymphoma (DLBCL), a hematological malignancy whose intestinal microecology had not previously been characterized. Fecal samples were analyzed using 16S rRNA gene sequencing to compare bacterial community composition and diversity. The researchers also used PICRUSt functional prediction to estimate differences in metabolic pathway activity between groups.
The study included 25 untreated patients with diffuse large B cell lymphoma and 26 healthy volunteers who served as controls. Fecal samples from these 51 total participants were the basis for the 16S rRNA sequencing analysis. The abstract does not provide further demographic details such as age or sex distribution.
Alpha-diversity (species diversity and abundance) did not differ significantly between DLBCL patients and healthy controls, but beta-diversity did differ significantly, indicating a distinct overall community structure. The DLBCL microbiota showed a continuous evolutionary relationship progressing from the phylum proteobacteria to the genus Escherichia-Shigella, both significantly more abundant than in controls. Allisonella, Lachnospira, and Roseburia were also more abundant at the genus level in DLBCL patients, while PICRUSt functional prediction showed significantly lower thiamine metabolism and phenylalanine, tyrosine, and tryptophan biosynthesis pathways in the DLBCL group.
The findings demonstrate that gut microbiota composition is significantly altered in untreated DLBCL, establishing a baseline microbial signature associated with this malignancy. This work lays groundwork for future prospective studies to determine whether these microbial differences contribute to disease development or progression. It also opens the door to microbiome-directed interventional trials aimed at improving outcomes for patients with DLBCL.
This study examined how gut microbial signatures relate across three common intestinal diseases: Crohn's disease, ulcerative colitis, and colorectal cancer. The authors performed a meta-analysis across 13 fecal metagenome data sets to identify species and functional pathway markers that were consistently altered within each disease. They then compared the phylogenetic relationships, metabolic preferences, and inter-connections among these disease-associated marker species to see what was shared and what was distinct between the three conditions.
The analysis drew on 13 existing fecal metagenome data sets covering patients with Crohn's disease, ulcerative colitis, and colorectal cancer, compared against controls. The abstract does not give specific participant counts, ages, or geographic origins for these cohorts. Because the work is a meta-analysis of previously published metagenomic data sets rather than a new patient recruitment, the population studied is best described as a compiled multi-cohort fecal metagenomic dataset spanning the three diseases.
The researchers identified 87 marker species and 65 marker pathways that were consistently changed across multiple data sets for the same disease. These markers grouped into disease-specific and disease-common clusters with distinct phylogenetic relationships: Crohn's disease-specific species were phylogenetically closely related, while colorectal cancer-specific species were more phylogenetically distant from one another. Ulcerative colitis-specific species were phylogenetically closer to the colorectal cancer cluster, which the authors suggest reflects the elevated colorectal cancer risk seen in ulcerative colitis patients. Marker species within the same cluster shared metabolic preferences, and a subset of markers correlated with an indicator of leaky gut, while cases showed more coordinated changes and tighter inter-connections among marker species than controls.
By mapping which microbial and pathway markers are shared versus disease-specific, this work provides a framework for building multidisease diagnostic models rather than treating each intestinal disease in isolation. The phylogenetic closeness of ulcerative colitis markers to colorectal cancer markers offers a microbiome-based rationale for the known clinical link between these two conditions. The association between marker species/pathways and a leaky gut indicator supports the idea that gut barrier dysfunction and dysbiosis are mechanistically connected. Overall, the findings suggest that cross-disease microbial signature comparisons could improve diagnostic precision for Crohn's disease, ulcerative colitis, and colorectal cancer.
This study examined whether the composition of the intestinal microbiome influences clinical outcomes in early breast cancer. Researchers used shotgun metagenomics to characterize fecal microbiota composition and paired this with plasma metabolomics. They then tested whether specific gut microbes causally affected tumor prognosis and treatment side effects using a mouse model colonized with patient-derived microbiota and challenged with a histo-compatible mouse breast cancer plus chemotherapy.
The human cohort consisted of 76 early breast cancer patients, from whom 121 fecal specimens were collected, including 45 patients sampled both before and after chemotherapy. These patients were enrolled in the CANTO prospective study, which was designed to record side effects associated with breast cancer clinical management. The findings were further tested in immunocompetent mice colonized with the patients' fecal microbiota.
Specific gut commensal bacteria were found to be overabundant in breast cancer patients compared with healthy individuals. These overabundant commensals were associated with worse breast cancer prognosis and were modulated by chemotherapy exposure. In the mouse model, microbiota from these patients appeared to influence weight gain and neurological side effects associated with breast cancer therapies.
The findings suggest the gut microbiome could serve as a modifiable factor influencing both breast cancer prognosis and treatment tolerability. This raises the possibility of using fecal microbiota composition to help predict outcomes or side effects in patients undergoing adjuvant or neoadjuvant chemotherapy. The authors explicitly state that these findings, obtained in adjuvant and neoadjuvant settings, warrant prospective validation before 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 evaluated whether oral microbiota contributes to colorectal cancer (CRC) progression by comparing saliva and stool microbial communities. Researchers used 16S rRNA analysis and next-generation sequencing to profile bacteria in both sample types. They then applied linear discriminant analysis effect size (LEfSe) to identify species that were differentially abundant between CRC patients and healthy controls, and between early- and advanced-stage CRC.
The study included 52 patients with colorectal cancer and 51 healthy controls, with saliva and stool samples collected from each participant. CRC patients were further divided into an early-stage group (Stage I or II, n = 26) and an advanced-stage group (Stage III or IV, n = 26). This design allowed comparison both between CRC patients and controls and across disease stages within the CRC group.
Indigenous oral bacteria, including Peptostreptococcus, Streptococcus, and Solobacterium species, were present at significantly higher relative abundance in both the saliva and stool of CRC patients compared with controls. Among species enriched in CRC patients, P. stomatis, S. anginosus, S. koreensis, and S. moorei were identified as oral in origin, appearing in both body sites. S. moorei showed a further significant increase in relative abundance in advanced-stage compared with early-stage CRC, and this pattern held true in both saliva and stool samples.
The consistent presence of the same oral-derived bacterial species in both saliva and stool of CRC patients suggests oral microbiota may translocate to, or otherwise influence, the gut environment during CRC progression. The stage-dependent rise of S. moorei raises the possibility that specific oral bacteria could serve as biomarkers tracking CRC advancement. These findings support further investigation into oral-gut microbial crosstalk as a factor in colorectal cancer biology and potential non-invasive monitoring.
This study examined whether the gut microbiome, and specifically its short-chain fatty acid (SCFA) byproducts, are needed for a normal sympathoadrenal stress response to hypoglycemia. Researchers depleted the gut microbiota of adult mice with broad-spectrum, non-absorbable antibiotics and then tested their epinephrine response to insulin-induced low blood sugar. They also tested whether simply recolonizing the gut with bacteria, without restoring SCFA production, could reverse any deficits.
The subjects were male C57Bl6 mice, divided into groups given either regular drinking water (controls) or a cocktail of non-absorbable broad-spectrum antibiotics (Abx) in their drinking water for two weeks. Mice from each group were then injected with either insulin, to induce hypoglycemia, or saline. A separate recolonization group (Abx plus R) was also included to assess reversal of antibiotic effects.
Antibiotic treatment sharply reduced microbial diversity and depleted Bacteroidetes and Firmicutes, enlarged the caecum, and eliminated detectable short-chain fatty acids such as acetate, propionate, and butyrate. These Abx mice showed blunted tonic and stress-induced epinephrine levels. Recolonization restored bacterial diversity but did not restore sympathoadrenal responsiveness or caecal SCFA levels, indicating that bacterial presence alone is insufficient.
The findings suggest that bacterial metabolites, particularly SCFAs, rather than the mere presence of gut bacteria, are what drive normal adrenal catecholamine responses to hypoglycemia. This points to SCFA restoration, not just microbial recolonization, as the relevant target for repairing stress-response deficits after antibiotic-induced dysbiosis. It also implies that antibiotic courses could carry a previously underappreciated risk of disrupting glucose counter-regulatory physiology.
This prospective cohort study evaluated whether intrapartum antibiotics, and specific classes of those antibiotics given during labor and delivery, affect the maturation of the infant gut microbiota over the first year of life. Intrapartum antibiotic exposure was abstracted from maternal medical records. Infant fecal samples were collected at six weeks and one year of age and characterized using 16S rRNA sequencing, with metagenomic analysis performed on a subset of samples to capture taxonomic and functional profiles.
The study population consisted of 266 full-term infants enrolled in the New Hampshire Birth Cohort Study (NHBCS), a prospective cohort based in rural New Hampshire, USA. Infants were classified according to their mothers' exposure to antibiotics, including specific antibiotic classes, during labor and delivery. Fecal samples from these infants were analyzed at two time points, six weeks and one year, to track microbiota development.
Exposure to intrapartum antibiotics, particularly to two or more antibiotic classes, was independently associated with lower microbial diversity and a distinct bacterial community composition at six weeks of age. At one year, infants exposed only to penicillins during labor and delivery had significantly lower alpha diversity scores compared with infants not exposed to any intrapartum antibiotics. Penicillin exposure specifically was also related to a significantly smaller increase over the first year in several bacterial taxa, including Bacteroides.
The findings suggest that not all intrapartum antibiotics affect infant gut microbiota development equally, with penicillin-class exposure and multi-class exposure showing the clearest associations with reduced diversity and altered taxa such as Bacteroides. This class-specific effect implies that clinical decisions about which antibiotic to use during labor and delivery could have lasting consequences for infant microbiome maturation. These results support more granular research into antibiotic stewardship during childbirth, distinguishing between antibiotic classes rather than treating intrapartum antibiotic exposure as a single uniform category.
This study examined whether travel undertaken by elite athletes in the build-up to the 2016 Cricket World Cup altered the composition of the gut microbiome. Researchers collected faecal samples at baseline and after travel and analyzed them using 16S rRNA amplicon sequencing. A subset of samples was also examined with shotgun metagenomic sequencing to look at antibiotic resistance and virulence genes in more detail. The work was motivated by concern that travel-related stress and antibiotic resistance gene spread could affect gut microbiome stability and, potentially, athletic performance.
The cohort consisted of Irish cricket players preparing for the 2016 Cricket World Cup, including 14 male and 7 female athletes. Faecal samples were collected from all 21 participants at baseline and after travel. A smaller subset of four participants had their samples additionally analyzed by shotgun metagenomic sequencing.
One particular travel time point was identified as having the potential to disrupt the gut microbiome, unlike other travel periods examined. Following this travel, alpha diversity of the gut microbiome decreased, accompanied by shifts in the taxonomic profile of the microbial community. Shotgun metagenomic analysis also revealed changes in antibiotic resistance genes and virulence genes after travel. These changes appeared to be linked, in particular, to episodes of gastrointestinal distress during travel.
The findings suggest that travel, especially when accompanied by gastrointestinal distress, can disrupt the gut microbiome of elite athletes, including reductions in diversity and changes in resistance and virulence gene content. Because this analysis was conducted in athletes, the authors note the findings may have broader relevance beyond sport. The results raise concern that travel-associated microbiome disruption could carry implications for health and, potentially, performance in populations that travel frequently. This underscores the value of monitoring gut microbiome stability during periods of travel.
This study examined which environmental and intrinsic factors shape gut microbiota composition and diversity in school-age children, and how these factors relate to metabolic health. Gut microbiota was characterized using 16S sequencing to identify clinical and environmental covariates associated with variation in microbial composition. The study also looked at how co-abundance groups of bacteria related to the presence of metabolic complications.
The cohort was ORSMEC, described as the largest gut microbial population-based study of school-aged children in Latin America, with 926 children aged 6 to 12 years. This is a school-age pediatric population from a developing-country setting, evaluated at a population level rather than in a clinical trial context.
Fourteen clinical and environmental covariates were associated with gut microbial variation, but together they explained only 15.7% of the inter-individual differences observed. Socioeconomic status markers had a major influence on the most abundant taxa and on how children's microbiota distributed across enterotypes. Age was positively correlated with higher microbial diversity in normal-weight children (rho = 0.138, P = 2 x 10-3), but this relationship was negative, though not statistically significant, in overweight and obese children. Co-abundance groups of bacteria were also associated with the presence of metabolic complications.
The findings suggest that socioeconomic and environmental exposures, not just intrinsic biology, are major drivers of gut microbiota composition in children, which helps explain inconsistent dysbiosis patterns reported across pediatric metabolic studies. The divergent relationship between age and diversity in normal-weight versus overweight or obese children implies that childhood weight status may alter normal patterns of microbiome maturation. Because so much of the individual variation remains unexplained, the results point to the need for larger, more comprehensive population-based studies, particularly in underrepresented regions like Latin America, to better characterize the drivers of gut dysbiosis and metabolic risk in children.
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 investigated whether gut microbiota composition in young children and their mothers is associated with different environmental exposures in rural Malawi. The researchers examined exposures such as socio-economic status, water source, sanitary facility, presence of domestic animals, maternal characteristics, season, antibiotic use, and delivery mode. They analyzed faecal samples using 16S rRNA sequencing to characterize bacterial OTU and genus abundances, along with measures of microbiota maturity, diversity, and UniFrac distances. The 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 who were participating in a nutrition intervention trial in rural Malawi. Children were sampled longitudinally at 1, 6, 12, 18, and 30 months after birth, while mothers were sampled once, at 1 month postpartum. This design allowed comparison of microbiota composition across a range of environmental exposures within a low-income, rural population.
The abstract indicates that measures of microbiota maturity and diversity in children were associated with the environmental exposure variables examined, though the specific results text is cut off in the excerpt provided. The study framework compared bacterial OTU and genus abundances and UniFrac distances between participants with differing exposures such as water source, sanitary facility, and domestic animal presence. Because the abstract does not provide the complete results, specific directions, magnitudes, or statistical values cannot be stated here.
This work addresses a gap in understanding how environmental conditions shape gut microbiota development in low-income settings where childhood malnutrition is common. By linking exposures like water source, sanitation, and antibiotic use to microbiota maturity and diversity, the findings could help inform strategies to support healthy microbiota development in vulnerable child populations. Further detail from the full results would be needed to specify which exposures matter most and how they might be targeted by interventions.
This study examined chronological changes in gut microbiota composition among children with acute lymphoblastic leukemia (ALL) using 16S ribosomal RNA sequencing. The researchers tracked microbiota profiles at multiple time points: before chemotherapy began, during treatment, and after chemotherapy was completed. The goal was to determine whether disruptions to the gut microbiota caused by leukemia and its treatment are reversible once therapy ends and disease remission is achieved.
The study population was a group of paediatric patients diagnosed with acute lymphoblastic leukemia, followed longitudinally through the course of their chemotherapy treatment. Their gut microbiota profiles were compared against those of age- and ethnicity-matched healthy children serving as controls. The abstract does not provide an exact number of participants.
Before chemotherapy started, children with ALL showed greater inter-individual variability in gut microbiota composition compared to healthy controls, along with enrichment of bacteria from the Bacteroidetes phylum and the Bacteroides genus. Once chemotherapy commenced, the relative abundance of Bacteroides decreased. Following cessation of chemotherapy, the gut microbiota composition shifted back toward a profile resembling that of the healthy control group.
The findings suggest that chemotherapy-associated disruption of the gut microbiota in pediatric ALL patients is not necessarily permanent and can be restored after treatment ends. This raises the possibility that gut microbiota status could serve as a marker to monitor recovery alongside disease remission. It also points to Bacteroides dynamics as a specific feature worth further investigation in the context of childhood leukemia and chemotherapy exposure.
This study used 16S rRNA gene sequencing to characterize and compare the fecal gut microbiota of children with autism spectrum disorder (ASD) and healthy children. The researchers examined differences at both the phylum and genus levels, including shifts in the Bacteroidetes to Firmicutes ratio. They also looked at species-level changes related to branched-chain amino acid (BCAA) synthesis and evaluated functional pathway differences between groups.
The study included 48 children with autism spectrum disorder and 48 healthy children as controls, all located in China. Fecal samples from these 96 children were analyzed via 16S rRNA sequencing. The abstract does not provide further demographic details such as age range or sex distribution.
Children with ASD showed decreased Firmicutes, Proteobacteria, and Verrucomicrobia, alongside a significantly higher Bacteroidetes/Firmicutes ratio driven by Bacteroidetes enrichment. At the genus level, Bacteroides, Prevotella, Lachnospiracea_incertae_sedis, and Megamonas were increased, while several genera including Clostridium XlVa, Escherichia/Shigella, Haemophilus, and Akkermansia were decreased relative to controls. Species that synthesize branched-chain amino acids, such as Bacteroides vulgatus and Prevotella copri, were significantly increased in ASD children, while Bacteroides fragilis and Akkermansia muciniphila were decreased compared to controls. Notably, the specific pathogenic bacteria present at the highest levels varied from child to child within the ASD cohort.
These findings suggest that gut microbiota alterations in ASD are not uniform but instead vary considerably between individual children, particularly regarding which pathogenic bacteria dominate. The reduction in Bacteroides fragilis and Akkermansia muciniphila, alongside enrichment of BCAA-synthesizing species, points to potential shifts in microbial metabolic output that could relate to gut-brain signaling. This heterogeneity implies that microbiome-based approaches to understanding or addressing ASD-associated GI dysbiosis may need to be individualized rather than applied uniformly across the ASD population.
This study examined how the gastric mucosal microbiota differs across distinct microhabitats within the stomach in the context of gastric cancer (GC). Researchers compared microbial diversity, composition, bacterial co-occurrence networks, and predicted functional profiles across normal, peritumoral, and tumoral tissue. The goal was to determine whether GC-associated stomach microhabitats, rather than cancer stage or type, shape the gastric microbiota.
The cohort consisted of 276 patients with gastric cancer who had not received preoperative chemotherapy and were enrolled retrospectively. Tissue samples were collected from three microhabitats: 230 normal, 247 peritumoral, and 229 tumoral samples. Microbial community composition was assessed using 16S rRNA gene sequencing on the MiSeq platform.
The composition and diversity of the gastric microbiota were determined by the specific stomach microhabitat rather than by GC stage or type. Bacterial richness was decreased in both peritumoral and tumoral microhabitats compared to normal tissue, and the co-occurrence network of abundant bacteria was simplified in the tumoral microhabitat. Helicobacter pylori, Prevotella copri, and Bacteroides uniformis were significantly decreased in tumoral tissue, while Prevotella melaninogenica, Streptococcus anginosus, and Propionibacterium acnes were increased there.
These findings indicate that the tumor microenvironment reshapes the local microbiota in a site-specific manner, with reduced diversity and simplified microbial networks marking the transition from normal to tumoral tissue. The consistent shifts in specific taxa across microhabitats suggest the gastric microbiota could serve as a biomarker of tissue state within the same stomach. This microhabitat-based framework highlights the importance of sampling location when characterizing microbiota changes associated with gastric cancer.
This study examined the relationship between early-life gut microbiome composition and childhood eczema using 16S rRNA gene sequencing. Researchers compared microbial profiles between healthy children and children with eczema, stratifying samples into four age brackets (0-0.5, 0.5-1, 1-2, and 2-3 years) to account for developmental and environmental changes in the gut microbiome. Bifidobacterium and Bacteroides abundance were further verified using quantitative PCR in the same samples.
The cohort included 172 children under age three, divided into a healthy group of 123 subjects and an eczema group of 49 subjects. Samples were further split into four age-based subgroups (0-0.5, 0.5-1, 1-2, and 2-3 years) to enable age-matched comparisons between healthy and eczema children.
Lower relative abundance of Bifidobacterium was associated with childhood eczema, and this reduction was significant in eczema cases from 0.5 to 3 years old but not in infants younger than six months. Microbial diversity was significantly decreased across all age groups in eczema samples, with the most pronounced reduction seen in children aged 2-3 years. Random Forest analysis identified Bifidobacterium operational taxonomic units as highly predictive of eczema status, achieving an AUC of 0.83 in ROC analysis, confirming Bifidobacterium as a key genus linked to the condition.
The findings suggest that reduced Bifidobacterium abundance and lower microbial diversity are meaningful, age-dependent markers of childhood eczema rather than a uniform signature present from birth. The high predictive power of Bifidobacterium-based classification (AUC = 0.83) indicates potential utility as a biomarker for eczema risk or diagnosis in young children. These results also point to Bifidobacterium as a plausible target for future microbiome-directed interventions aimed at eczema prevention or management in early childhood.
This study examined whether gut microbiome changes linked to colorectal cancer (CRC) hold up across different patient cohorts and populations. The researchers combined data from five publicly available datasets with two newly generated cohorts, then tested their conclusions on two further validation cohorts. They looked at overall microbial richness, functional pathways such as gluconeogenesis, putrefaction, fermentation, and carbohydrate degradation, and specific genes including the choline trimethylamine-lyase gene, to see which features consistently distinguished CRC from controls.
The analysis drew on a combined total of 969 fecal metagenomes assembled from multiple public and newly collected cohorts. These samples came from people with colorectal cancer as well as control subjects without the disease, spanning several independent study populations. The abstract does not give individual demographic details, but the design explicitly used multiple geographically and methodologically distinct cohorts to test reproducibility.
The gut microbiome in CRC showed reproducibly higher species richness than in controls (P < 0.01), driven partly by expansion of species normally found in the oral cavity. Gluconeogenesis and putrefaction and fermentation pathways were associated with CRC, while stachyose and starch degradation pathways were associated with controls. A predictive microbiome signature trained across multiple datasets achieved high accuracy in cohorts it had not been trained on, with an average area under the curve of 0.84, and the choline trimethylamine-lyase gene was significantly overabundant in CRC (P = 0.001), pointing to a link between microbial choline metabolism and the disease.
By validating microbiome signatures across multiple independent cohorts, the study shows that certain CRC-associated microbial features are reproducible rather than cohort-specific artifacts. These consistent, high-accuracy signatures could form the basis for microbiome-based diagnostic or prognostic tests for colorectal cancer. The identified link to choline metabolism also opens a concrete, testable mechanistic hypothesis for how gut bacteria might contribute to CRC development.
This study examined whether the oral microbiome influences the development of oral squamous cell carcinoma (OSCC), the most common head and neck malignancy. Researchers used 16S rRNA gene sequencing and metatranscriptomic analysis to track longitudinal changes in oral microbiome composition and function. They did this in a 4-nitroquinoline-1-oxide (4-NQO) induced mouse model of OSCC, comparing colonized gnotobiotic mice to controls lacking a microbiome. Two different microbiome inocula were tested: one from healthy mice and one from mice already bearing a 4-NQO induced tumor.
The subjects were gnotobiotic mice, animals raised germ-free and then deliberately colonized with defined microbial communities, rather than human patients. Mice were divided into groups based on which oral microbiome inoculum they received (healthy-derived versus tumor-derived) and whether they were exposed to the carcinogen 4-NQO. Control groups included mice exposed to 4-NQO but lacking any microbiome, and mice not exposed to 4-NQO at all. The abstract does not report specific sample sizes for these groups.
Mice colonized with either oral microbiome and exposed to 4-NQO developed more numerous and larger tumors than 4-NQO exposed controls without a microbiome, indicating the microbiome promoted tumorigenesis. Overall microbial diversity increased in tumorigenic samples compared to the nontumor group not exposed to 4-NQO. Despite variability in how communities changed over time, consistent patterns emerged as disease progressed. Notably, the two groups inoculated with the OSCC-associated microbiome showed opposite abundance trends for Parabacteroides and Corynebacterium, with Parabacteroides decreasing in the control group.
The findings support a causal role for the oral microbiome in promoting oral squamous cell carcinoma development, rather than the microbiome merely reflecting tumor presence. The identification of specific taxa, such as Parabacteroides and Corynebacterium, with divergent abundance patterns during disease progression suggests these organisms could serve as markers or contributors to tumorigenesis. This gnotobiotic mouse model provides a controlled system for further dissecting how oral microbial communities interact with carcinogen exposure to drive cancer. These results underscore the potential value of monitoring or modulating the oral microbiome as part of understanding OSCC risk.
This randomized, controlled, parallel-arm trial examined whether 8 weeks of daily almond snacking changes the composition of the gut (fecal) microbiome compared with an isocaloric graham cracker snack. Almonds are rich in fiber, unsaturated fats, and polyphenols, nutrients thought to favorably shift gut microbial ecology. The researchers measured gut microbiome alpha-diversity and the abundance of specific bacterial taxa, including the pathogenic bacterium Bacteroides fragilis, using stool samples collected at baseline and after the intervention.
The study enrolled 73 college freshmen aged 18 to 19 years, including 41 women and 32 men, with body mass indexes ranging from 18 to 41 kg/m2. None of the participants had cardiometabolic disorders at enrollment. Participants were randomly assigned to an almond snack group (56.7 g/d, 364 kcal; n = 38) or a graham cracker control group (77.5 g/d, 338 kcal/d; n = 35).
After 8 weeks, the almond group showed 3% greater quantitative alpha-diversity (Shannon index) and 8% greater qualitative alpha-diversity (Chao1 index) than the cracker group. Almond snacking also decreased the abundance of the pathogenic bacterium Bacteroides fragilis by 48% relative to the control snack. Both differences reached statistical significance (P < 0.05), indicating that the almond snack produced measurable shifts in gut microbial ecology beyond what the isocaloric cracker snack achieved.
The findings suggest that a simple dietary substitution, swapping a processed snack for a nutrient-dense whole food like almonds, can meaningfully increase gut microbial diversity and reduce the abundance of a pathogenic organism, Bacteroides fragilis, over a relatively short period. Because reduced gut diversity and altered Bacteroides fragilis levels have been linked to cardiometabolic disturbances, this points to almond snacking as a low-cost, food-based strategy worth further study in populations at higher metabolic risk. The results also support the broader idea that fiber-, unsaturated-fat-, and polyphenol-rich foods can be used deliberately to reshape the gut microbiome.
This study examined how the mode of delivery affects the earliest establishment of the infant gut microbiota during the neonatal period, defined as the first month of life. The researchers used longitudinal sampling and whole-genome shotgun metagenomic analysis to track microbial colonization over time. They focused specifically on whether caesarean section birth disrupts normal transmission of maternal gut bacteria and permits colonization by environmental or hospital-associated microbes.
The cohort included 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 into infancy. For a subset of these infants, matched maternal samples were also collected, comprising 175 mothers paired with 178 babies. This design allowed direct comparison of microbial strains shared, or not shared, between mothers and their infants.
Babies delivered by caesarean section showed disrupted transmission of maternal Bacteroides strains compared with vaginally delivered infants. These caesarean-born babies instead showed high-level colonization by opportunistic pathogens associated with the hospital environment, including Enterococcus, Enterobacter, and Klebsiella species. Similar, though less pronounced, disruptions 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 delivery mode and related perinatal factors, such as antibiotic exposure and breastfeeding, shape whether a newborn's gut is colonized by beneficial maternal strains or by opportunistic hospital-associated pathogens. Because early microbiota disruption has been linked to later disease risk, these results raise concerns about the downstream health consequences of stunted maternal strain transmission after caesarean birth. The study underscores the importance of considering delivery practices, antibiotic prophylaxis, and breastfeeding support as factors that influence the trajectory of infant gut microbiome development.
This study examined whether gut microbiome associations with colorectal cancer (CRC) that have been documented mainly in developed, high-incidence countries also hold in a distinct population. The researchers performed combined metagenomic and metabolomic association analyses on fecal samples to characterize bacterial taxa and metabolic pathways linked to CRC. They then compared their findings against CRC microbiome data available from other populations to test for conservation or divergence of these associations.
The cohort consisted of fecal samples from 30 CRC patients and 30 healthy controls, all recruited from two different locations in India. This design allowed the authors to test whether host-microbiome relationships identified in other, mostly Western, cohorts generalize to an Indian population. The comparison also drew on previously published CRC microbiome data from other countries.
The study confirmed associations between Bacteroides and other bacterial taxa with CRC that had been previously reported in other populations, supporting some generalizability of prior findings. A novel finding specific to the Indian cohort was the association of Flavonifractor plautii, a flavonoid-degrading bacterium, with CRC. The abundance of F. plautii correlated significantly with enzymes and metabolic modules involved in flavonoid degradation in the Indian CRC samples.
The findings suggest that F. plautii may contribute to CRC risk by degrading beneficial anticarcinogenic flavonoids, reducing their protective availability in the gut. This population-specific association highlights that CRC-microbiome relationships are not fully uniform across global populations and that some associations may be context dependent. The results underscore the importance of studying diverse, non-Western cohorts to build a complete picture of microbiome contributions to CRC.
This study examined patterns of gut microbiota composition in people living with HIV/AIDS compared to HIV-uninfected healthy individuals. Stool samples were profiled by sequencing bacterial 16S rRNA genes to characterize community structure and abundance of specific taxa. The researchers also compared microbiota differences between treated and untreated HIV patients, and between patients grouped by mode of HIV transmission (homosexual versus heterosexual).
The study enrolled 33 patients with HIV/AIDS from a population in South China, including 14 participants who had received highly active antiretroviral therapy (HAART) for more than 3 months and 19 who had not received treatment. A comparison group of 35 healthy controls was also enrolled. This was a cross-sectional design using stool samples collected from these participants.
Dysbiosis was more common in patients with AIDS than in healthy controls, marked by decreased alpha-diversity. Patients with AIDS had lower mean counts of Bacteroidetes, Faecalibacterium, Prevotella, Bacteroides vulgatus, Dialister, and Roseburia inulnivorans, alongside higher mean counts of Proteobacteria, Enterococcus, Streptococcus, Lactobacillus, Lachnoclostridium, Ruminococcus gnavus, and Streptococcus vestibularis. Bacilli abundance was increased specifically in homosexual patients, while Proteobacteria abundance was higher among heterosexual patients with HIV.
These findings reinforce that HIV/AIDS is associated with a distinct, reproducible gut dysbiosis signature involving both reduced beneficial commensals and increased pro-inflammatory or opportunistic taxa. The differences observed by transmission route and treatment status suggest that host behavioral and clinical factors may shape the gut microbiome in HIV infection beyond the virus itself. Characterizing these shifts could help identify microbial targets relevant to the gastrointestinal disease and systemic immune activation seen in AIDS.
This study examined how cervical microbiota composition relates to the severity of cervical intraepithelial neoplasia (CIN), distinguishing direct associations from indirect associations mediated through HPV infection. Prior research had only measured the total association between cervical microbiota and either HPV infection or CIN, without separating these two pathways. The researchers used 16S rRNA gene sequencing to profile cervical microbiota and a sensitive PCR method to detect HPV, then modeled direct and indirect (HPV-mediated) associations with CIN status separately.
The study included 126 women classified as CIN 1- (normal cytology and CIN 1) and 40 women classified as CIN 2+ (CIN 2 and CIN 3), for a total of 166 women. Cervical samples from these women were analyzed for microbiota composition using Illumina sequencing of the 16S rRNA gene, and HPV status was determined using the SPF1/GP6+ PCR primer set.
Several taxa, including Pseudomonas stutzeri, Bacteroides fragilis, Lactobacillus delbrueckii, Atopobium vaginae, and Streptococcus agalactiae, showed indirect associations with CIN status mediated by HPV infection. For Ps. stutzeri, the direct and indirect associations with CIN status ran in opposite directions, while for A. vaginae the direct and indirect associations ran in the same direction. B. fragilis, L. delbrueckii, and S. agalactiae showed only indirect associations with CIN status, with no independent direct effect detected.
The findings suggest that some cervical microbial populations, including B. fragilis, influence CIN risk primarily by way of their relationship with HPV infection rather than through a direct pathway. Distinguishing direct from HPV-mediated indirect associations offers a more precise picture of how the cervical microbiome contributes to cervical disease progression. This approach could help refine future research into microbiota-based risk assessment or intervention strategies for cervical neoplasia.
This study examined the association between gut microbiota composition and Helicobacter pylori-related gastric lesions in a population at high risk for gastric cancer. Researchers used deep sequencing of the microbial 16S ribosomal RNA gene in fecal samples to characterize gut bacterial communities. The work was motivated by concern that H. pylori eradication, while effective for gastric cancer prevention, may carry adverse consequences such as microbial dysbiosis.
The study included 47 subjects from a high-risk population for gastric cancer. Participants were grouped by H. pylori infection status (negative, past infection, or current infection) and by gastric lesion category, including normal, gastritis, and metaplasia. Fecal samples from these subjects were used for the microbiota analysis.
Bacteroidetes, Firmicutes, and Proteobacteria dominated the fecal microbiota, with average relative abundances of 54.77%, 31.37%, and 12.91% respectively. Microbial diversity, measured by observed species and the Shannon index, was higher in subjects with past or current H. pylori infection than in H. pylori-negative subjects. Bacteroidetes abundance significantly decreased from H. pylori-negative subjects (66.16%) to those with past infection (33.01%), and also declined progressively from normal (76.49%) to gastritis (56.04%) to metaplasia (46.83%). Firmicutes and Proteobacteria showed elevated trends in the past infection group compared with the negative group, though these differences did not reach statistical significance.
The findings suggest that H. pylori infection history and the severity of associated gastric lesions are linked to measurable shifts in gut bacterial diversity and composition, particularly reductions in Bacteroidetes. This raises the possibility that gut microbial dysbiosis accompanies both H. pylori infection and its downstream gastric pathology, which is relevant to concerns about consequences of eradication therapy. The results support further investigation into how gut microbiota patterns might serve as markers or contributors to gastric lesion progression in high-risk 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 to profile gut bacteria. Bacterial reads were grouped into Operational Taxonomic Units (OTUs) using the RDP classifier and RDP 16S rRNA database. 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 exact age range, sex distribution, or geographic location of the participants. Sample material was presumably fecal, consistent with standard 16S rDNA gut microbiome protocols, though this is not explicitly stated.
Obese children showed lower intestinal flora diversity than normal-weight controls, based on the alpha diversity measure. Significant differences in the relative abundance of specific bacterial taxa were detected at multiple levels of classification between the two groups. The abstract does not name Bacteroides fragilis, polysaccharide A, or the B. fragilis toxin as part of these findings. The beta diversity analysis further confirmed dissimilarity in overall community composition between obese and normal children.
Identifying the specific bacterial taxa that differ between obese and normal-weight children may help clarify the role of gut microbiota in childhood obesity development. This information could support future research into the mechanisms linking intestinal flora composition to weight gain in children. Such findings may also inform the search for new microbiome-based strategies to address or prevent childhood obesity, though the abstract does not describe any specific intervention tested.
This study evaluated whether faecal metagenomes could serve as non-invasive diagnostic biomarkers for colorectal cancer (CRC). Researchers performed metagenome-wide association studies on stool samples to identify microbial species and gene markers that differ between CRC patients and controls. They then tested whether these markers could be validated across independent cohorts from different countries and confirmed using targeted quantitative PCR (qPCR) assays.
The discovery cohort included 74 patients with CRC and 54 controls from China. Validation used 16 patients and 24 controls from Denmark, plus two previously published cohorts from France and Austria. A further independent Chinese cohort of 47 patients with CRC and 109 controls was used for qPCR validation of selected biomarkers.
The analysis confirmed known associations of Fusobacterium nucleatum and Peptostreptococcus stomatis with CRC, and identified new associations including Parvimonas micra and Solobacterium moorei. Twenty microbial gene markers differentiated CRC from control microbiomes, and four of these were validated in the Danish cohort. In the French and Austrian cohorts these four genes distinguished CRC from controls with AUCs of 0.72 and 0.77, and qPCR measurement of two of the genes classified CRC patients in the independent Chinese cohort with an AUC of 0.84 and an odds ratio of 23. These marker genes were also enriched in early-stage disease.
The findings suggest that faecal microbial gene markers can distinguish CRC from controls with reasonably strong accuracy across geographically and methodologically distinct cohorts, supporting their potential as generalizable, non-invasive screening tools. Enrichment of these markers in early-stage CRC suggests they could help with earlier detection, which is important given the survival benefit of early diagnosis. The use of a simple qPCR assay to reproduce diagnostic performance also points toward a practical, scalable path from metagenomic discovery to clinical stool-based testing.
This study examined whether the gut microbiota (GMB) is associated with brain amyloidosis in cognitively impaired elderly patients. The researchers measured stool abundance of selected bacterial taxa with known pro- and anti-inflammatory activity, including Escherichia/Shigella, Pseudomonas aeruginosa, Eubacterium rectale, Eubacterium hallii, Faecalibacterium prausnitzii, and Bacteroides fragilis. They also measured blood levels of pro-inflammatory cytokines (CXCL2, CXCL10, IL-1B, IL-6, IL-18, IL-8, NLRP3 inflammasome, TNF-alpha) and anti-inflammatory cytokines (IL-4, IL-10, IL-13). The goal was to test whether a specific pro-inflammatory GMB profile and peripheral inflammation track with amyloid buildup, a hallmark of Alzheimer's disease pathogenesis.
The study included cognitively impaired patients with brain amyloidosis (n = 40, labeled Amy+) and cognitively impaired patients without brain amyloidosis (n = 33, labeled Amy-). A control group of 10 individuals with neither cognitive impairment nor brain amyloidosis was also included. All participants were assessed for stool bacterial taxa abundance and blood cytokine expression.
Amy+ patients showed higher levels of certain markers compared with the other groups, consistent with a link between brain amyloidosis and both pro-inflammatory gut bacterial taxa and peripheral inflammation. The abstract text was truncated before the specific comparative results were given, so exact taxa-level or cytokine-level differences cannot be restated here beyond what is confirmed: Amy+ patients had elevated findings relative to Amy- and control groups. Bacteroides fragilis was among the taxa specifically measured in this comparison.
The findings support the idea that a pro-inflammatory gut microbiota profile, combined with peripheral inflammatory activation, may be associated with brain amyloid deposition in cognitively impaired elderly patients. This suggests the gut microbiota could play a role in the pathogenesis of sporadic, nongenetic Alzheimer's disease through inflammatory pathways. If confirmed, gut bacterial taxa and peripheral cytokines could serve as investigational markers or targets in relation to amyloid pathology, though the abstract does not specify treatment or diagnostic applications.
This study examined the bacterial community composition of the bronchial airway, sampled by protected bronchial brushing, in relation to atopic asthma. The researchers used 16S rRNA gene sequencing to characterize the bronchial bacterial microbiome and inferred community-level functional profiles from the sequencing data. They compared microbiome composition across groups and examined associations with clinical and inflammatory features, including type 2-related inflammation markers and the change in airway hyperresponsiveness following six weeks of inhaled fluticasone treatment.
The study included 42 adults with steroid-naive atopic asthma, 21 adults with atopy but no asthma, and 21 nonatopic healthy control subjects. All participants underwent bronchial brushing to obtain airway samples for bacterial profiling. The asthmatic group had not yet received corticosteroid treatment at the time of initial sampling, allowing comparison before and after six weeks of fluticasone.
The bronchial microbiome differed significantly among the three groups. Asthmatic subjects were uniquely enriched in members of the Haemophilus, Neisseria, Fusobacterium, and Porphyromonas genera compared with the atopy-only and healthy control groups. These compositional differences suggest that microbiome features are more closely tied to the asthma phenotype itself than to atopy or aeroallergen sensitization alone.
By comparing steroid-naive asthmatics, atopic non-asthmatics, and healthy controls, the study helps disentangle whether bronchial microbiome changes reflect asthma, atopy, or corticosteroid treatment. Enrichment of specific bacterial genera in asthmatic airways points to potential microbial targets or biomarkers relevant to asthma pathophysiology. The examination of microbiome relationships to corticosteroid responsiveness also raises the possibility that airway bacterial composition could inform understanding of treatment response in asthma.
This study examined whether gut dysbiosis correlates with clinical progression of Parkinson's disease (PD) over a two-year period. Researchers tracked changes in gut microbiota composition alongside demographic and clinical features across that follow-up window. The work builds on a prior report from the same group describing gut dysbiosis in PD patients. The aim was to link baseline microbial counts to later changes in motor and non-motor symptom severity.
The cohort consisted of 36 patients with Parkinson's disease who were followed for two years. Patients were later divided evenly into a deteriorated group and a stable group based on how much their total UPDRS scores worsened over that period. The abstract does not provide further demographic details such as age, sex distribution, or disease duration at enrollment.
Change in total UPDRS score over two years was predicted by baseline counts of Bifidobacterium and the Atopobium cluster, with a correlation coefficient of 0.52. Low baseline counts of Bifidobacterium and Bacteroides fragilis were associated with worsening of UPDRS I scores over two years. Low baseline Bifidobacterium was specifically linked to worsening hallucinations and delusions, while low baseline B. fragilis was linked to worsening motivation and initiative. The deteriorated group had lower baseline counts of Bifidobacterium, B. fragilis, and Clostridium leptum than the stable group at year zero, though not at year two, suggesting an accelerated decline in these bacteria preceded clinical worsening.
These findings suggest that baseline levels of specific gut bacteria, including Bifidobacterium and Bacteroides fragilis, may serve as early indicators of which PD patients are likely to experience faster clinical deterioration. The distinct associations between particular taxa and specific symptom domains (psychiatric versus motivational) point toward possible microbiota-linked pathways influencing different aspects of PD progression. This raises the possibility that monitoring or modulating these bacterial populations could eventually inform prognostic assessment or intervention strategies in PD, though the abstract does not describe any mechanistic or interventional testing.
This study examined whether asthma during pregnancy alters the composition of the infant gut microbiota, with a focus on lactobacilli and other microbes. Infant fecal microbiota were profiled by gene sequencing at 3-4 months of age. The researchers compared microbiota abundance between infants born to mothers with and without asthma treatment during pregnancy, and tested whether these effects differed by infant sex.
The study drew on 1021 mother-infant pairs from the Canadian Healthy Infant Longitudinal Development (CHILD) full-term birth cohort. Infant fecal samples were collected and profiled at 3-4 months of age. Covariates examined alongside maternal asthma status included infant sex, maternal ethnicity, pre-pregnancy overweight and atopy status, birth mode, breastfeeding status, and intrapartum antibiotic treatment.
Male, Caucasian infants born to mothers with prenatal asthma had fewer lactobacilli in the gut at 3-4 months of age, independent of birth mode and other covariates. When asthmatic mothers were also overweight before pregnancy, Lactobacillus abundance in male infants was reduced further, while female infants instead showed enrichment of Bacteroidaceae. These sex-specific microbiota differences linked to maternal prenatal asthma status were also more evident in certain subgroups of women, as described in the abstract.
The findings suggest that maternal asthma during pregnancy shapes infant gut microbiota development in a sex-specific manner, rather than affecting all infants uniformly. Because lactobacilli influence infant growth, reduced lactobacilli in male infants of asthmatic mothers may connect maternal respiratory disease to sex-specific patterns of infant development. Maternal pre-pregnancy weight status appears to compound these effects, pointing to a need for sex-stratified approaches when studying maternal health influences on infant microbiota.
This study examined whether specific faecal bacterial groups are correlated with body mass index (BMI) in children. Researchers measured the occurrence and concentration of the Bacteroides fragilis group, Clostridium spp., Bifidobacterium spp., Escherichia coli, Lactobacillus spp., and Methanobrevibacter smithii in stool samples. Both culture-based techniques and quantitative PCR were used to detect and quantify these organisms, and the resulting bacterial levels were statistically correlated with BMI.
The study population consisted of 84 faecal samples collected from children classified into three weight groups: 30 obese, 24 overweight, and 30 lean children. This design allowed direct comparison of faecal microbial profiles across the BMI spectrum within a paediatric cohort. No further demographic details are given in the abstract.
Bacteroides vulgatus, Clostridium perfringens, and Bifidobacterium adolescentis were the most prevalent species detected by culture across all samples. The Bacteroides fragilis group was present at significantly higher concentrations in obese and overweight children than in lean children (p 0.015), and its faecal levels were positively correlated with BMI (r = 0.24, p 0.026). Lactobacillus spp. were also higher in obese and overweight children (p 0.022) and showed an even stronger positive correlation with BMI (r = 0.44, p 0.002), while Bifidobacterium spp. were found in higher numbers in lean children than in overweight or obese children (p 0.042).
These findings suggest that specific faecal bacterial taxa, including the Bacteroides fragilis group and Lactobacillus spp., track with higher BMI in children, while Bifidobacterium spp. track with leanness. This supports the idea that childhood weight status is associated with distinct, quantifiable shifts in gut microbial composition. Such associations may inform future research into microbiome-based markers or targets relevant to paediatric obesity risk.
This study compared the colonic microbial composition of patients with systemic sclerosis (SSc) to that of healthy controls. Researchers used 16S ribosomal RNA sequencing on mucosal lavage samples collected from the cecum and sigmoid colon during colonoscopy. They also examined whether specific bacterial genera were associated with the presence and severity of gastrointestinal tract symptoms in the SSc patients.
The study included 17 adult patients with systemic sclerosis, 88 percent of whom were female, with a median age of 52.1 years. Healthy controls were matched to the SSc patients by age and sex on a one-to-one basis. Gastrointestinal symptom burden in the SSc group was assessed with the GI Tract 2.0 score, which averaged 0.7 with a standard deviation of 0.6.
Principal coordinate analysis showed significant differences in microbial community structure between SSc patients and healthy controls in both the cecum and sigmoid regions. Patients with SSc had decreased levels of commensal bacteria such as Faecalibacterium and Clostridium, a pattern similar to that seen in other inflammatory disease states. The abstract text provided is cut off before detailing which genera were increased in SSc patients or which specific genera correlated with GI symptoms, so those findings cannot be reported here.
The findings suggest that systemic sclerosis is associated with a distinct colonic microbial consortium that departs from that of healthy individuals, marked by loss of beneficial commensal genera. Because this shift parallels patterns observed in other inflammatory conditions, it raises the possibility that the gut microbiome contributes to or reflects the inflammatory processes underlying SSc. This supports further investigation into the colonic microbiota as a potential factor in SSc-related gastrointestinal symptoms and as a possible target for future research or intervention.
This study examined whether the enteric virome, alongside the bacterial microbiome, contributes to HIV infection and the resulting immunodeficiency seen in AIDS. Researchers characterized viral and bacterial communities in stool samples to see how they related to disease status and antiretroviral therapy (ART). The work addressed a gap in knowledge, since prior research had linked HIV to microbial translocation and enteropathy but had not clarified the virome's role.
The study drew on a cohort of Ugandan patients that included HIV-uninfected individuals and HIV-infected individuals. Among the HIV-infected participants, some were treated with antiretroviral therapy (ART) and others were untreated. Peripheral CD4 T cell counts were measured across these groups and used to stratify findings.
Patients with low peripheral CD4 T cell counts showed an expansion of enteric adenovirus sequences, and this expansion occurred independent of ART treatment. These same lower-CD4 patients also had a bacterial microbiome with reduced phylogenetic diversity and richness. Specific bacteria differed in abundance by CD4 status, including increases in Enterobacteriaceae, a group previously associated with inflammation.
The findings indicate that immunodeficiency in progressive HIV infection is accompanied by coordinated shifts in both the enteric virome and the bacterial microbiome. These combined viral and bacterial alterations may contribute to AIDS-associated enteropathy and to disease progression more broadly. The results suggest that the virome, not just bacteria, deserves attention as a potential factor in HIV-related gut dysfunction.
This case-control study examined whether the composition of the gut bacterial community differs in children with early onset relapsing-remitting multiple sclerosis (MS) compared to children without autoimmune disease. Researchers used 16S ribosomal RNA sequencing of fecal samples to characterize microbial community composition, and applied PICRUSt (phylogenetic reconstruction of unobserved states) to predict functional pathways associated with the identified taxa. Associations between subject characteristics, including immunomodulatory drug (IMD) exposure, and microbiota measures such as beta diversity and taxa abundance were tested using non-parametric tests, permutational multivariate analysis of variance, and negative binomial regression.
The study included 18 children with relapsing-remitting MS and 17 control children, matched for age and sex, recruited from a pediatric clinic at the University of California, San Francisco. Participants were 18 years old or younger, with a mean age of 13 years (range 4 to 18). The MS cases had short disease duration, with a mean of 11 months since onset (range 2 to 24 months), and about half of the cases had never been exposed to immunomodulatory drugs.
Overall gut bacterial beta diversity was not significantly related to MS status itself, but it was significantly associated with immunomodulatory drug exposure (Canberra distance, P < 0.02). Despite the lack of an overall diversity difference by disease status, MS cases showed a significant enrichment in the relative abundance of certain bacterial taxa compared to controls. The abstract text was truncated before specifying which taxa were enriched, so the exact organisms identified in this excerpt cannot be stated. This study does not mention Bacteroides fragilis, polysaccharide A, or the B. fragilis toxin.
The findings suggest that gut microbiota alterations may be detectable even in the earliest stages of pediatric MS, supporting the broader hypothesis that gut microbial communities could play a role in neurological autoimmune disease. The significant link between immunomodulatory drug exposure and microbial beta diversity highlights that treatment status is an important variable to control for in microbiome studies of MS. These results support further investigation into gut bacteria as potential biomarkers or contributors to early MS pathophysiology in children.
This study examined how the infant gut microbiota develops during the first six months of life. Researchers measured 33 bacterial taxa and 8 bacterial metabolites in fecal samples using qPCR and RT qPCR. They then used regression analysis to look for associations between microbiota composition and early-life factors over time.
The study followed 108 healthy neonates who were sampled repeatedly during their first half year of life. Alongside the fecal samples, questionnaires collected information on each infant's gender, place and mode of birth, presence of siblings or pets, feeding pattern, and antibiotic use. This allowed the researchers to relate microbiota measurements directly to these early-life exposures within the same cohort.
Bacterial DNA was detected in most meconium samples, suggesting that bacterial exposure may begin in utero, before birth itself. After birth, colonization by Bifidobacterium, Lactobacillus, and Bacteroides species was shaped by mode of delivery, type of feeding, and the presence of siblings. These effects were evident at the species level and changed over the first six months of life. Infant-type bifidobacterial species such as B. breve and B. longum subsp. infantis showed distinct patterns tied to these early-life factors.
The findings support the idea that mode of delivery, feeding type, siblings, and gender are meaningful, modifiable or identifiable factors shaping early gut colonization. Because altered early colonization has been linked to higher disease risk later in life, understanding these influences could inform strategies to support healthy infant microbiota development. The detection of bacterial DNA in meconium also raises the possibility that microbial exposure begins earlier than birth, a question worth further investigation.
This study examined whether the composition of gut microbiota differs between infants with eczema and healthy infants. Researchers used high-throughput sequencing of the V3-V4 hypervariable regions of the 16S rRNA gene to profile fecal bacterial communities. The analysis focused on identifying specific bacterial genera and species whose abundance differed between eczematous and healthy infants, rather than broad differences in overall taxonomic composition.
The study was a case-control comparison of 50 infants with eczema (cases) and 51 healthy infants (controls). Fecal samples from these 101 infants were used to generate a total of 12,386 operational taxonomic units (OTUs) at 97% similarity. The abstract does not provide further demographic details such as age range, feeding method, or geographic location.
Gut microbiota differed between the two groups in taxa abundance, not in overall taxonomic composition. Healthy infants showed enrichment of Bifidobacterium, Megasphaera, Haemophilus, and Streptococcus, while infants with eczema showed enrichment of Escherichia/Shigella, Veillonella, Faecalibacterium, Lachnospiraceae incertae sedis, and Clostridium XlVa. At the species level, Faecalibacterium prausnitzii and Ruminococcus gnavus, both previously linked to atopy or inflammation, were significantly enriched in infants with eczema, and Akkermansia muciniphila was also more abundant in this group.
The findings support a model in which specific shifts in gut bacterial abundance, rather than wholesale changes in community composition, accompany eczema in infancy. The enrichment of Faecalibacterium prausnitzii, Ruminococcus gnavus, and Akkermansia muciniphila points to potential roles for these organisms in intestinal barrier integrity and inflammatory processes relevant to atopic disease. These associations suggest candidate microbial targets for further mechanistic study and potential early-life markers of eczema risk.
This study examined the gut mucosal microbiome across successive stages of colorectal tumorigenesis, from precancerous adenoma through invasive carcinoma. The researchers catalogued microbial communities in mucosal tissue and used probabilistic partitioning of relative abundance profiles to identify recurring community configurations, or metacommunities, associated with disease stage. They also examined paired lesion and adjacent-mucosa samples to track how bacterial correlation patterns shift as tissue progresses toward cancer.
The analysis drew on 47 paired samples of adenoma and adenoma-adjacent mucosae, 52 paired samples of carcinoma and carcinoma-adjacent mucosae, and 61 healthy control samples, all from human gut mucosal tissue. These findings were then validated against two previously published, independently collected data sets. The abstract does not specify further demographic details such as age, sex, or geographic origin of the participants.
A metacommunity dominated by members of the oral microbiome was primarily associated with colorectal cancer, distinguishing cancerous tissue from healthy mucosae. Paired-sample analysis revealed distinct community configurations between lesions and their adjacent mucosae, indicating localized microbial changes tied to the lesion itself. Correlation analyses of bacterial taxa showed early signs of dysbiosis already present in adenoma, with co-exclusive (mutually exclusive) taxon relationships becoming more common as tissue progressed to carcinoma. These alterations were reproducible when compared against two independent, previously published data sets.
The findings suggest that a taxonomically defined microbial consortium, rather than a single organism, is implicated in the development of colorectal cancer. Because dysbiosis and shifting bacterial co-exclusion patterns are detectable as early as the adenoma stage, mucosal microbiome profiling could help flag precancerous changes before invasive cancer develops. The prominence of oral-associated taxa in cancerous mucosae also points to oral-gut microbial translocation as a process worth further investigation in colorectal carcinogenesis.
This study examined whether patients with anorexia nervosa (AN) show gut dysbiosis, a microbial imbalance, that could relate to the disease's unclear pathophysiological mechanism. The researchers compared fecal microbiota composition between AN patients and healthy controls using the Yakult Intestinal Flora-SCAN, a 16S or 23S rRNA-targeted RT-quantitative PCR method. They also broke down the AN group into restrictive (ANR) and binge-eating (ANBP) subtypes to see whether dysbiosis patterns differed by clinical presentation.
The study included 25 female patients with anorexia nervosa, split into 14 with the restrictive subtype (ANR) and 11 with the binge-eating/purging subtype (ANBP). These patients were compared against 21 age-matched healthy female controls. All participants were assessed through stool sampling for fecal bacterial quantification.
AN patients had significantly lower total bacterial counts and lower obligate anaerobes, including the Clostridium coccoides group, Clostridium leptum subgroup, and the Bacteroides fragilis group, compared to healthy controls. Streptococcus counts were also lower in the AN group than in controls. When broken down by subtype, both ANR and ANBP patients showed significantly lower Bacteroides fragilis group counts than controls, while the Clostridium coccoides group reduction was significant specifically in the ANR subgroup.
These findings support the idea that gut dysbiosis, marked by reduced obligate anaerobes such as the Bacteroides fragilis group and Clostridium groups, is present in anorexia nervosa and may play a role in its pathophysiology. The subtype-specific differences suggest that dysbiosis patterns may vary with clinical presentation (restrictive versus binge-eating/purging), which could inform more tailored understanding of gut-related mechanisms in AN. Because the abstract describes findings from a single comparative study, further research would be needed to establish causality or therapeutic relevance of these microbial changes.
This study examined the gut microbiome in new-onset, treatment-naive Crohn's disease (CD), a form of inflammatory bowel disease genetically linked to host pathways involved in immune responses to intestinal microbiota. Researchers collected samples from multiple gastrointestinal locations before any treatment began. They compared microbial community composition between CD patients and controls, and also examined the effect of prior antibiotic exposure on the microbiome. The goal was to identify consistent dysbiosis patterns and evaluate which sampling site best reflects early disease.
The study drew on the largest pediatric Crohn's disease cohort assembled to date at the time, focused specifically on new-onset cases that had not yet received treatment. Samples were collected from multiple gastrointestinal sites, including the ileum and rectum, as well as fecal samples, within this pediatric population. The abstract does not give an exact number of participants or specific demographic details beyond the pediatric, treatment-naive, new-onset CD designation.
An axis of dysbiosis strongly correlated with disease status: increased abundance of Enterobacteriaceae, Pasteurellaceae, Veillonellaceae, and Fusobacteriaceae alongside decreased abundance of Erysipelotrichales, Bacteroidales, and Clostridiales. Comparing CD patients with and without antibiotic exposure showed that antibiotic use amplified this microbial dysbiosis pattern. Comparisons across ileal, rectal, and fecal samples revealed that the rectal mucosa-associated microbiome captured the disease signature distinctly at this early stage.
Because dysbiosis is detectable even before treatment, this composition shift appears to be an early feature of Crohn's disease rather than a consequence of therapy. The finding that antibiotics amplify dysbiosis suggests antibiotic exposure should be accounted for when interpreting microbiome studies in CD patients. Most notably, the rectal mucosal-associated microbiome offers a convenient and potentially earlier diagnostic sampling site compared with fecal or ileal sampling, which could support development of non-invasive early diagnostic approaches.
This study examined whether fecal microbiota composition, measured through metagenomic sequencing of stool samples, could detect colorectal carcinoma (CRC) as an alternative or complement to the standard fecal occult blood test (FOBT). Researchers searched for taxonomic markers in the gut microbiome that distinguished CRC patients from tumor-free controls. They also investigated whether microbial gene pool differences in stool reflected microbial community composition at the tumor site itself, and examined metabolic shifts associated with CRC.
The initial study population consisted of 156 participants whose fecal samples underwent metagenomic sequencing to identify CRC-associated microbial markers. The findings were then validated in an independent set of patient and control populations totaling 335 individuals drawn from different countries. Together these cohorts included both early-stage and late-stage cancer patients as well as tumor-free controls.
Metagenomic detection of CRC achieved accuracy similar to the standard FOBT, and when the two methods were combined, sensitivity improved by more than 45 percent relative to FOBT alone while specificity was maintained. Detection accuracy did not differ significantly between early-stage and late-stage cancer, and the results held up in the independent validation cohorts from different countries. CRC-associated changes in fecal microbiota partly mirrored microbial community composition at the tumor itself, and the data revealed a metabolic shift from fiber degradation in controls toward utilization of host carbohydrates and amino acids in CRC patients, accompanied by increased lipopolysaccharide metabolism.
These findings suggest fecal microbiota profiling could serve as a non-invasive screening tool for colorectal cancer, particularly valuable because it performed comparably well for early-stage disease when combined with FOBT. The parallel between tumor-site and fecal microbial signatures suggests these stool-based markers may reflect genuine host-microbe interactions occurring at the tumor rather than incidental changes. The metabolic shift toward host-carbohydrate and amino-acid utilization, along with increased lipopolysaccharide metabolism, points to potential microbial contributions to the tumor-associated gut environment worth further mechanistic investigation.
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 used a deep, global microarray-based method to characterize the diversity and temporal changes of the intestinal microbiota during infancy. The researchers aimed to define specific bacterial signatures associated with atopic eczema, since prior work had linked deviations in microbiota composition and diversity in infancy to both the development and recurrence of eczema. Faecal samples were profiled at two time points, 6 and 18 months of age, to track how the microbiota changed alongside eczema status.
The study analyzed faecal microbiota from 34 infants, 15 with eczema and 19 healthy controls, selected from a prospective follow-up study based on availability of faecal samples. These infants were considered at-risk for atopic disease and had originally been randomized to receive either Lactobacillus rhamnosus GG or placebo. This gives the cohort a defined clinical and interventional context rather than being an anonymous public dataset.
Children with eczema harboured a more diverse total microbiota than controls, as measured by the Simpson's reciprocal diversity index of the microarray profiles. Microbiota composition did not differ between groups at 6 months, but became significantly different by 18 months (MCPP, p=0.01). At 18 months, healthy children had a 3-fold greater abundance of Bacteroidetes, while children with eczema showed increased abundance of Clostridium clusters IV and XIVa, groups typically abundant in adults rather than infants.
The findings suggest that eczema in infancy is associated with a microbiota that matures toward an adult-like, Clostridium-dominated profile earlier and with reduced Bacteroidetes compared to healthy at-risk infants. Because the groups looked similar at 6 months but diverged by 18 months, the results point to a developmental window in which microbiota trajectory, not just baseline composition, may matter for eczema risk. This supports using compositional and diversity signatures of the maturing infant microbiota as candidate markers or targets related to atopic eczema.
This study examined how the composition of the human intestinal microbiota relates to intestinal permeability and both local and systemic inflammation in obesity. Researchers profiled fecal microbiota, measured fecal calprotectin (a marker of intestinal inflammation) and plasma C-reactive protein (a marker of systemic inflammation), and assessed HbA1c and plasma transaminase and lipid levels. Intestinal permeability at the gastroduodenal, small intestinal, and colonic levels was tested using a multisaccharide test.
The study population consisted of 28 subjects spanning a wide range of body mass index, from 18.6 to 60.3 kg/m2, so it included both nonobese and obese individuals. Based on their fecal microbiota composition, the subjects separated into two clusters: one made up predominantly of obese subjects (15 of 19) and one made up exclusively of nonobese subjects (9 of 9). The abstract does not give further demographic detail such as age, sex, or geographic origin.
Intestinal permeability did not differ between the two microbiota-based clusters. However, the cluster dominated by obese subjects showed reduced bacterial diversity, a decreased Bacteroidetes/Firmicutes ratio, and an increased abundance of potentially proinflammatory Proteobacteria. Fecal calprotectin was detectable only in a subset of subjects within the obese microbiota cluster (8 of 19, p = 0.02), and plasma C-reactive protein was also increased in these subjects.
The findings suggest that a distinct, less diverse microbiota composition in obesity is linked to low-grade local and systemic inflammation rather than to altered intestinal permeability itself. This supports the idea that shifts in microbial community structure, including a lower Bacteroidetes/Firmicutes ratio and more Proteobacteria, may contribute to the inflammatory state associated with obesity. These results point to fecal microbiota profiling and inflammatory markers like calprotectin and C-reactive protein as potential tools for identifying obese individuals at greater inflammatory risk.
This study examined whether human intestinal microbes are involved in the development of autoimmunity that often precedes type 1 diabetes (T1D), an autoimmune disorder marked by destruction of insulin-secreting pancreatic islet cells. Prior work had shown a role for gut bacteria in diabetes in murine and rat models, but the human picture was unclear. The researchers used high-throughput, culture-independent sequencing approaches to identify bacteria that correlate with the onset of T1D-associated autoimmunity. They tracked changes in gut microbial composition and diversity over time in relation to autoimmune status.
The study population was young children who are at high genetic risk for type 1 diabetes. Children who went on to develop T1D-associated autoimmunity were compared with age-matched and genotype-matched children who did not develop autoimmunity. The abstract does not give an exact sample size, so the specific number of children enrolled cannot be stated.
Bacterial diversity diminished over time in children who developed autoimmunity, relative to nonautoimmune, age- and genotype-matched controls. A single species, Bacteroides ovatus, accounted for nearly 24% of the total increase in the phylum Bacteroidetes seen in cases compared with controls. In contrast, a human Firmicute strain (CO19) accounted for nearly 20% of the increase in Firmicutes observed in controls over time compared with cases. The abstract frames these shifts as part of three lines of evidence that healthy infants' microbiomes become more stable approaching toddlerhood, while children destined for autoimmunity show a different trajectory.
The findings suggest that specific shifts in gut microbial composition and a loss of microbial diversity may track with, and possibly contribute to, the development of T1D-associated autoimmunity in genetically at-risk children. Identifying taxa such as Bacteroides ovatus and the Firmicute strain CO19 as differentially associated with case versus control trajectories offers candidate microbial markers for further study. This work supports the broader premise that the composition and stability of the early-life gut microbiome may be relevant to autoimmune disease risk in humans, not just in animal models. Longitudinal microbiome monitoring in high-risk children could eventually inform strategies to identify or intervene in the path toward autoimmunity.
This study examined whether the fecal microbiota of patients with irritable bowel syndrome (IBS) differs from that of healthy people, using global and deep molecular profiling rather than the more limited methods used in earlier work. Researchers used a comprehensive, highly reproducible phylogenetic microarray combined with quantitative polymerase chain reaction (qPCR) to characterize bacterial and methanogen populations in fecal samples. The goal was to identify microbial signatures that could discriminate IBS from healthy states and to relate those signatures to intestinal symptom scores.
The study analyzed fecal samples from 62 patients with IBS and 46 healthy individuals who served as controls. The abstract does not provide further demographic detail such as age, sex distribution, or IBS subtype. Sample analysis was performed using the phylogenetic microarray and qPCR platforms described above.
The intestinal microbiota of IBS patients differed significantly from that of controls (P = .0005). IBS patients had a two-fold increased ratio of Firmicutes to Bacteroidetes (P = .0002), driven by roughly 1.5-fold increases in Dorea, Ruminococcus, and Clostridium species (P < .005), a two-fold decrease in Bacteroidetes (P < .0001), and a 1.5-fold decrease in Bifidobacterium and Faecalibacterium species (P < .05). When present, methanogens were about four-fold lower on average in IBS patients than in controls. The abstract does not mention Bacteroides fragilis, B. fragilis toxin, or polysaccharide A.
These findings support a distinct, quantifiable microbial signature associated with IBS, characterized by shifts in the Firmicutes-to-Bacteroidetes ratio and reductions in specific taxa such as Bifidobacterium and Faecalibacterium. Because the analysis used a comprehensive, deep, and reproducible molecular platform, it strengthens confidence that these microbiota differences are real rather than artifacts of limited detection methods used in prior studies. Such signatures could eventually inform microbiota-based diagnostic or classification approaches for IBS, pending correlation with clinical symptom scores and further validation.
This study compared the fecal gut microbiota of children eating a high-fiber, agrarian-style diet against children eating a modern Western diet. Researchers used high-throughput 16S rDNA sequencing along with biochemical analyses to characterize bacterial composition and metabolic byproducts. The goal was to test whether long-term dietary habits shape gut microbial communities in ways relevant to health.
The comparison involved children from Europe (EU) and children from a rural village in Burkina Faso (BF). The BF children ate a diet high in fiber and plant polysaccharides, resembling the diets of early agricultural human settlements. The abstract does not give an exact number of children in each group.
BF children showed significant enrichment in Bacteroidetes and depletion in Firmicutes compared to EU children (P < 0.001). They uniquely harbored bacteria from the genera Prevotella and Xylanibacter, which carry genes for cellulose and xylan hydrolysis and were completely absent in EU children. BF children also had significantly higher short-chain fatty acid levels (P < 0.001) and significantly fewer Enterobacteriaceae, including Shigella and Escherichia, than EU children (P < 0.05).
The findings suggest that gut microbiota coevolved with a polysaccharide-rich diet, allowing hosts to extract more energy from fiber and potentially resist pathogen overgrowth. This supports the idea that modern Western diets, low in fiber, may shift gut microbial ecology away from a configuration linked to metabolic efficiency and gut protection. The results also underscore diet as a major driver of human gut microbial variation across populations.
2026-07-04
Bacteroides fragilis majorTaxon page created: biology (morphology, polysaccharide-A immunomodulation, pathogenicity, antibiotic resistance), virulence factors including the enterotoxigenic BFT toxin, the good-and-bad vulnerabilities, interventions, the data-derived Conditions table across 83 conditions, and the full research feed.
Mazmanian SK, Liu CH, Tzianabos AO, Kasper DL.
An immunomodulatory molecule of symbiotic bacteria directs maturation of the host immune system.Cell. 2005
Mazmanian SK, Round JL, Kasper DL.
A microbial symbiosis factor prevents intestinal inflammatory disease.Nature. 2008
Dejea CM, Fathi P, Craig JM, et al. (Sears CL).
Patients with familial adenomatous polyposis harbor colonic biofilms containing tumorigenic bacteria.Science. 2018
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