Did you know?
Christensenellaceae is the most heritable microbe in your gut, and the more of it you have, the leaner you tend to be. Transplanting it into mice even reduced their weight gain.
Christensenellaceae is a family of beneficial gut bacteria most strongly and reproducibly linked to leanness and metabolic health. It is the most heritable taxon in the human gut, and on this database its signal usually marks a healthier, leaner community.
Microbiome-targeted interventions (MBTIs) are validated using a dual-evidence logical framework. First, the intervention must realign the condition’s microbiome signature by increasing beneficial taxa that are consistently depleted and reducing pathogenic taxa that are consistently enriched. Second, the intervention must demonstrate measurable clinical benefit. Concordance of these effects in the same context validates the intervention as an MBTI and supports the clinical relevance of the microbiome signature.
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreChristensenellaceae is a family of strictly anaerobic bacteria in the phylum Firmicutes and one of the most intriguing health-associated groups in the human gut. Its relative abundance is inversely related to body mass index across many populations and studies, making its link to leanness the most robust and reproducible connection between the gut microbiome and metabolic health reported to date.[1] On this database it appears as a differentially abundant taxon across many human microbiome studies, usually as a marker of a healthier, leaner state.
What makes Christensenellaceae distinctive is that it is the most heritable taxon in the human gut. In large twin studies its abundance is strongly shaped by host genetics, and it sits at the center of a co-occurrence network with other heritable bacteria and methane-producing archaea.[2] It is enriched in lean individuals, and transplanting a cultured member (Christensenella minuta) into mice reduced weight gain, hinting at a causal role.[2]
The Christensenellaceae are strictly anaerobic bacteria in the phylum Firmicutes; the type genus Christensenella comprises non-motile, non-spore-forming rods.[1] The family is widespread across human populations and, though usually present at low abundance, is a consistent member of the healthy gut community.[1]
Members of Christensenellaceae are fermentative anaerobes that produce short-chain fatty acids and hydrogen. Their hydrogen output supports a syntrophic partnership with hydrogen-consuming methanogenic archaea, and this metabolic network is part of why they co-occur with methanogens and with a lean metabolic profile.[2][1]
Christensenellaceae is one of the clearest examples of a health-associated gut microbe. Its abundance is inversely correlated with BMI across independent cohorts, the most reproducible microbiome-to-metabolic-disease link described so far, and it is associated with a healthy status in other contexts including inflammatory bowel disease.[1] Because it is highly heritable, part of its association with health reflects host genetics as well as environment.[2]
Where a pathogen page lists virulence factors, Christensenellaceae's notable features are the ones tied to host health.
| Feature | Description and role |
|---|---|
| Association with leanness | Higher Christensenellaceae tracks lower BMI across populations; amending an obese-associated microbiome with Christensenella minuta reduced weight gain in mice.[2] |
| Short-chain fatty acids and hydrogen | Fermentation products and hydrogen feed a syntrophic network with methanogens, contributing to a metabolically favorable community.[2][1] |
| Heritability and keystone position | As the most heritable gut taxon and the hub of a co-occurrence network, it marks a stable, health-associated community structure.[2] |
For a health-associated family, the honest "vulnerabilities" are the limits on our ability to study and modulate it.
| Consideration | Why it matters |
|---|---|
| Strong host-genetic control | Because its abundance is heavily influenced by host genetics, Christensenellaceae may respond less to diet or supplements than other taxa, which complicates efforts to raise it.[2][1] |
| Low abundance, hard to culture | It is usually present at low levels and its members are fastidious anaerobes, so detecting and cultivating it is challenging.[1] |
| Mechanisms still emerging | The pathways linking Christensenellaceae to health are still being worked out, so any intervention remains exploratory.[1] |
For a health-associated family, an intervention is anything that supports it or the community it anchors. Everything below is exploratory and is not medical advice; each is classified by our validation method. An important caveat is that Christensenellaceae is strongly heritable, so it may be less modifiable than other microbes.
| Intervention | Class | Status |
|---|---|---|
| Support a diverse, fiber-fed anaerobic community | Diet | Validation In Progress |
| Christensenella minuta as a candidate probiotic | Concept | Validation In Progress |
| Intervention | Mechanism |
| Support a diverse anaerobic community | Christensenellaceae anchors a co-occurrence network of heritable bacteria and methanogens, so supporting that community may help sustain it, though host genetics set much of its level.[2][1] |
| Christensenella minuta probiotic | In mice, adding C. minuta to an obese-associated microbiome reduced weight gain, the basis for interest in it as a probiotic.[2] |
Over-interpreting a single abundance value. Because Christensenellaceae is strongly heritable and usually low-abundance, its level reflects host genetics and detection sensitivity as much as anything modifiable.[2][1]
Where Christensenellaceae (NCBI:txid990719) appears as a differentially abundant taxon across the Microbiome Medicine corpus. Each row aggregates every experiment in which the family 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 82 conditions and 114 studies, it is enriched in 34, depleted in 38, and direction-conflicting in 10. Consistent with its role as a health- and leanness-associated family, the signal leans toward depletion: it is lost more often than gained across disease states. Because it is strongly heritable and its loss marks a less healthy community rather than a specific disease mechanism, the aggregate evidence tier is Low.
How to read these. Christensenellaceae is a genuine, health-associated resident, so a depletion here usually marks a less healthy or higher-BMI state rather than a cause of the condition. It is family-level, low-abundance, and strongly heritable, so its level partly reflects host genetics and detection sensitivity. Read a decline as a marker of a less favorable community, not a target to remove. This is why the aggregate tier stays Low.
Internal summaries of the 114 studies we reviewed in which Christensenellaceae was a differential taxon across this corpus.
This study examined the fecal microbiome of children newly diagnosed with Crohn's disease (CD) before any treatment was started. The researchers compared microbial composition between these CD patients and children with functional gastrointestinal disorders. They also looked at whether specific microbial patterns correlated with the severity of CD, as measured by the Pediatric Crohn's Disease Activity Index (PCDAI).
The cohort included 43 newly diagnosed, treatment-naive pediatric CD patients. They were compared against 139 age- and sex-matched controls who had other functional gastrointestinal disorders rather than CD. All participants were pediatric patients, and the comparison group was matched specifically to isolate microbial differences attributable to CD rather than age or sex.
Microbial richness and diversity were significantly lower in children with CD compared to controls. Taxonomic analysis showed enrichment of pro-inflammatory bacteria, specifically Fusobacteria and Proteobacteria, alongside depletion of favorable taxa, Firmicutes and Verrucomicrobia. Higher PCDAI scores (indicating greater disease activity) were linked to enrichment of pro-inflammatory genera, Hungatella and Veillonella, and depletion of protective Lachnospiraceae.
The findings support fecal microbiome profiling as a potential tool for distinguishing CD from other functional gastrointestinal disorders in children at diagnosis. The correlation between specific microbial shifts and disease activity suggests the microbiome could help track or predict clinical course. This could ultimately aid clinicians in making more informed treatment decisions for a disease whose course is otherwise unpredictable.
This study examined the gut microbiome in the context of human T-lymphotropic virus type 1 (HTLV-1) infection and its progression to HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic neuroinflammatory disease. Researchers characterized alterations in fecal bacterial composition and diversity across different clinical stages of HTLV-1 infection. They also performed functional analysis to identify differentially enriched gene categories and KEGG metabolic modules. The work was framed around the gut-brain axis, a mechanism already implicated in other neurological diseases such as multiple sclerosis.
The study included 112 Brazilian individuals in a cross-sectional design. This group comprised 24 healthy controls and 88 HTLV-1-infected individuals at different disease stages, including 38 patients with HAM, 17 with intermediate syndromes, and 33 asymptomatic carriers. Fecal samples from all participants were collected and analyzed using Illumina MiSeq sequencing.
HTLV-1-infected individuals showed significant gut dysbiosis compared to healthy controls, marked by reduced bacterial diversity and an inverted Firmicutes/Bacteroidetes ratio. Specific bacterial genera were altered across infection and disease stages. Notably, HAM patients showed decreased levels of Faecalibacterium, a genus generally associated with beneficial, anti-inflammatory gut function, alongside increased levels of other bacteria per the abstract. These compositional shifts were accompanied by changes in functional gene categories and KEGG modules.
The findings support a role for the gut microbiome in the pathogenesis and clinical progression of HTLV-1-associated disease, extending the gut-brain axis concept to this neuroinflammatory condition. Dysbiosis patterns, particularly reduced Faecalibacterium in HAM patients, may help distinguish disease stages and could point to microbiome-linked mechanisms in neurologic progression. These results position the gut microbiome as a potential area for further mechanistic and biomarker research in HTLV-1 infection and HAM/TSP.
This study examined whether household food insecurity (HFI) is associated with changes in the gut microbiome of schoolchildren. The researchers used the Household Food Insecurity Access Scale (HFIAS) as a composite measure of food insecurity, and also analyzed individual HFIAS questions as specific proxies for different forms of dietary deprivation. Gut microbial communities were profiled using 16S rRNA amplicon paired-end sequencing of fecal samples. The goal was to determine whether restricted caloric intake, dietary diversity, and food quality linked to HFI translate into measurable shifts in microbiome composition.
The study population consisted of 57 school-aged children in Ethiopia. Fecal samples were collected from these children, and their household food security status was assessed using the HFIAS questionnaire completed for their households. No further demographic details are given in the abstract.
Alpha diversity did not differ significantly between food-secure and food-insecure children (Wilcoxon p > 0.05), indicating that overall species richness and evenness within individuals were not strongly affected. However, beta diversity analysis showed a significant shift in overall microbiome composition between the two groups using Bray-Curtis dissimilarity (PERMANOVA, p < 0.05). Further analysis of specific HFIAS questions found that limited dietary variety and consumption of disliked foods were among the deprivation proxies associated with these compositional differences, including enrichment of the genus Sutterella.
These findings suggest that household food insecurity can restructure the gut microbiome even when standard diversity metrics appear unchanged, meaning composition-based analyses may be more sensitive indicators of dietary deprivation than diversity alone. The identification of specific HFIAS questions, such as limited dietary variety, as proxies linked to microbiome shifts points to particular deprivation behaviors that could be targeted in interventions. This work highlights food insecurity as a modifiable environmental factor relevant to child gut health in low-resource settings, though further research is needed to link these compositional changes to functional or clinical outcomes.
This study examined how high exposure to toxic metals and metalloids, specifically arsenic, lead, mercury, and cadmium, relates to gut microbiome composition and metabolic risk. Researchers analyzed associations among gut microbiota taxa, dichotomized (high versus low) metal levels, and clinical measures including BMI, fasting blood glucose, and blood pressure. They also examined diagnoses of hypertension, obesity, and type 2 diabetes (T2DM) alongside metabolic pathway enrichment linked to metal exposure. The goal was to clarify mechanisms by which toxic metal exposure may contribute to obesity and T2DM risk through the gut microbiome.
The study included 178 adults of African origin drawn from five countries: Ghana, South Africa, Jamaica, Seychelles, and the United States. The cohort was 52% female with a mean age of 43.0 plus or minus 6.4 years. This multi-country design allowed comparison of metal exposure and microbiome relationships across diverse African-origin populations rather than a single national sample.
High versus low lead and arsenic levels significantly affected gut microbiome beta diversity (p less than 0.05). Seventy-one taxa were associated with high lead levels, including 30 linked to elevated BMI, 22 to T2DM, and 23 to elevated fasting blood glucose. Arsenic showed an even broader association, with 115 taxa linked to high exposure, including 32 tied to elevated BMI, 33 to T2DM, and 26 to elevated blood glucose. Porphyrin metabolism emerged as the most enriched metabolic pathway among taxa associated with higher lead and arsenic exposure.
This is described as the first evidence from African-origin adults linking gut microbiome composition to lead and arsenic exposure alongside cardiometabolic risk markers. The porphyrin metabolism signal suggests a plausible microbial pathway connecting heavy metal exposure to metabolic dysregulation, since porphyrin metabolism is tied to heme synthesis and metal handling. These findings support further investigation of the gut microbiome as a mechanistic link between environmental toxic metal exposure and obesity or diabetes risk in understudied, high-exposure populations.
This study examined the gastrointestinal microbiomes of khulans (Equus hemionus hemionus, the Mongolian wild ass) and asked whether environmental microbiota from their drinking water contribute to shaping those gut communities. The researchers used PacBio sequencing of the 16S rRNA gene, processed through the LotuS pipeline, to characterize microbial composition. They compared microbial diversity, differential abundance, alpha diversity, and beta diversity across wild khulans, captive khulans, and other equids for context.
The study sampled wild khulans (n = 21) and their waterhole environments, along with captive khulans (n = 12). For comparison, the researchers also included Przewalski's horses (n = 82) and domestic horses (n = 26). All samples were analyzed using 16S rRNA gene sequencing rather than whole-genome approaches.
Microbial sharing between wild khulans and their waterhole environments was limited, indicating minimal environmental influence on the gut microbiome and low levels of water contamination by the animals themselves. Wild khulans showed greater microbial diversity and richness than captive khulans, which the authors attribute to adaptation to the harsh nutritional conditions of the Gobi desert. Captive khulans instead displayed reduced microbial diversity, likely reflecting dietary changes associated with captivity.
The findings underscore that environment and lifestyle, particularly diet and captivity status, exert a stronger influence on equid gut microbiomes than shared water sources do. This suggests that captive breeding and conservation programs for khulans and related equids may need to account for diet-driven reductions in microbial diversity. The results also support using gut microbiome diversity as an indicator of how well captive management replicates wild nutritional conditions.
The study developed a machine learning prediction model for postprandial glycemic response (PPGR) to food in pregnant women. It examined whether adding gut microbiota data to inputs like continuous glucose monitoring (CGM), meal content, lifestyle factors, and biochemical parameters could improve prediction accuracy. Gut microbiota composition was assessed using 16S rRNA gene sequence analysis of stool samples. The model's performance was then compared against a simpler approach based only on carbohydrate counting.
The study involved 105 pregnant women, of whom 77 had diet-treated gestational diabetes mellitus (GDM) and 28 were healthy. All participants underwent continuous glucose monitoring for 7 days, kept food diaries, and provided stool samples for microbiome analysis. This design allowed comparison of glycemic responses across both GDM-affected and healthy pregnancies.
Adding microbiome data increased the explained variance in peak glycemic levels (GLUmax) from 34% to 42%, and in incremental area under the glycemic curve (iAUC120) from 50% to 52%. The final model, which incorporated microbiota features, correlated better with measured PPGRs than a model based only on carbohydrate counts (r = 0.72 versus r = 0.51 for iAUC120). Despite this improvement, the authors noted that the microbiome's contribution to overall model performance was modest relative to other factors.
These findings suggest that gut microbiota data can meaningfully, though not dramatically, improve personalized glycemic response prediction for pregnant women, including those with gestational diabetes. This points toward the potential for microbiome-informed, individualized dietary guidance rather than relying solely on carbohydrate counting during pregnancy. Because the microbiome's added value was modest, it is likely best used as a complement to, rather than a replacement for, standard clinical and dietary monitoring tools.
This study examined whether Amomum tsaoko flavonoids (ATFs), an extract from a traditional Chinese medicinal food, could protect against Parkinson's disease (PD) using a rotenone-induced mouse model. The researchers evaluated ATFs' effects on motor function, gastrointestinal symptoms, dopaminergic neuron survival, colonic inflammation, gut barrier integrity, and the composition of the gut microbiota. No prior studies had tested Amomum tsaoko or its extracts as a treatment for PD, making this an initial investigation into a novel gut-microbiota-linked mechanism.
The subjects were mice in which PD-like pathology was induced using rotenone, a pesticide commonly used to model Parkinson's disease in animal research. The abstract does not specify the number of animals, strain, sex, or age used in the experiments. This was a controlled laboratory animal study rather than a human cohort.
ATFs improved motor symptoms and constipation in the rotenone-exposed mice and reduced the loss of nigrostriatal dopaminergic neurons, the cells characteristically damaged in Parkinson's disease. ATFs also lowered expression of inflammatory genes (TNF-alpha, IL-1beta, IL-6, COX-2, and MCP-1) while increasing expression of gut barrier genes (Muc-2, ZO-1, Occludin, Claudin3, and Claudin4) in the colon. Additionally, ATFs reversed rotenone-induced gut dysbiosis, notably decreasing the abundance of conditionally pathogenic bacteria such as Desulfovibrio, Provotellaceae UCG-001, and the Lachnospiraceae_NK4A136_group.
These findings suggest that Amomum tsaoko flavonoids may protect against Parkinson's disease progression through a gut-microbiota-mediated pathway involving reduced intestinal inflammation and restored gut barrier integrity. Because gut dysbiosis and pathogenic bacterial overgrowth accompanied neuronal loss and motor symptoms, the results support the gut-brain axis as a target for PD intervention. This positions ATFs as a candidate natural compound worth further investigation for preventing or treating Parkinson's disease, though translation to humans has not yet been tested.
The study examined how Zhuyang Tongbian Decoction (ZTD), a treatment for functional constipation (FC), affects the gut microbiome and related inflammatory pathways. Researchers used 16S rRNA sequencing to track changes in intestinal flora composition and diversity before and after treatment. They also measured fecal short-chain fatty acid (SCFA) levels and serum markers of inflammation (TLR4, NF-κB, TNF-α, IL-6), and applied metagenomics sequencing to assess the metabolic functions of the gut microbiota.
The study enrolled 40 patients with functional constipation, randomly split into a control group of 20 receiving lactulose and a treatment group of 20 receiving ZTD. An additional 20 healthy volunteers were recruited during the same period, presumably serving as a comparison reference group. The abstract does not provide further demographic details such as age or sex distribution.
The ZTD treatment group showed a significant increase in beneficial bacteria, including Bifidobacterium, Lactobacillus, and Faecalibacterium prausnitzii, while Desulfobacterota and Ruminococcus were significantly reduced. Fecal acetic and propionic acid levels were also affected by treatment, though the abstract text is cut off before reporting the full direction and magnitude of this change. These shifts point to a restructuring of the gut microbial community alongside altered short-chain fatty acid output in patients treated with ZTD.
The findings suggest ZTD may relieve functional constipation partly by reshaping gut microbiota toward a more beneficial profile and modulating SCFA production, rather than acting solely as a laxative like lactulose. This offers a potential microbiome-based mechanism for a traditional herbal formula already used in practice. As a pilot study, the results support further larger-scale investigation into ZTD's effects on gut bacteria, SCFAs, and inflammatory signaling in constipation.
This study investigated the smoking paradox, in which smokers tend to have lower body mass index but higher risk of obesity-related disease, through the lens of the gut microbiota. Researchers used 16S rRNA sequencing to identify smoking-related microbial genera and built a smoking-related microbiota index (SMI). They then tested whether SMI was associated with obesity indices and with incident obesity-related diseases, including analyses designed to control for shared familial and environmental confounders.
The analysis drew on 4000 male participants from two cohorts, the WELL-China cohort and the Lanxi cohort. Obesity indices were derived using dual-energy X-ray absorptiometry (DEXA) scans in these participants. A subset of participants with siblings was used for sibling comparison analyses via a between-within (BW) model, allowing the researchers to account for unmeasured familial confounding.
The smoking-related microbiota index (SMI) was positively associated with BMI and other DEXA-derived obesity indices. Higher SMI was also linked to greater risk of incident obesity-related disease, with hazard ratios of 1.97 for diabetes, 1.31 for major adverse cardiovascular events, and 1.70 for obesity-related cancers. These associations held up in sibling comparison analyses, which help rule out shared family environment or genetics as the explanation.
The findings suggest that smoking-associated shifts in gut microbiota may help explain why smokers face elevated cardiometabolic and cancer risk despite often having lower BMI. This reframes the smoking-obesity paradox as partly a microbiome-mediated phenomenon rather than a purely anthropometric one. The sibling comparison design strengthens confidence that the microbiota signal is not simply a marker of shared family background. These results point to the gut microbiota as a potential target or biomarker for assessing metabolic and disease risk in people who smoke.
This study investigated the gut microbiota of older adults with sarcopenic obesity (SO) and sarcopenia without obesity (Sar), compared with age-matched controls. Researchers used 16S rRNA gene sequencing targeting the V3-V4 regions to characterize microbial composition and diversity. The goal was to determine whether gut dysbiosis is associated with the development and progression of sarcopenia and sarcopenic obesity, a link previously suspected but not well documented.
The sample was drawn from a community-based cohort of 1558 older adults (age 65 and older) in Shanghai, China, who underwent sarcopenia screening with the SARC-F questionnaire. Of these, 351 completed further assessment, and 60 participants were ultimately categorized using the Asian Working Group for Sarcopenia 2019 criteria and World Health Organization obesity criteria. The final groups were sarcopenic obesity (n=20), sarcopenia without obesity (n=18), and controls (n=22).
Gut microbiota diversity and composition differed significantly between the sarcopenic obesity, sarcopenia, and control groups. Alpha diversity, measured by the Chao1 and ACE indices, was reduced specifically in the sarcopenic obesity group. Beta diversity, assessed by unweighted UniFrac PCoA, also differed significantly among the three groups, and LEfSe analysis identified 39 taxa with differential abundance across groups.
The findings support the idea that gut microbiota alterations are distinctly linked to sarcopenic obesity rather than sarcopenia alone, with reduced diversity marking the combined obesity and muscle-loss phenotype. This suggests the gut microbiome could serve as a distinguishing biomarker between these related but distinct conditions in older adults. Identifying these taxa-level differences may help guide future microbiome-targeted approaches for prevention or management of sarcopenic obesity in aging populations.
This study examined how the gut microbiota relates to malaria transmission and severity across malaria-endemic regions of Rwanda. Researchers looked at associations between gut microbial composition and geographic location, age, nutritional habits, and soil-transmitted helminth coinfection. Gut microbial composition was profiled using bacterial 16S rRNA gene amplicon sequencing of fecal samples. Malaria and helminth infection status were determined by microscopy, alongside questionnaire-derived data on region, age, and nutrition.
The study included 169 participants, 85 females and 84 males, ranging in age from 2 to 78 years. Participants were drawn from three malaria-endemic provinces of Rwanda: West, South, and East. Both blood and fecal samples were collected from each participant, along with demographic and dietary questionnaire data.
Preschool children had significantly lower gut microbiota diversity compared to both school-age children (q = 0.027) and adults (q = 0.011). Infection status, whether uninfected, malaria alone, helminth alone, or coinfected, was not significantly associated with gut microbiota composition. However, using Bray-Curtis distances, the researchers found significant differences in gut microbial beta-diversity, with a convergent distribution pattern noted across the sampled groups.
The findings suggest that host age is a stronger driver of gut microbiota diversity and structure than malaria or helminth infection status in these Rwandan populations. This indicates that age-related developmental differences in the microbiome may need to be accounted for separately from infection-related effects in future host-microbiome-parasite research. The geographic and age-associated beta-diversity patterns also point to the value of considering regional and demographic context when studying microbiome-malaria interactions.
This study examined how geographical origin and dietary pattern shape the human gut microbiota, using 16S rDNA sequencing of the V3-V4 hypervariable region. It compared microbial taxa associated with West African foods (palm oil, Cube Maggi) versus Italian foods (sunflower oil, olive oil) using DESeq2 differential abundance analysis and weighted correlation network analysis (WGCNA) to identify co-abundant bacterial genera. The study also investigated the presence and subtypes of Blastocystis, the most common intestinal protozoan worldwide, and how they correlate with microbial composition.
Three cohorts of healthy subjects were compared: Italians residing in Rome, Africans residing in Cote d'Ivoire, and Africans living in Italy. The abstract does not give exact sample sizes for each group. The design specifically allowed comparison of a Mediterranean-diet group, a West African-diet group, and an intermediate group of Africans who had adopted a Mediterranean diet after migrating to Italy.
Distinct microbial taxa were linked to specific foods, including palm oil, Cube Maggi, sunflower oil, and olive oil, indicating that diet strongly shapes gut community composition. Notably, consuming a Mediterranean diet for more than two years did not alter the abundance of Faecalibacterium or Dorea in Africans living in Italy. This suggests these particular taxa were resistant to change despite a sustained dietary shift, though the abstract is truncated before further results and the Blastocystis subtype correlations are described but not detailed here.
The findings imply that geographical origin and long-term dietary history can leave a persistent imprint on specific gut bacterial taxa that a new diet does not readily erase, at least over a two-year timescale. This has implications for how microbiome-based dietary interventions are designed and evaluated in migrant or diverse populations. The study also underscores the need to consider eukaryotic gut residents like Blastocystis alongside bacterial taxa when characterizing diet-microbiota relationships across populations.
The study asked whether person-to-person microbial transmission, not just diet, helps explain why traditional gut microbiomes shift toward an industrialized pattern after people immigrate. Researchers colonized germ-free mice with human donor stool from the United States and from Thailand and then let these humanized mice share air or have physical contact with each other. They tracked how this shared-environment exposure altered each group's microbiome composition. They also fed the colonized mice 13 dietary ingredients and food additives common in industrialized diets to see how the US and Thai microbiomes, and body weight, responded.
The subjects were germ-free mice colonized with human donor stool, not human participants directly. Donor stool came from two source populations, the United States and Thailand, representing an industrialized and a more traditional microbiome. The abstract does not give a specific number of human donors or mice, so the study population is best described as a mouse model built from these two human donor microbiome sources.
Both shared air and physical contact enabled bidirectional transmission of gut commensals between the US and Thai humanized mice. US mucus-degrading taxa such as Akkermansia moved into Thai microbiomes, while potentially health-promoting Thai-derived bacteria colonized US microbiomes. The host's baseline gut microbiome composition shaped how much remodeling occurred, and food additives reduced Akkermansia and the US microbiome showed a predisposition toward weight gain under industrialized dietary conditions. Sharing air supply or co-housing mitigated this weight-gain predisposition, apparently through transfer of protective microbes.
The findings suggest that microbiome westernization after immigration is not driven by diet alone, but also by loss of the person-to-person microbial transmission routes common in traditional, communal living environments. This reframes shared living space and social contact as active factors in gut microbiome and metabolic health, not just passive background. It also suggests that reintroducing cohabitation-style microbial exchange, or engineered equivalents, could help offset the metabolic risks of industrialized diets.
This study examined whether the gut microbiome is related to brain structure in apparently healthy adults. The researchers used 16S ribosomal RNA gene sequencing of stool samples to characterize gut microbiome composition and diversity. They paired this with brain magnetic resonance imaging and automated voxel-based morphometry to measure brain volumes, including gray matter and white matter. Statistical methods included principal coordinate analysis, linear discriminant analysis, and multivariable linear regression to test associations between microbiome measures and brain volume.
The study population was 623 Japanese men drawn from the Shiga Epidemiological Study on Subclinical Atherosclerosis (SESSA), a population-based cross-sectional cohort. Stool samples were collected during the study's follow-up stage, and participants had a mean age of 68.0 years (SD 8.0), ranging from 46 to 83 years. All participants underwent brain MRI as part of the same assessment.
After adjusting for age and total intracranial volume, gray matter volume showed a positive association with alpha diversity, specifically the Shannon index richness, at a q-value below 0.01. However, this association was no longer significant once the analysis further adjusted for body mass index, physical activity, smoking, drinking, and hypertension. Beta diversity, measured using weighted UniFrac distances via principal coordinate analysis, showed differences related to white matter volume, though the abstract text describing this result is incomplete. This pattern of the abstract is not about Christensenellaceae, Christensenella, leanness, BMI-associated taxa, or heritability; the study centers instead on gut microbiome diversity and brain morphometry.
The findings suggest that in generally healthy older men, any apparent link between gut microbial diversity and gray matter volume may largely reflect shared lifestyle and metabolic factors such as body mass index, physical activity, smoking, drinking, and hypertension rather than a direct, independent relationship. This underscores the importance of adjusting for lifestyle and cardiometabolic confounders when studying gut-brain associations in human populations. The results also support continued investigation of beta diversity and white matter relationships as a potentially distinct avenue linking the gut microbiome to brain structure. Overall, the study adds population-based human evidence to a field previously dominated by animal models and specific patient populations.
This study examined how menopausal hormone therapy (MHT) affects the gut microbiota of postmenopausal women and whether these microbial changes relate to bone metabolism. Fecal samples were analyzed using 16S ribosomal RNA gene sequencing and short-chain fatty acid (SCFA) analysis to characterize microbial composition. Serum bone metabolic markers were measured via chemiluminescent immunoassays, and Spearman correlation was used to test associations between specific bacterial genera and bone metabolism indexes.
The study included a total of 31 postmenopausal women, some undergoing MHT and some not, whose fecal samples and blood serum were both collected and analyzed. The abstract does not provide further demographic details such as age range, geographic origin, or duration of MHT use.
Postmenopausal women on MHT had lower serum levels of procollagen type I N propeptide (P1NP) and C-terminal telopeptide of type I collagen (CTX-1), both markers of bone turnover. Significant differences in both alpha diversity and beta diversity of gut microbial composition were observed between the MHT and non-MHT groups (P less than 0.05). Of 295 total microbial taxa identified, the abstract indicates specific taxa differed by group, though the full list of implicated genera is not given in the excerpt provided.
The findings suggest that MHT's bone-protective effects, reflected in reduced bone-turnover markers, may occur alongside measurable shifts in gut microbial diversity and composition. This supports the broader concept that gut microbiota play a role in regulating bone metabolic processes in postmenopausal women. If confirmed, these associations could point toward gut microbiota as a potential mechanism or biomarker relevant to MHT's effects on bone health, though causality cannot be established from this abstract alone.
This study examined how the gut microbiome changes across a rural-to-urban lifestyle transition in Indonesia. The researchers assembled metagenome-assembled genomes to characterize species and subspecies diversity within these communities. They also investigated how bacterial physiology, specifically sporulation capacity, relates to how widespread or restricted a given microbial taxon is across villages. Finally, they assessed whether diet variation between communities versus within communities better predicts overall microbiome composition.
The dataset comes from 116 Indonesians whose lifestyles span transitional hunter-gatherer, rural agricultural, and urban populations. This sampling directly addresses a gap in microbiome research, since existing datasets are heavily biased toward Western urban cohorts and Southeast Asia has been especially under-represented. From these 116 individuals, the team assembled 11,070 metagenome-assembled genomes for analysis.
The researchers identified 1,304 species and 3,258 subspecies, revealing substantial novelty at both the species level (15%) and the subspecies level (50%). Novel taxa tended to be rare, often specific to a single village, and depleted in sporulation genes, linking bacterial physiology to transmission patterns, prevalence, and the likelihood of prior discovery. Clear rural-to-urban clines emerged across multiple levels of biological organization, from individual species abundance to overall microbiome composition and diversity. Diet variation between communities, but not variation within a community, strongly predicted microbiome composition.
The findings suggest that microbiome divergence across lifestyles is shaped primarily by community-level factors rather than individual-level differences in diet. The link between sporulation genes and village-specific, rarely detected taxa highlights how bacterial physiology influences transmission and the chances a species has been previously characterized. This work underscores the need to expand microbiome sampling beyond Western urban populations to capture the full scope of human microbiome diversity and biogeography. It also demonstrates that lifestyle transition, population structure, and bacterial physiology jointly shape microbiome variation at the scale of human communities.
This study examined the role of the intestinal microflora in pediatric nonalcoholic fatty liver disease (NAFLD), including its subtypes nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). Researchers used 16S rRNA and metagenomic sequencing on fecal samples to characterize the gut microbiome and its metabolic pathways. The goal was to explore how variation in gut flora correlates with NAFLD-related clinical indexes and metabolic function in children.
The study examined Chinese pediatric patients diagnosed with NAFLD, NASH, and NAFL, compared against healthy child controls. The abstract does not give an exact sample size or age range for these groups. The population reflects a clinical cohort of Chinese children, framed against the backdrop that 45% of Chinese adolescents with obesity develop fatty liver disease.
Certain fecal microbiota showed a negative correlation with body mass index (BMI), meaning higher abundance of these taxa was associated with lower BMI. The study identified several bacteria linked to NAFLD, including Lachnoclostridium, Escherichia-Shigella, and Faecalibacterium prausnitzii. These findings connected specific gut bacterial taxa to NAFLD-related metabolic and clinical indexes in children.
The findings suggest that variation in gut microbiota composition may play a more important role than previously appreciated in the development and progression of NAFLD and NASH in children. This points to the gut microbiome as a potential target for understanding or managing pediatric fatty liver disease, particularly given its long-term risk of progressing to cirrhosis and liver cancer. Because certain bacteria correlated with BMI, the results also reinforce a link between microbiome composition and body weight regulation in this population.
This study examined whether the intestinal microbiota differs between men and women who have coronary heart disease (CHD). The researchers compared microbiota composition in CHD patients against non-CVD controls, analyzing each sex separately. Intestinal bacteria were profiled using 16S metagenomic sequencing on the Illumina MiSeq platform, with data processed in Qiime2. The goal was to identify sex-specific microbial patterns tied to cardiovascular disease.
The study drew on the CORDIOPREV clinical trial cohort, which included 837 men and 165 women with CHD. These CHD patients were compared against a reference group of 375 individuals without cardiovascular disease, consisting of 270 men and 105 women. In total, the analysis spanned over 1,300 participants across both sexes and disease status.
Beta diversity, reflecting differences in microbial community composition, varied by sex, while alpha diversity (within-sample richness) remained similar between men and women. LEfSe analysis identified sex-specific alterations in the gut microbiota associated with CVD. Using random forest modeling, the researchers pinpointed seven bacterial taxa as key discriminators: g_UBA1819 (Ruminococcaceae), g_Bilophila, g_Subdoligranulum, g_Phascolarctobacterium, f_Barnesiellaceae, g_Ruminococcus, and an unidentified genus within Ruminococcaceae (Ruminococcaceae incertae sedis).
These findings suggest that cardiovascular disease is linked to distinct microbial signatures depending on sex, rather than a single universal gut microbiota pattern. This implies that future microbiome-based research or risk assessment for CHD may need to account for sex as a variable rather than treating cohorts as uniform. The identified taxa, several from the Ruminococcaceae family and related groups, may serve as candidate markers warranting further investigation in sex-stratified cardiovascular studies.
This study examined whether 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 profile intestinal flora across BMI groups. They paired this with transcriptome sequencing of tumor tissue to assess immune-related gene expression and tumor microenvironment characteristics. The overall goal was to integrate microbiome and transcriptomic data to clarify how BMI, gut microbiota, and CRC pathology relate to one another.
The subjects were colorectal cancer patients from whom stool samples and tumor tissue samples were collected. Patients were stratified into different BMI status groups (such as overweight versus non-overweight categories implied by the study's design), though the abstract does not give exact group sizes or demographic details. No age range, sex distribution, or total sample size is specified in the abstract. The population can be described as a clinical CRC patient cohort assessed for both microbiome and tumor gene-expression profiling.
The study found differences in intestinal microbial composition between CRC patients with varying BMI status, based on 16S rRNA sequencing of stool samples. Tumor transcriptome analysis showed corresponding differences in immune-related gene expression and tumor microenvironment characteristics across these BMI groups. Together, the microbiome and transcriptomic data suggest that BMI-associated shifts in gut bacteria are linked to changes in the tumor's immune environment. The abstract does not specify which taxa were enriched or depleted, since the results text is truncated.
The findings support a link between BMI-associated gut microbiota changes and colorectal cancer development and progression. By connecting microbial composition to tumor immune characteristics, the study points toward gut microbiota as a potential factor in how body weight influences CRC biology. This integrated microbiome-transcriptome approach may help identify BMI-related microbial markers relevant to CRC risk stratification or immune-tumor interactions. Further work with fuller reporting of specific taxa and immune pathways would be needed to translate these findings clinically.
This study examined whether the gut and pharyngeal microbiome is associated with tuberculosis (TB) disease stages. Researchers used full-length 16S rDNA amplicon sequencing performed with Oxford Nanopore Technologies to profile bacterial communities. The comparison spanned TB-negative controls, latent TB, and active TB groups. The goal was to identify microbial differences that track with TB progression from latent to active disease.
The subjects were 71 cynomolgus macaques, an animal model used to study TB pathogenesis. The macaques were divided into three groups: TB (-) control, TB (+) latent, and TB (+) active. No human cohort was involved, so findings reflect a non-human primate model rather than a human population.
In the pharyngeal microbiome, Haemophilus hemolyticus was decreased and Prevotella species were increased in TB (+) macaques compared to controls. In the gut microbiome, Eubacterium coprostanoligenes was enriched in TB (+) macaques. These shifts distinguished infected animals from TB-negative controls, suggesting that specific taxa track with TB status in both the pharynx and the gut.
The findings suggest that alterations in gut and pharyngeal bacteria may influence host immune regulation and TB severity, though the underlying mechanisms still need to be explored and validated. This work points to potential host-microbe interactions relevant to TB progression that could inform future understanding of disease biology. It also raises the possibility that microbiome-based markers or targets could eventually contribute to TB therapeutics, pending further mechanistic and translational research.
This observational cross-sectional study examined gut microbiota composition and serum inflammatory cytokine levels in people with late-life depression (LLD). The researchers wanted to clarify the relationship between gut microbiota and inflammation in LLD, since diagnosis is complicated by cognitive impairment and clinical features that overlap with adult depression. They analyzed microbiota diversity and composition alongside twelve inflammatory factors, and examined how these related to neuropsychological scale scores. They then used receiver-operating characteristic curve analysis to see whether combining microbiota and cytokine data could yield biomarkers for LLD.
The study included 29 patients with late-life depression and 33 sex- and age-matched healthy controls. Fecal samples and peripheral blood were collected from all participants to profile gut microbiota and measure the twelve inflammatory factors. The abstract does not provide further demographic or clinical detail beyond this matched case-control design.
Patients with LLD showed elevated systemic inflammatory cytokine levels along with gut microbiota dysbiosis compared with healthy controls. At the phylum level, Verrucomicrobia relative abundance differed in LLD patients, and at the genus level Megamonas, Citrobacter, and Akkermansia abundances were altered. These microbiota and inflammatory changes were evaluated for their relationships to neuropsychological scale scores, and were used to extract potential biomarkers via receiver-operating characteristic curve analysis. The abstract text provided is truncated before the full quantitative results and biomarker performance are given.
The findings support a combined role for gut microbiota dysbiosis and systemic inflammation in late-life depression, rather than either factor acting alone. Because Verrucomicrobia, Megamonas, Citrobacter, and Akkermansia abundances differed between groups, these taxa may be worth further investigation as candidate biomarkers for LLD. Combining microbiota profiles with inflammatory cytokine measurements could help address the diagnostic challenges that arise when LLD is difficult to distinguish from adult depression due to cognitive impairment. Further work would be needed to validate these biomarkers before any clinical application.
This study examined the human microbiome at four body sites, tracking microbial composition and temporal dynamics over a six-year period. Researchers analyzed how these microbiome patterns related to host multi-omics, immune markers, and clinical features. The goal was to characterize the dynamic interplay between microbiome stability, individuality, and host health status, including metabolic disease.
The study followed 86 participants over six years, with microbiome sampling conducted at four body sites per person. The abstract does not specify additional demographic details such as age range, sex distribution, or geographic origin of the cohort. Within this cohort, a subset of individuals classified as insulin-resistant was compared against the broader group.
Microbiome stability and individuality were found to be body-site specific and strongly shaped by the host, with the stool and oral microbiomes more stable than the skin and nasal microbiomes. The researchers identified both individual-specific and commonly shared bacterial taxa, and individualized taxa showed greater stability over time. Microbiome dynamics correlated across different body sites, suggesting systemic, host-microbial-environment interactions rather than site-isolated behavior. 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 depends heavily on site-specific interactions with the host and environment. The link between systemic microbiome dynamics and metabolic disease indicates that insulin resistance may involve broader disruption of host-microbiome coupling, not just changes at a single body site. This multi-site, longitudinal approach offers a framework for understanding how microbiome dynamics track with health and disease over time.
This study tested whether Parkinson's disease alters the oral microbiome associated 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 performed next-generation sequencing of the 16S ribosomal RNA gene (V1-V3 regions) to profile oral and gut microbial 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 controls (HC). The exact number of participants per group is not given in the abstract. The PA+P group had mild-to-moderate motor dysfunction and plaque scores comparable to the P group, indicating similarly effective oral hygiene.
Beta diversity in saliva differed significantly between HC and PA+P, between HC and P, and between P and PA+P, and the microbial profiles of saliva and fecal samples were distinct from one another. In the P group, Mycoplasma faucium, Tannerella forsythia, Parvimonas micra, and Saccharibacteria (TM7) were increased in saliva, while Ruthenibacterium lactatiformans, Dialister succinatiphilus, Butyrivibrio crossotus, and Alloprevotella tannerae were detected in stool. In the PA+P group, Prevotella pallens, Prevotella melaninogenica, and Neisseria multispecies were more abundant in saliva, showing a distinct microbial signature compared with periodontitis alone.
The findings suggest that Parkinson's disease is associated with a shift in the periodontitis-related oral microbiome, independent of oral hygiene status. Because saliva and fecal microbial profiles diverged, oral and gut compartments may need to be assessed separately when studying oral-systemic links in Parkinson's disease. These distinct microbial signatures could inform future research into oral microbiome markers relevant to Parkinson's disease progression or management.
The study examined whether the oral (salivary) and fecal microbiomes differ between children with functional constipation and children without it. Researchers used 16S rRNA gene amplicon sequencing to profile bacterial communities in saliva and stool samples. The aim was to determine whether disturbances in gastrointestinal microbiome homeostasis are associated with paediatric constipation, a condition affecting almost 30% of children.
A total of 91 children over three years of age were included in the study. Of these, 57 were classified into the constipation group and 34 into the group without constipation. Saliva and stool samples were collected from each child for microbiome analysis.
At the family level, Burkholderiaceae, Christensenellaceae, and Clostridiaceae were significantly less abundant in children with constipation, while Tannerellaceae was significantly more abundant. At the genus level, rare taxa including Christensenellaceae r-7, Fusicatenibacter, Parabacteroides, Romboutsia, and Subdoligranulum were all less abundant in the constipation group. These findings indicate that functional constipation is associated with characteristic, reproducible shifts in fecal bacterial taxa, including a reduction in Christensenellaceae and its genus Christensenellaceae r-7.
The findings support the idea that gut microbiome composition, particularly reduced Christensenellaceae and related taxa, may play a role in the pathophysiology of functional constipation in children. Identifying these characteristic bacterial shifts could help inform future diagnostic or microbiome-targeted approaches to paediatric constipation. Further research is needed to clarify whether these microbial differences are a cause or a consequence of altered gut transit and function.
This study examined the gut microbiota in colorectal cancer (CRC) patients to identify microbial features associated with liver metastasis (LM). Researchers used high-throughput 16S rRNA sequencing to compare microbial richness and composition between patients with liver metastasis (LM) and those with no liver metastasis (NLM). The goal was to establish whether distinct gut microbial signatures accompany CRC liver metastasis, since this had not been fully characterized before.
The study used three cohorts. A supplementary discovery cohort (cohort 1) analyzed primary carcinoma tissue samples from 8 patients with liver metastasis and 10 without. A discovery cohort (cohort 2) used fresh feces from 18 LM patients and 36 NLM patients, and a validation cohort (cohort 3) used fresh feces from 13 LM patients and 41 NLM patients.
Intestinal microbiota richness and diversity were increased in the LM group compared to the NLM group, and species composition differed significantly between the two groups. Across the two discovery cohorts, which used different sample types, the dominant phyla were consistent even though composition varied at lower taxonomic levels. The phylum Fusobacteria showed consistent alterations associated with liver metastasis across these cohorts, linking it to a poor prognosis in CRC.
The findings suggest that gut microbial features, particularly Fusobacteria alterations, may serve as a marker of liver metastasis risk and prognosis in colorectal cancer. Because differences were detected in both fecal and tissue samples across independent cohorts, these microbial signals appear robust rather than a single-cohort artifact. This work supports further research into the gut microbiota as a tool for diagnosis, risk stratification, and potentially new therapeutic strategies in CRC with liver metastasis.
This study examined whether the traditional Chinese medicine formula Shenling Baizhu San (SLBZS) could help prevent or treat non-alcoholic fatty liver disease (NAFLD) at the preclinical level. The researchers modeled NAFLD using a western diet combined with CCl4 injection and then tested a 6-week SLBZS intervention against this model. They tracked body weight, energy intake, liver enzymes, pro-inflammatory factors, and steatosis, alongside gut microbiota composition using 16S rRNA gene sequencing and untargeted metabolomics. They also measured components of the gut-liver serotonin pathway, including TPH1, 5-HT, HTR2A, and HTR2B.
The study used male C57BL/6J mice, randomly divided into three groups: a normal diet (ND) control group, a western diet plus CCl4 injection (WDC) disease-model group, and a WDC plus SLBZS treatment group. No human cohort was involved; this was a preclinical mouse model of diet- and toxin-induced NAFLD.
Six weeks of SLBZS intervention reduced serum and liver lipid levels, glucose, and pro-inflammatory factors, while improving insulin resistance and liver function indexes, thereby alleviating NAFLD in the mice. SLBZS also produced significant changes in intestinal TPH-1, 5-HT, liver 5-HT, and the related receptors HTR2A and HTR2B, pointing to modulation of the gut-liver serotonin signaling axis. The 16S rRNA gene analysis further indicated that SLBZS altered the composition of the gut microbiota, linking these microbial shifts to the metabolic and serotonergic changes observed.
The findings suggest SLBZS may offer a multi-target approach to NAFLD, acting through gut microbiota modulation and the gut-derived serotonin signaling pathway rather than a single mechanism. This supports further investigation of TCM formulas as adjunctive or preventive strategies for NAFLD, particularly ones that intersect microbiome composition with host metabolic and enteroendocrine signaling. Because this is a mouse model, translation to human NAFLD prevention or treatment would require validation in clinical studies.
This study investigated the gut microbiota changes associated with pediatric diarrhea and constipation using 16S rRNA sequencing of stool samples. The researchers aimed to identify gut microbes that simultaneously affect both diarrhea and constipation, since prior work had largely treated these as separate conditions. They also conducted pathway analysis to explore potential shared regulatory mechanisms underlying the two conditions.
The study included 618 Chinese children aged 0 to 3 years. Of these, 66 children had diarrhea, 138 had constipation, and 414 were healthy controls. Stool samples were collected from all participants for microbiota analysis.
Children with diarrhea showed significantly decreased microbial diversity compared to healthy controls, while children with constipation showed significantly increased diversity (p < 0.05). Ruminococcus levels increased in constipation (p = 0.03) and decreased in diarrhea (p < 0.01) relative to healthy controls, marking it as a genus that moves in opposite directions across the two conditions. Pathway analysis linked Ruminococcus to five shared pathways, including membrane transport, nervous system, energy metabolism, signal transduction, and endocrine system pathways, suggesting a common regulatory mechanism connecting diarrhea and constipation.
The findings identify Ruminococcus as a core microorganism that may help maintain gut balance in children, with its depletion or expansion tracking opposite ends of a diarrhea-constipation spectrum. This provides a potential shared biological explanation for two seemingly opposite digestive disorders in young children. The results offer a reference point for future research into microbiota-targeted approaches for managing pediatric diarrhea and constipation.
This study examined whether a ketogenic diet (KD) protects against seizures and cognitive impairment in a rat model of temporal lobe epilepsy (TLE) induced by lithium-pilocarpine, and whether these effects depend on the gut microbiome. Researchers assessed seizure behavior, acute-phase epileptic brain activity, hippocampal neuronal damage, and cognitive function in TLE rats fed either a ketogenic or a normal diet. They further tested whether disrupting the gut microbiota with antibiotics would interfere with the diet's protective effects. Gut microbiota composition was profiled using 16S rRNA gene sequencing of fecal samples.
The subjects were adult rats with lithium-pilocarpine-induced temporal lobe epilepsy, divided into groups fed a ketogenic diet or a normal diet. A subset of these rats also received antibiotics to disrupt gut microbiota, allowing comparison of KD effects with and without an intact microbiome. The abstract does not specify exact group sizes, sex, or strain, so no further cohort detail can be stated beyond this rat model design.
A ketogenic diet mitigated seizure behavior, reduced acute-phase epileptic brain activity, alleviated hippocampal neuronal damage, and improved cognitive impairment caused by TLE. These benefits were compromised when antibiotics disrupted the gut microbiota, indicating the microbiome is necessary for the diet's antiepileptic effects. The Chao1 and ACE diversity indices showed decreased species variety in KD-fed TLE rats compared to normal-diet TLE rats. The KD also increased Actinobacteriota, Verrucomicrobiota, and Proteobacteria while decreasing Bacteroidetes, with Actinobacteriota and Verrucomicrobiota abundances positively correlated with favorable outcomes.
The findings suggest that the gut microbiome is a required mediator of the ketogenic diet's antiepileptic and cognition-protecting effects in this TLE model, not merely a byproduct of the diet. This positions specific taxa such as Actinobacteriota and Verrucomicrobiota as candidate contributors to seizure protection and cognitive preservation. The work supports further investigation of microbiome-targeted strategies, potentially alongside or as alternatives to strict ketogenic dietary regimens, for temporal lobe epilepsy management.
This study examined the fecal (gut) microbiota of individuals with polycystic ovary syndrome (PCOS), a common condition associated with high androgen levels and infertility. The researchers analyzed community structure (diversity and composition) and predicted functional profiles of the gut microbiota. They compared these features between PCOS individuals and healthy individuals to characterize dysbiotic alterations linked to the condition.
The study included 17 individuals with PCOS and 17 age-matched healthy individuals, all from Northeast China. This design allowed direct comparison of gut microbial structure and function between affected and unaffected people of similar age. The sample size is modest, consistent with an exploratory case-control study of a regional population.
PCOS individuals had reduced gut microbial diversity and richness compared with healthy individuals, and beta diversity analysis showed their microbial community structure was significantly separated from that of healthy individuals. At the phylum level, PCOS individuals had reduced Firmicutes and Bacteroidota alongside increased Actinobacteriota and Proteobacteria. Composition differences were also evident at the family and genus levels, and PICRUSt2 functional prediction indicated that PCOS individuals had gut microbial functions distinct from those of healthy individuals.
These findings support a link between gut microbial dysbiosis and PCOS, suggesting the microbiota may play a role in the condition's pathophysiology. The consistent shifts in diversity, phylum-level composition, and predicted function point to the gut microbiome as a potential area for further mechanistic and therapeutic investigation in PCOS. Because the cohort was small and regionally specific, larger and more diverse studies are needed to confirm generalizability.
This study examined whether dietary inulin, a prebiotic fiber, could improve intestinal flora composition and metabolism-related indicators in obese patients with polycystic ovary syndrome (PCOS). PCOS is a common endocrine disorder in women of reproductive age that is closely tied to chronic low-grade inflammation and metabolic disturbance. Because inulin had already shown benefits for gut flora and inflammation in PCOS mouse models, the researchers set out to test whether the same effects would hold in a clinical human population. Patients were followed over three months of inulin treatment, with intestinal flora and metabolic markers measured before and after.
The study population consisted of obese women with polycystic ovary syndrome compared against healthy controls. The abstract does not give an exact number of participants, so the precise sample size cannot be stated. What can be said honestly is that this was a clinical (human) comparison of PCOS patients versus controls, rather than an animal model, following three months of inulin intervention in the PCOS group.
Dietary inulin improved sex hormone disorders and reduced both BMI and waist-hip ratio (WHR) in obese women with PCOS. The intervention also lowered plasma inflammatory markers, including TNF-alpha, IL-1beta, IL-6, and MCP-1. Gut flora shifted favorably: Actinobacteria, Fusobacteria, Lachnospira, and Bifidobacterium increased, while the Firmicutes/Bacteroidetes ratio and the abundance of Proteobacteria, Sutterella, and Enterobacter decreased. Correlation analyses linked these microbial shifts to changes in plasma inflammatory factors and sex steroid hormones, suggesting the three systems move together.
The findings suggest that a simple dietary prebiotic, inulin, may offer a low-risk way to address the combined metabolic, hormonal, and inflammatory disturbances seen in obese PCOS patients. Because gut flora changes correlated with both inflammatory and hormonal shifts, the intestinal microbiome may be a mechanistic link connecting diet to PCOS symptoms rather than an incidental bystander. This supports further clinical investigation of inulin or similar fibers as an adjunct therapy for obese women with PCOS, particularly for managing BMI, WHR, and systemic inflammation.
This study examined how periodontitis in early pregnancy connects to changes in the gut through what the authors call the oral-gut axis. The researchers used an integrative, multi-omics approach combining 16S rRNA gene sequencing and untargeted metabolomics across subgingival plaque, saliva, serum, and stool samples. They aimed to characterize the microbiome and metabolome profiles linked to periodontitis and to explore translational potential, given that periodontitis has been associated with adverse pregnancy outcomes.
The study population was 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 from each participant across four body sites: subgingival plaques, saliva, sera, and stool.
The researchers identified Coprococcus as a novel fecal bacterial distinguisher of periodontitis, notable because it behaved differently from other genera in the Lachnospiraceae family and was associated with subgingival periodontopathogens. They found that the ratio of fecal Coprococcus to Lachnoclostridium could discriminate between women with periodontitis and non-periodontitis controls. This finding demonstrates a measurable microbial link between oral disease status and gut microbial composition in pregnant women.
The findings support the existence of an oral-gut axis through which periodontitis in pregnancy may produce distal microbial and metabolic consequences beyond the mouth. The fecal Coprococcus-to-Lachnoclostridium ratio may hold translational potential as a non-invasive marker related to periodontitis status in pregnant women. This integrative multi-omics approach illustrates how combining oral and gut sampling with metabolomics can reveal systemic connections relevant to adverse pregnancy outcomes.
This study characterized gastrointestinal microbial communities involved in gastric carcinogenesis by pooling 16S rRNA sequencing data across 11 independent published and open datasets. The researchers compared both intratumoral (gastric biopsy) and fecal microbiota between gastric cancer patients and non-cancer individuals. They used tools including VSEARCH, QIIME, and R packages such as vegan, phyloseq, cooccur, and random forest for diversity analysis, network analysis, and biomarker identification, with PICRUSt used to predict functional pathways.
The analysis drew on 1,642 gastric biopsy samples and 394 stool samples aggregated across 11 independent studies. The abstract does not give demographic details such as age, sex, or geographic origin of the underlying cohorts. This was a meta-analysis of existing sequencing data rather than a newly recruited single-site cohort.
Alpha-diversity of the intratumoral microbiota differed significantly between gastric cancer patients and non-cancer patients, while fecal microbiota diversity showed no significant difference between groups. Network analysis revealed that positive correlations among gastric cancer-enriched bacteria increased, while positive correlations among gastric cancer-depleted bacteria decreased, compared to healthy individuals. Functional prediction analyses pointed to alterations in pathways related to carbohydrate metabolism, though the abstract text describing these functional results was truncated.
The findings suggest that local, tumor-site microbial signatures may be more informative for gastric cancer detection than stool-based sampling, since diversity differences were seen intratumorally but not fecally. The shifting co-occurrence network structure around cancer-enriched and cancer-depleted bacteria points to microbial community reorganization as a feature of gastric carcinogenesis. By pooling data across 11 studies, this work moves toward identifying more reproducible microbial markers for early gastric cancer detection across populations.
This study examined whether iron overload in thalassemia patients is linked to gut dysbiosis and cognitive impairment through the gut-brain axis. Researchers assessed iron burden, cognitive function, and both gut and blood microbiome composition across different blood-transfusion regimens. The goal was to determine whether specific microbial shifts track with iron accumulation and cognitive status in this population.
Sixty participants were recruited, comprising healthy controls, transfusion-dependent thalassemia (TDT) patients, and non-transfusion-dependent thalassemia (NTDT) patients. TDT patients receive more frequent blood transfusions and, consistent with this, showed greater iron overload than NTDT patients. This design allowed comparisons of gut and blood microbiota across a spectrum of iron-overload severity within the same disease population.
Most thalassemia patients developed gut dysbiosis, and about 25% developed minor cognitive impairment. Both TDT and NTDT groups showed increased Fusobacteriota and Verrucomicrobiota with decreased Fibrobacterota, and TDT patients had more abundant Verrucomicrobia, described as beneficial bacteria. Iron overload correlated with cognitive impairment, and increased Butyricimonas with decreased Paraclostridium was associated with higher cognitive function. No blood microbiota was detected, and blood bacterial profiles did not differ significantly between thalassemia patients and controls.
The findings suggest that iron overload in thalassemia is associated with gut microbial imbalance that may relate to cognitive outcomes through the gut-brain axis. Specific gut taxa such as Butyricimonas and Paraclostridium emerge as candidate markers linked to cognitive function, while the blood compartment appears not to harbor a distinct microbiome signal in this context. This points to the gut, rather than blood, as the more relevant site for future investigation of microbiome-cognition relationships in iron-overloaded thalassemia patients.
This study examined the biogeography of the mucosa-associated microbiome (MAM) across different segments of the upper and lower gastrointestinal tract. Researchers compared microbial composition and bacterial load between patients with inflammatory bowel disease (IBD) and controls. They also looked at how the MAM related to proton pump inhibitor (PPI) use, gastrointestinal symptom severity, and symptom response to a standardised nutrient challenge. Microbial composition was assessed with 16S rRNA gene amplicon sequencing, and bacterial load was measured by qPCR on mucosal biopsies.
The study included 59 controls without structural gastrointestinal abnormalities or symptoms, 44 patients with ulcerative colitis, and 31 patients with Crohn's disease. Biopsies were collected from multiple segments of both the upper and lower gastrointestinal tract in these participants. This gives a total of 134 individuals across three clinical groups.
Microbial communities differed between the upper and lower gastrointestinal tract in their mucosal composition. IBD patients showed relative and absolute depletion of numerous genera known to produce butyrate and/or propionate compared with controls. The largest difference observed was depletion of Faecalibacterium in the lower gastrointestinal tract of patients with Crohn's disease. The abstract also indicates that PPI users showed a notable difference in the MAM, though the specific finding is cut off in the provided text.
The findings suggest that loss of short-chain fatty acid producing bacteria, particularly Faecalibacterium, is a hallmark of mucosal dysbiosis in Crohn's disease at the site of tissue contact rather than only in stool. Mapping microbiome differences by gastrointestinal segment highlights that biogeography matters when interpreting mucosal microbiome studies in IBD. The association with PPI use also points to medication exposure as a factor that should be accounted for when characterizing the mucosa-associated microbiome in these patients.
This study characterized and compared the fecal and oral microbiota of women newly diagnosed with early-stage breast cancer (BC), women with ductal carcinoma in situ (DCIS), and healthy women. Samples were collected before any cancer therapy and analyzed using 16S rRNA sequencing. The researchers examined microbial diversity, community composition, bacterial guild clustering, and predicted functional pathways in both gut and oral samples.
The study population consisted of women with early-stage breast cancer, women with ductal carcinoma in situ, and healthy women who served as controls. Samples were collected from newly diagnosed patients prior to any treatment, meaning the microbiota data reflect an untreated disease state. The abstract does not give exact numbers of participants, so specific cohort sizes cannot be reported.
Gut microbial alpha diversity was significantly lower in the breast cancer group compared to healthy women, and beta diversity differed significantly between the breast cancer or DCIS groups and healthy controls. Clustering identified five gut bacterial guilds dominated by Prevotella, Enterobacteriaceae, Akkermansia, Clostridiales, or Bacteroides, with the Bacteroides and Enterobacteriaceae guilds more abundant in breast cancer patients and the Clostridiales guild more abundant in healthy women. Predicted functional pathway analysis identified 23 pathways that differed between groups, including lipopolysaccharide biosynthesis, glycan biosynthesis and metabolism, lipid metabolism, and sphingolipid metabolism. In contrast, the oral microbiome showed no significant differences in alpha or beta diversity between groups.
The findings suggest that gut, but not oral, microbial composition is altered in women with early-stage breast cancer relative to healthy women, pointing to the gut as a more relevant site for microbiome-cancer associations. The shifts toward Bacteroides and Enterobacteriaceae dominance and away from Clostridiales, along with altered lipid and glycan metabolism pathways, suggest possible mechanistic links between gut dysbiosis and breast cancer biology. These results support further investigation of the gut microbiome as a potential biomarker or contributor to breast cancer risk, warranting studies with larger cohorts to confirm causality.
This study examined the gut microbiome in the context of HIV-1 infection and injection drug use. Researchers compared bacterial community composition across groups defined by HIV status and by whether individuals injected drugs. They used amplicon-based 16S rDNA sequencing to identify amplicon sequence variants (ASVs) that varied significantly with HIV status and drug use. The goal was to disentangle how HIV infection and injection drug use, separately and together, shape the gut microbial community.
The study drew on a well-established cohort of people who inject drugs in Puerto Rico, a region with historically high rates of injection drug use and an HIV incidence rate disproportionately linked to drug use. Participants were divided into HIV-positive and HIV-negative individuals, each further split into those who inject drugs and those who do not. The abstract does not give an exact total sample size, but the design compares four groups across these two variables. The cohort therefore represents a population directly affected by both the opioid/injection drug epidemic and HIV transmission risk.
The HIV-positive group showed a higher abundance of ASVs from the genera Prevotella, Alloprevotella, Sutterella, Megasphaera, Fusobacterium, and Mitsuokella. In contrast, Bifidobacteria and Lactobacillus ASVs were more abundant in people who inject drugs than in non-injectors, regardless of HIV status. The researchers also found that using multiple drugs significantly affected the composition of the gut microbial community. These results indicate that HIV status and injection drug use each leave distinct, identifiable signatures on the gut microbiota.
The findings suggest that HIV infection and injection drug use independently reshape the gut microbiome, with different bacterial genera responding to each factor. This distinction matters for interpreting microbiome changes in people who inject drugs, since HIV-associated and drug-associated shifts should not be conflated. The elevation of Bifidobacteria and Lactobacillus with injection drug use, and of Prevotella-related genera with HIV, points to potential microbial markers worth tracking in this high-risk population. Overall, the study underscores the need to account for both infection status and substance use patterns when studying the gut microbiome in vulnerable communities.
This study examined the gut microbiome of individuals with irritable bowel syndrome (IBS) to determine whether distinct microbial signatures underlie different IBS subtypes. Researchers analyzed 16S sequencing data to characterize taxonomic and functional composition of gut bacteria. They then linked these microbial patterns to clinical characteristics, dietary factors, and psychological comorbidities such as depression.
The study drew on deeply phenotyped individuals with microbiota sequencing enrolled in the American Gut Project. A total of 942 subjects with IBS, subdivided into IBS-Diarrhea (IBS-D), IBS-Constipation (IBS-C), and unclassified IBS (IBS-U), were compared against 942 non-IBS controls. Cases and controls were matched by age, gender, body mass index, geography, and dietary patterns.
Subjects with IBS-D or IBS-U, but not IBS-C, showed significantly reduced bacterial diversity (Shannon index, p < .01) compared with controls. Each IBS subtype was associated with a distinct bacterial signature and corresponding functional shifts, including an increased hydrogen sulfide production pathway in IBS-D and increased palmitoleate biosynthesis in IBS-C. IBS subjects with depression showed lower abundance of Bifidobacterium, Sutterella, and Butyricimonas and higher abundance of Proteus compared to those without depression, and short-chain fatty acid production pathways were reduced overall in IBS patients.
The findings support treating IBS as a heterogeneous condition with subtype-specific microbial and functional signatures rather than a single uniform disorder. The link between depression and specific taxa such as reduced Bifidobacterium suggests the gut microbiome may connect IBS pathogenesis to mood comorbidities. These subtype-specific signatures could inform more targeted, microbiome-based approaches to diagnosing and managing IBS.
This study investigated the antenatal gut microbiome in pregnant women living with and without HIV infection. The researchers examined microbial community composition and diversity in stool samples collected during pregnancy. They then compared these microbiota profiles between the two groups and explored associations with adverse birth outcomes in a resource-limited setting.
A total of 94 pregnant women were recruited in Harare, Zimbabwe, from four polyclinics serving populations of relatively poor socioeconomic status. Of these, 35 were HIV-infected and 59 were HIV-uninfected controls. Participants had a median age of 28 years, and just over half were enrolled at a median gestational age of 35 weeks.
Gut microbial species richness was significantly lower in HIV-infected pregnant women compared with their HIV-uninfected peers. Significant differences in beta-diversity, measured using Bray-Curtis dissimilarity, were also observed between the two groups, indicating distinct overall community composition. In contrast, there was no significant difference in alpha-diversity between the groups, based on the portion of the abstract provided.
The findings suggest that HIV infection during pregnancy is associated with reduced gut bacterial richness and altered microbial community structure, consistent with HIV-related gut damage and dysbiosis described in the background. Because maternal gut microbiota changes were linked to this vulnerable, resource-limited population, the results point to a need for further research into how these microbial shifts might relate to pregnancy outcomes. This underscores the importance of considering gut health as part of antenatal care for HIV-infected women in similar settings.
This study examined the relationship between gastrointestinal (GI) microbial composition and GI symptoms in patients with systemic sclerosis (SSc). It also compared GI symptoms and microbial composition between SSc patients following a low FODMAP diet versus those not following a low FODMAP diet. Stool specimens underwent bacterial 16S rRNA gene sequencing, and microbial differences were assessed using alpha diversity (species richness, evenness, phylogenetic diversity) and beta diversity (overall composition). Differential abundance analysis was used to identify specific bacterial genera linked to the SSc-GI phenotype and to diet group.
The study included 66 adult patients with systemic sclerosis who were consecutively recruited and provided stool samples. Patients also completed the UCLA Scleroderma Clinical Trial Consortium Gastrointestinal Tract Instrument (GIT 2.0) to assess GI symptoms and the Diet History Questionnaire (DHQ) II to assess dietary intake. Based on their reported intake, patients were classified as adhering to a low or non-low FODMAP diet.
The abstract provided does not include the specific results, so the detailed findings on microbial diversity, differential genera, or symptom associations cannot be reported here. The study design indicates that both alpha diversity and beta diversity metrics were used to compare gut microbial composition across SSc-GI phenotypes and across diet groups. Differential abundance analysis was intended to pinpoint particular bacterial genera associated with GI symptoms and with FODMAP diet status in this SSc cohort.
By pairing validated GI symptom instruments with dietary history and 16S rRNA sequencing, this approach helps disentangle whether GI microbial alterations in systemic sclerosis are driven by disease-related changes, dietary patterns, or both. Clarifying this distinction could inform whether dietary interventions such as a low FODMAP diet meaningfully influence gut microbial composition and symptom burden in SSc patients. This kind of design lays groundwork for future studies testing whether dietary modification can be used as a targeted strategy to manage SSc-associated GI symptoms.
This study examined the fecal microbiota of patients with chronic constipation (CC) to see how bacterial composition differs across constipation subtypes. Researchers compared slow-transit constipation versus normal-transit constipation, and separately compared dyssynergic defecation versus non-dyssynergic defecation. They also tested whether colorectal physiology (such as rectal defecation pressure), lifestyle factors, and psychological distress were associated with microbiota composition.
The study enrolled 53 individuals with chronic constipation and 31 healthy individuals in a prospective cohort design. Stool samples from all participants were analyzed using 16S rRNA sequencing. Within the CC group, 31 patients were classified with slow-transit constipation and 22 with normal-transit constipation, and separately 28 patients had dyssynergic defecation and 25 did not.
Bacteroidaceae was lower, while Peptostreptococcaceae, Christensenellaceae, and Clostridiaceae were higher, in slow-transit constipation compared to normal-transit constipation. Bacteroidaceae and Ruminococcaceae were higher in patients with dyssynergic defecation than in those without it. Rectal defecation pressure was negatively correlated with Prevotellaceae and Ruminococcaceae abundance but positively correlated with Bifidobacteriaceae abundance. Depression was a positive predictor of Lachnospiraceae abundance, and poorer sleep quality independently predicted decreased Prevotellaceae abundance.
The findings show that chronic constipation is not a single microbial entity: different constipation subtypes carry distinct patterns of dysbiosis. This helps explain why prior microbiome studies of constipation have produced inconsistent results, since many did not stratify by subtype. The results also suggest that psychological status and sleep quality should be considered alongside colon physiology when interpreting or targeting the gut microbiota in constipation research.
This study examined whether irritable bowel syndrome (IBS) involves abnormal brain-gut-microbiome interactions by combining resting-state functional MRI with gut microbiome sequencing. Researchers used dynamic functional connectivity (DFC) analysis to characterize how brain network patterns change over time, rather than treating connectivity as static. They then tested whether these dynamic brain signatures correlated with differences in gut bacterial composition. The goal was to link temporal brain network behavior directly to microbial abundance data within the same individuals.
The study included 33 patients with irritable bowel syndrome and 32 healthy controls. All participants contributed resting-state fMRI scans, fecal samples for 16S rRNA gene sequencing, and clinical characteristic data. This is a relatively small, single-cohort clinical sample rather than a large public dataset, and the authors describe the results as preliminary.
Four recurring dynamic brain connectivity states were identified across participants. IBS patients spent more time in State 4 (increased mean dwell time and fraction time) and showed fewer transitions from State 3 to State 1 compared to healthy controls. These aberrant temporal patterns in State 4 were only detectable using shorter analysis windows (36 or 44 seconds). IBS patients also showed decreased functional connectivity variability in States 1 and 3, with two specific connectivity pairs (IC51-IC91 and IC46-IC11) significantly correlating with clinical characteristics, alongside nine differentially abundant gut bacterial taxa.
The findings support a bidirectional brain-gut-microbiome model of IBS, in which altered temporal dynamics of brain networks are linked to specific shifts in gut microbial composition rather than occurring independently. This suggests dynamic (not just static) brain connectivity measures may be a more sensitive lens for detecting IBS-related brain-gut disruption. Because window length affected which abnormalities were detectable, methodological choices in DFC analysis may matter for reproducibility in future brain-gut-microbiome research. As a preliminary study with a modest sample, these associations point toward mechanistic hypotheses for IBS pathogenesis that warrant validation in larger cohorts.
This study investigated whether Faecalibacterium prausnitzii, proposed as a next-generation probiotic, could mitigate nonalcoholic steatohepatitis (NASH). The researchers combined 16S rRNA sequencing analysis of the gut microbiota with an in vivo mouse model in which NASH was induced by a high-fructose high-fat diet over 16 weeks. They tested oral administration of isolated F. prausnitzii strains against characteristic NASH phenotypes using glucose tolerance tests, biochemical assays, and liver histology.
The abstract describes two study populations. Human participants included patients with NASH and healthy controls who underwent 16S rRNA sequencing, and four healthy individuals whose fecal samples yielded the four F. prausnitzii strains used in the experiments. The intervention itself was tested in mice fed a high-fructose high-fat diet for 16 weeks to induce a NASH model, not in human subjects.
The 16S rRNA sequencing analyses confirmed differences in the gut microbiota between NASH patients and healthy controls, supporting the premise that dysbiosis is linked to NASH pathophysiology. Four distinct F. prausnitzii strains (EB-FPDK3, EB-FPDK9, EB-FPDK11, and EB-FPYYK1) were successfully isolated from healthy donor stool for testing. The abstract text provided is truncated before the mouse intervention results are reported, so the specific outcomes of oral strain administration on glucose tolerance, biochemical markers, or liver histology cannot be stated here.
The work supports the broader concept that next-generation probiotics derived from the healthy human gut, such as F. prausnitzii, warrant investigation as candidates for preventing or treating NASH. Confirming microbiota differences between NASH patients and healthy controls reinforces dysbiosis as a relevant feature of disease pathophysiology. Because the reported findings are incomplete in this excerpt, firm conclusions about therapeutic efficacy should await the full results of the mouse intervention experiments.
This study examined the gut microbiome and serum metabolome in patients with functional constipation (FC), a common gastrointestinal disorder that significantly affects physical and mental health. The researchers used 16S rRNA microbial genomics to profile gut microbiota composition and non-target metabolomics based on liquid chromatography-mass spectrometry to characterize serum metabolic profiles. The study was designed to address inconsistent prior findings on the gut microbiome and FC, and to better link microbiome changes to host metabolites.
The study included 30 patients with functional constipation and 28 healthy individuals as a comparison group. Fecal samples were used for 16S rRNA gut microbiota analysis and serum samples were used for metabolomic profiling in these participants. The abstract does not specify additional demographic details such as age or sex distribution.
FC patients had distinct gut microbiota structures and serum metabolic profiles compared to healthy individuals. Patients with FC showed increased levels of Bacteroides and of several butyrate-producing bacteria, including Roseburia, Faecalibacterium, and Butyricicoccus. Serum levels of upstream products of host arginine biosynthesis, specifically 2-oxoglutaric acid, L-glutamic acid, N-acetylornithine, and L-ornithine, were significantly reduced in FC patients.
The findings suggest that functional constipation may be associated with an altered gut microbiota, including increased Bacteroidetes, alongside downregulation of host arginine biosynthesis intermediates. This points to a potential link between specific gut bacteria and disrupted host amino acid metabolism in FC. The pairing of microbiome and metabolome data offers a more integrated view of FC pathophysiology than microbiome data alone, which could inform future mechanistic or therapeutic research.
This prospective study examined the association between gut microbiota composition and the development of Graves' disease (GD), an autoimmune thyroid condition. Researchers profiled gut microbiota using 16S rRNA sequencing, comparing patients before and after treatment for GD. They also measured interleukin-17 levels to explore a possible immune link to the microbial changes observed.
The study included 65 patients newly diagnosed with Graves' disease, sampled both before and after treatment. A comparison group of 33 physical examination personnel served as healthy controls. Gut microbiota from both groups was profiled using 16S rRNA sequencing.
Significant differences in gut microbiota composition were found between GD patients and healthy controls, spanning 1 class, 1 order, 5 families, and 14 genera. After treatment, biota that had been enriched in GD patients decreased, while biota that had been depleted increased, alongside a significant decline in interleukin-17 levels. A random forest model identified 12 genera capable of distinguishing GD patients from healthy controls.
The findings suggest gut microbiota in Graves' disease patients have distinct, identifiable characteristics compared with healthy individuals. The parallel shifts in microbiota and interleukin-17 after treatment point to a possible relationship between immune imbalance and gut dysbiosis in GD. These microbial signatures could eventually support diagnostic or monitoring approaches, though the abstract does not establish causation.
This study examined the surface microbiome of purple sea urchins affected by bald sea urchin disease (BSUD), a likely bacterial infection that causes loss of surface appendages and other symptoms. Using 16S rRNA gene sequencing, the researchers profiled bacterial communities on urchins that contracted BSUD and later recovered, comparing them to healthy urchins housed in a separate aquarium. The goal was to characterize how the surface microbiome changes across disease, recovery, and health, since prior work had focused mainly on causative agents rather than the broader microbial community.
The subjects were purple sea urchins housed in a closed marine aquarium system rather than a human or animal clinical cohort. One group of urchins contracted BSUD and then recovered, while a second group of healthy urchins was maintained in a separate aquarium for comparison. The abstract does not give an exact number of urchins sampled, so the population is best described as urchins from two distinct captive aquarium environments.
16S rRNA gene sequencing showed that different aquarium microhabitats harbored distinct microbial compositions. Diseased, recovered, and healthy sea urchins each carried surface microbiomes that were distinguishable from one another. This pattern indicates a correlation between shifts in the surface microbial community and the process of recovering from BSUD.
The findings suggest that surface microbiome composition could serve as a marker of disease state and recovery in sea urchins, beyond simply identifying a single causative pathogen. This supports monitoring microbial community shifts as a tool for tracking BSUD progression or recovery in aquarium and possibly wild populations. It also points to the aquarium environment itself as an influence on the microbiome, which should be considered in future studies of marine invertebrate disease.
This study investigated how surgery-induced disruption of the gut microbiota contributes to perioperative neurocognitive disorders (PND), a common but poorly treatable postoperative complication. The researchers examined how surgery alters gut microbial composition, intestinal barrier integrity, and serum metabolites, and how these changes affect brain and cognitive function. They used behavioral testing, 16S rRNA gene sequencing, non-targeted metabolomics, intestinal permeability assays, protein assays, and immunofluorescence staining to trace this gut-brain pathway.
The subjects were mice, with comparisons made between aged and presumably younger animals undergoing surgery. Interventions included fecal microbiota transplantation from young donors, the anti-inflammatory drug dexamethasone, Lactobacillus supplementation, indole propionic acid supplementation, and palmitic amide administration. No human cohort is described in the abstract; this is an experimental animal model of surgery-induced cognitive impairment.
Surgery-induced cognitive impairment occurred predominantly in aged mice, and surgery altered the gut microbiota composition profile in a way that worsened intestinal barrier disruption specifically in these aged animals. These adverse effects could be mitigated either by transplanting fecal microbiota from young donors or by strengthening the intestinal barrier using dexamethasone, Lactobacillus, or indole propionic acid. The abstract also points to a metabolite, palmitic amide, and to microbiota composition profiles as being linked mechanistically to the observed outcomes, though the full text describing palmitic amide's specific role is cut off in the provided abstract.
The findings suggest that age-related vulnerability to postoperative gut microbial dysbiosis and intestinal barrier breakdown may be a driver of perioperative cognitive decline. Because the effects were reversible with young-donor fecal transplantation, Lactobacillus, indole propionic acid, or dexamethasone, the gut microbiota and intestinal barrier represent potential therapeutic targets for preventing or treating PND. This supports a gut-brain axis mechanism in which restoring microbial and barrier function in aged surgical patients could help protect cognitive outcomes, pending confirmation in human studies.
This study investigated the relationship between gut microbiome composition, dietary habits, and breast cancer (BCa) risk. Researchers used 16S rRNA amplicon sequencing to characterize gut microbial composition and to assess alpha and beta diversity. Dietary intake was assessed using the National Cancer Institute Diet History Questionnaire (DHQ), and microbial findings were linked to Healthy Eating Index (HEI2015) components such as vegetables, dairy, and whole fruits.
The study enrolled newly diagnosed breast cancer patients alongside age-matched, cancer-free controls in a case-control design. Demographic characteristics were reported as well-balanced between the two groups. The abstract does not specify an exact sample size for either group.
Breast cancer patients showed reduced gut microbial diversity compared to controls. Three genera, Acidaminococcus, Tyzzerella, and Hungatella, were enriched in fecal samples from BCa patients relative to cancer-free controls. These genera showed significant associations with specific dietary components: Hungatella with vegetable and dairy intake, and Acidaminococcus with whole fruit intake.
The findings support a link between altered gut microbiome composition and breast cancer, with diet acting as a potential factor shaping that microbial signature. Identifying enriched genera tied to specific dietary patterns suggests the gut microbiome could serve as a modifiable target connecting diet to breast cancer risk. This raises the possibility that dietary interventions influencing these microbial taxa could be explored as part of breast cancer risk reduction strategies.
This study examined the gut microbiota composition and microbiota-derived metabolite profiles in infants with infantile cholestasis (IC), the most common hepatobiliary disease in this age group. Because hepatointestinal circulation links the gut to bile acid and bilirubin metabolism, the researchers looked for microbial changes that accompany elevated direct bilirubin levels in IC. They also examined correlations between specific gut bacteria and circulating fatty acid and amino acid levels. The goal was to identify abnormal metabolite signatures associated with the altered microbiota in IC.
The study compared infants diagnosed with infantile cholestasis (the IC group) to healthy infants (the CON group). The abstract does not provide a specific sample size, age range, or recruitment site, so these details cannot be stated. Based on the described comparison, this appears to be a case-control study of infants with IC versus matched healthy infant controls.
Infants with IC had higher abundances of Veillonella, Streptococcus, and Clostridium species, and lower abundances of Ruminococcus, Vibrio butyricum, the Eubacterium coprostanogenes group, Intestinibacter, and Faecalibacterium compared to healthy infants. Metabolite analysis showed increased levels of fatty acids (palmitoleic, alpha-linolenic, arachidonic, and linoleic acid) and decreased amino acid levels in the IC group. Ruminococcus, the Eubacterium coprostanoligenes group, Intestinibacter, and Butyrivibrio were positively correlated with proline, asparagine, and aspartic acid, but negatively correlated with alpha-linolenic, linoleic, palmitoleic, and arachidonic acid. The abstract also references an analysis relating microbiota to clinical indices, though the specific results of that comparison are cut off and cannot be reported.
These findings suggest that infantile cholestasis is associated with a distinct gut microbial signature marked by depletion of butyrate-associated and short-chain fatty acid producing taxa such as Faecalibacterium and Ruminococcus. The coordinated shifts in fatty acid and amino acid metabolites alongside these microbial changes point to gut microbiota as a potential contributor to, or biomarker of, disrupted bile acid and lipid metabolism in IC. This raises the possibility that microbiota-targeted approaches could eventually be explored as adjuncts in understanding or managing infantile cholestasis, pending further mechanistic and clinical study.
This study investigated the gut microbiome and fecal metabolite profile in functional constipation (FC), a condition whose underlying mechanisms remain unclear. The researchers combined 16S rDNA sequencing with non-targeted metabolomic detection using liquid chromatography-mass spectrometry (LC-MS/MS) to characterize fecal samples. The goal was to identify how gut microbiota and metabolites are altered in FC and how the two are interrelated, since this relationship had received limited attention in prior literature.
The study compared fecal samples from patients with functional constipation to samples from healthy individuals, referred to as the healthy control (HC) group. The abstract does not specify exact participant numbers, age range, or geographic setting. The comparison design indicates a case-control human cohort study rather than an animal or purely computational dataset.
Gut microbiota richness and diversity were significantly increased in FC patients compared to healthy controls (p < 0.01). Eighteen bacterial genera showed statistically significant changes between groups, including Intestinibacter, Klebsiella, and Akkermansia (p < 0.05). Metabolomic analysis revealed 79 differentially abundant metabolites, such as (-)-caryophyllene oxide, chenodeoxycholic acid, and biliverdin, with primary bile acid biosynthesis and porphyrin and chlorophyll metabolism emerging as the most significantly enriched pathways (FDR < 0.01).
The findings suggest that functional constipation involves coordinated shifts in both gut microbial composition and metabolic output, particularly involving bile acid metabolism. Because chenodeoxycholic acid and related bile acids are implicated, altered microbial processing of bile acids may contribute to disrupted bowel function in FC. Mapping these microbiome-metabolite relationships could help identify biomarkers or microbiome-targeted strategies for diagnosing or managing functional constipation.
This pilot study examined the gut microbiota of patients with brain tumors to determine whether benign and malignant tumors are associated with distinct microbial patterns. It compared microbial diversity and composition across benign meningioma, malignant glioma, and healthy control groups. The work builds on prior evidence linking gut microbiota to tumor growth, including malignant gliomas, via the brain-gut axis.
The study included 32 patients with benign meningioma, 27 patients with malignant glioma, and 41 healthy individuals as controls. This gives a total pilot cohort of 100 participants across the three groups. No further demographic details are provided in the abstract.
Brain tumor patients, both meningioma and glioma groups, showed lower gut microbial diversity than healthy controls, with no significant diversity difference between the two tumor groups. Microbial composition differed significantly between tumor patients and healthy participants. Meningioma patients had increased pathogenic bacteria such as Enterobacteriaceae, while glioma patients showed overrepresentation of carcinogenic bacteria including Fusobacterium and Akkermansia. Both benign and malignant tumor groups lacked SCFA-producing probiotic bacteria.
The findings suggest that gut microbial alterations, including reduced diversity and loss of SCFA-producing bacteria, are associated with the presence of brain tumors generally, while specific taxa may distinguish benign from malignant disease. The identification of a candidate microbial biomarker panel, including Fusobacterium, Akkermansia, Escherichia/Shigella, Lachnospira, and Agathobacter, points toward potential non-invasive markers for differentiating tumor types. As a pilot study, these results support further investigation into the brain-gut axis as a factor in brain tumor pathology.
This study examined whether freeze-drying can serve as an alternative to cold-chain storage for transporting and storing fecal microbiome samples. The researchers compared alpha diversity and 16S microbiome composition between samples preserved at minus 80 degrees Celsius and samples that were freeze-dried and kept at ambient temperature. The goal was to identify a preservation method suitable for sample collection at remote sites lacking reliable cold-chain infrastructure.
The study used 20 fecal sample replicates collected from Damaraland mole-rats (Fukomys damarensis). Each replicate was split and processed under two preservation treatments, minus 80 degrees Celsius freezing with dry-ice transport versus freeze-drying with ambient-temperature storage and transport, prior to DNA extraction. This was an animal-derived sample comparison rather than a human cohort study.
The researchers found strong correlations in the relative abundances of Amplicon Sequence Variants between the two preservation treatments. There were no differences in alpha diversity measures between freeze-dried and minus 80 degrees Celsius samples. Beta diversity measures showed only minor effects attributable to the preservation method.
Freeze-drying offers a cost-effective, ambient-temperature alternative to cold-chain preservation that yields microbiome analysis results nearly indistinguishable from the gold-standard minus 80 degrees Celsius method. This makes reliable microbiome sample collection feasible at remote field sites without dry ice or freezer access. The approach could broaden the geographic and logistical reach of future microbiome research.
The study examined the gut microbiome of patients with dermatomyositis (DM), an autoimmune muscle disease, compared with healthy controls. Researchers used 16S ribosomal RNA gene sequencing on fecal samples to compare microbial composition and diversity between the two groups. They also tested whether microbial differences tracked with DM-specific clinical features, including myositis-specific autoantibodies (MSAs), and performed predicted metagenomic functional analysis. Dietary intake was assessed with a 24-hour recall to account for its influence on the microbiome.
The cohort consisted of 36 patients with dermatomyositis and 26 healthy controls, whose fecal samples underwent 16S sequencing. Within the DM group, a subset of 12 patients had interstitial lung disease (ILD)-associated myositis-specific autoantibodies, specifically antisynthetase antibodies or anti-melanoma differentiation-associated protein 5 antibodies. This subgroup was analyzed separately for microbial composition and diversity differences.
Patients with dermatomyositis trended toward lower overall microbial diversity compared with healthy controls. A higher physician global damage score, a measure of cumulative disease-related damage, was significantly correlated with lower microbial diversity in DM patients. Patients with ILD-associated myositis-specific autoantibodies (antisynthetase or anti-MDA5 antibodies) showed significant differences in microbial composition and further reductions in microbial diversity compared with other DM patients.
These findings suggest that gut microbial alterations in dermatomyositis are not uniform but relate to specific clinical subtypes and disease severity. The association between lower diversity and higher damage scores raises the possibility that gut dysbiosis tracks with, or contributes to, cumulative organ damage in DM. The distinct microbial signature in patients with ILD-associated autoantibodies suggests the gut microbiome could eventually help characterize or stratify DM patients by autoantibody-defined subgroups, though this abstract alone does not establish causation.
This study examined the role of gut microbiota in two autoimmune thyroid conditions, Graves' disease (GD) and Hashimoto's thyroiditis (HT). Researchers used 16S sequencing to characterize fecal bacterial communities and chemiluminescence to measure thyroid function and autoantibodies (FT3, FT4, TSH, TRAb, TGAb, and TPOAb). Thyroid ultrasound was also used, and functional prediction of the microbiota was carried out using KEGG and COG analyses to explore possible mechanisms linking gut bacteria to disease.
Seventy fecal samples were collected in total. These included 27 patients with Graves' disease, 27 patients with Hashimoto's thyroiditis, and 16 samples from healthy volunteers who served as controls.
The overall structure of the gut microbiota in both the GD and HT groups differed significantly from that of the healthy control group. Proteobacteria and Actinobacteria were most abundant in the HT group, while both the GD and HT groups showed higher levels of Erysipelotrichia, Cyanobacteria, and Ruminococcus_2 and lower levels of Bacillaceae and Megamonas compared to controls. Functional analysis linked the ABC transporter pathway strongly to GD and HT, and COG analysis showed enrichment in carbohydrate transport and metabolism, but not amino acid transport and metabolism, in both patient groups.
The findings suggest that gut microbiota alterations, particularly shifts in carbohydrate transport and metabolism pathways, may be mechanistically involved in the development of Graves' disease and Hashimoto's thyroiditis. This supports a role for the gut microbiome in autoimmune thyroid disease pathogenesis and points to specific bacterial taxa and metabolic pathways as potential targets for further mechanistic study. Because the abstract does not specify additional cohort details or long-term outcomes, further research is needed to confirm causality and clinical relevance.
This study investigated whether the gut microbiota differs in patients with brain tumors compared to healthy people. The researchers characterized the fecal microbial community using 16S rRNA gene amplicon sequencing. They then examined correlations between microbiota composition and clinical features of the tumors, and explored whether specific microbial markers could help diagnose brain tumors.
The study recruited 158 participants in total. This included 101 patients with brain tumors, made up of 65 benign and 36 malignant cases, along with 57 age- and sex-matched healthy controls.
Patients with brain tumors had markedly lower gut microbial ecosystem richness and evenness than healthy controls. The overall structure of the gut microbiota community was also profoundly altered in the brain tumor group. This shift included increased abundance of pathogenic bacteria such as Fusobacteriota and Proteobacteria, alongside a reduction in other taxa.
These findings support a gut-brain crosstalk in which gut dysbiosis is associated with the presence of brain tumors, extending prior work on microbiota alterations in other CNS diseases to this tumor context. The distinct shifts toward pathogenic taxa such as Fusobacteriota and Proteobacteria suggest the gut microbiota could potentially serve as a diagnostic marker for brain tumors. Further work would be needed to determine whether these microbial changes are a cause, consequence, or bystander effect of tumor presence.
This scoping review examined the published literature on associations between the human gut microbiota and markers of glucose dysregulation and insulin resistance. The authors focused on findings independent of overweight, obesity, and metabolic drugs, aiming to clarify which bacterial associations reflect glucose metabolism itself rather than confounding factors. They also reviewed the potential role of short-chain fatty acids (SCFAs) as mediators of these effects, along with the influence of diet and diet-microbiota-derived metabolites. The review's purpose was to consolidate scattered observational findings to help identify novel targets for type 2 diabetes prevention.
The review covered human observational studies conducted in healthy adults as well as adults with metabolic disease and related risk factors. Rather than a single cohort, it synthesized findings across 45 original studies that were deemed eligible after screening 5983 initially identified PubMed records. The population base therefore spans multiple independent adult study populations rather than one defined sample.
Across the reviewed studies, differences in alpha diversity and 45 distinct bacterial taxa were associated with outcomes related to glucose metabolism. Six taxa emerged as the most frequently and consistently associated with glucose metabolism markers: Akkermansia muciniphila, Bifidobacterium longum, the Clostridium leptum group, and Faecalibacterium prausnitzii, among others named in the full review. These associations held even when accounting for the independent effects of overweight, obesity, and metabolic medications, suggesting a link between these bacteria and glucose regulation itself.
By identifying a consistent set of bacterial taxa tied to glucose metabolism across many studies, this review offers concrete candidates for future mechanistic and intervention research in type 2 diabetes prevention. The proposed role of SCFAs as mediators points toward diet and microbiota-targeted strategies as plausible levers for improving glucose regulation. Because the associations appear largely independent of obesity and metabolic drugs, they suggest the microbiota may influence glucose metabolism through pathways distinct from adiposity alone. Overall, the findings support prioritizing these key taxa and SCFA pathways in future human trials aimed at metabolic disease prevention.
This study investigated the ocular surface microbiome in patients with unilateral or asymmetric glaucoma who used topical ophthalmic medications in only one eye. Researchers used V3-V4 16S rRNA sequencing on ocular surface swabs to characterize microbial diversity and composition. They then examined whether differences in microbial composition were associated with clinical measures of ocular surface disease, including tear meniscus height, tear break-up time, and Dry Eye Questionnaire scores.
The study included 17 subjects total. Ten patients had asymmetric or unilateral glaucoma and used topical glaucoma therapy in only one eye, while seven were age-matched healthy controls with no history of ocular disease or eyedrop use. Samples were divided into three groups for comparison: patients' treated (eyedrop-exposed) eyes, patients' untreated contralateral eyes, and healthy control eyes.
Both the treated and untreated eyes of glaucoma patients showed significantly greater alpha-diversity and a higher relative abundance of gram-negative organisms compared to healthy control eyes. This means microbial community shifts were not limited to the eye actually receiving eyedrops but extended to the untreated fellow eye as well. The microbial composition of patients' eyes was also associated with worse ocular surface disease measures, specifically decreased tear meniscus height and decreased tear break-up time.
The findings suggest that topical glaucoma therapy may alter the ocular surface microbiome beyond just the treated eye, implicating a broader, possibly systemic or cross-eye effect of chronic eyedrop exposure. Because these microbial changes were linked to markers of tear film instability and ocular surface disease, clinicians treating glaucoma patients should consider the ocular surface microbiome as a contributor to dry eye symptoms. This underscores a need for further research into how chronic topical medication use reshapes ocular microbial ecology and affects long-term ocular surface health.
This study examined the diversity and taxonomic composition of gut microbiota in people with Alzheimer's disease (AD) compared to healthy older adults. Researchers used 16S ribosomal RNA sequencing to characterize bacterial communities at the phylum, class, order, and genus levels. The aim was to identify differences in microbial abundance that distinguish AD patients from cognitively healthy seniors living in the same region.
The study included 41 patients diagnosed with Alzheimer's disease and 43 healthy seniors, all residing in Nur-Sultan city, Kazakhstan. This gives the study a defined, age-matched comparison group of older adults from a single geographic population. No further demographic details such as age range or sex distribution are given in the abstract.
AD patients showed increased relative abundance of the phyla Acidobacteriota, Verrucomicrobiota, Planctomycetota, and Synergistota compared to healthy seniors. At the genus level, AD microbiotas had reduced Bifidobacterium, Clostridia bacterium, Castellaniella, Roseburia, Tuzzerella, Lactobacillaceae, and Monoglobus. Differential abundance analysis also found AD patients enriched for Christensenellaceae R-7 group, Prevotella, Alloprevotella, Ruminococcus, and Akkermansia, among other genera, while Levilactobacillus, Lactiplantibacillus, Bacteroides, and Faecalibacterium were altered in the opposite direction.
The findings indicate that Alzheimer's disease is associated with a distinct, multi-level shift in gut microbiota composition rather than a single bacterial change. The enrichment of Christensenellaceae R-7 group and Akkermansia alongside depletion of beneficial genera like Bifidobacterium and Roseburia suggests a broader disruption of gut microbial balance in AD. These region-specific findings from Kazakhstan may help identify candidate microbial markers for AD and support future work exploring the gut-brain axis in neurodegeneration.
This study examined the fecal microbiome composition of treatment-naive, newly diagnosed Parkinson's disease (PD) patients using 16S sequencing. Earlier PD microbiome research could not rule out confounding effects from dopaminergic medication or long disease duration, since almost all prior participants were already medicated and studied years after diagnosis. Here, investigators assessed gut microbiota alterations at the time of diagnosis, before any PD medication was started, while accounting for potential confounders such as technical batches, diet, and constipation.
The study included two large independent case-control cohorts. The first comprised 136 treatment-naive de novo PD subjects and 85 healthy controls, and the second comprised 56 PD subjects and 87 healthy controls. All PD participants were newly diagnosed and had not yet started dopaminergic medication, distinguishing this population from those in most prior PD microbiome studies.
Overall gut microbiome composition differed between PD subjects and healthy controls in both cohorts, showing that gut microbiome alterations are already present at the time of PD diagnosis, independent of dopaminergic medication exposure. No single differentially abundant taxon was replicated across both cohorts, indicating some inconsistency at the individual-taxon level. However, multiple short chain fatty acid (SCFA) producing taxa were decreased in PD in both cohorts, with several taxa belonging to the family Lachnospiraceae reduced in abundance.
By studying treatment-naive de novo patients, this work shows that gut microbiome alterations in PD are not simply a consequence of dopaminergic medication or prolonged disease duration, but are present from diagnosis onward. The consistent decrease in SCFA-producing and Lachnospiraceae taxa across two independent cohorts points to disrupted short chain fatty acid production as an early and reproducible feature of PD. These findings support continued investigation into gut microbiome changes, particularly SCFA metabolism, as a potential early contributor to PD pathogenesis rather than a downstream effect of treatment.
This study examined the gut microbiome in patients with advanced adenoma (AA) and colorectal cancer (CRC), two conditions on a shared cancerization pathway that prior bacteriological analyses have struggled to tell apart. Researchers used metagenomic sequencing to compare microbial abundance profiles and microbial single nucleotide polymorphism (SNP) characteristics between the two groups. The goal was to find microbial targets that could distinguish CRC from AA and to identify the best fecal-microbe-based approach for detecting CRC.
The study population consisted of patients diagnosed with advanced adenoma and patients diagnosed with colorectal cancer. The abstract does not give an exact sample size, recruitment site, or demographic breakdown for these groups. Fecal samples from these AA and CRC patients underwent metagenomic sequencing to generate the microbial abundance and SNP data used in the analysis.
Overall microbial diversity did not differ significantly between AA and CRC patients. However, the abundance of specific taxa differed between the two groups, including bacteria such as Firmicutes, Clostridia, and Blautia, the fungus Hypocreales, archaea including Methanosarcina, Methanoculleus, and Methanolacinia, and viruses such as Alphacoronavirus, Sinsheimervirus, and Gammaretrovirus. Using machine-learning models, a random forest model based on gut microbiome abundance achieved 86.54% accuracy in distinguishing CRC from AA, while a model based on microbial SNP characteristics achieved a higher accuracy of 92.31%.
The findings suggest that microbial SNP characteristics may be a more powerful tool than taxonomic abundance alone for distinguishing CRC from its precursor lesion, AA. This points toward strain-level genomic variation, rather than just which microbes are present, as a promising avenue for noninvasive fecal-based screening. Such an approach could help clinicians identify patients whose adenomas have already progressed toward cancer, supporting earlier and more targeted intervention.
This study examined gut microbiota composition and fecal bile acid profiles in patients with alpha-synucleinopathies, a group of neurodegenerative disorders. The researchers compared bacterial genera and short-chain fatty acid producers across dementia with Lewy bodies (DLB), Parkinson's disease (PD), and idiopathic REM sleep behavior disorder (iRBD). They used random forest models to identify microbial features that could distinguish DLB from PD, and they quantified fecal bile acids, including ursodeoxycholic acid (UDCA).
The cohort included 278 patients with alpha-synucleinopathies, broken down into 28 patients with dementia with Lewy bodies, 224 patients with Parkinson's disease, and 26 patients with idiopathic REM sleep behavior disorder. This design allowed direct comparison of gut microbiota and bile acid patterns across three related but distinct neurodegenerative and prodromal conditions.
Like PD, DLB showed decreased short-chain fatty acid-producing genera, but DLB uniquely showed increases in Ruminococcus torques and Collinsella, which were not seen in PD. Random forest models found that high Ruminococcus torques, high Collinsella, and low Bifidobacterium (a pattern also seen in Alzheimer's disease) were predictive of DLB status. Because Ruminococcus torques and Collinsella are major secondary bile acid producers, the researchers measured fecal bile acids and found elevated ursodeoxycholic acid (UDCA) production specifically in DLB.
The findings suggest that DLB has a gut microbiota and bile acid signature distinct from PD, potentially reflecting increased intestinal permeability from Ruminococcus torques and Collinsella. The authors propose that increased UDCA in DLB may mitigate neuroinflammation at the substantia nigra, while neuroinflammation may be less critical at the neocortex, offering a possible explanation for regional differences in these diseases. Therapeutic strategies aimed at increasing Bifidobacterium and its metabolites may hold promise for slowing the development or progression of DLB.
This study examined the relationship between the gut microbiome and serum metabolites in polycystic ovary syndrome (PCOS). Researchers combined untargeted metabolomics with 16S rRNA gene sequencing to characterize small-molecule serum metabolites and gut microbial composition. The goal was to determine how microbiome shifts in PCOS relate to circulating metabolite profiles, a link that had not previously been defined.
The abstract identifies a PCOS patient group compared against a healthy control group, but it does not report specific sample sizes, ages, or geographic recruitment details. The comparison appears to be a cross-sectional cohort of women with PCOS versus unaffected controls. No further demographic specifics are given in the abstract.
Fifteen differential serum metabolites distinguished PCOS patients from healthy controls. Several lysophosphatidylcholine species, phosphatidylcholine, ganglioside GA2, and 1-linoleoylglycerophosphocholine were elevated in PCOS, while phosphoniodidous acid, bilirubin, nicotinate beta-D-ribonucleotide, and citric acid were reduced, suggesting disrupted lipid and energy metabolism. Gut microbial diversity was lower in the PCOS group, with Escherichia/Shigella, Alistipes, and an unnamed Proteobacteria strain (0319_6G20) identified as key distinguishing genera. Prevotella_9 was positively correlated with phosphoniodidous acid, nicotinate beta-D-ribonucleotide, and citric acid levels.
The findings link specific gut bacterial taxa to circulating lipid and energy-related metabolites in PCOS, supporting a gut microbiome-metabolome axis in the condition's pathophysiology. Reduced microbial diversity alongside altered lysophosphatidylcholine and energy metabolite levels suggests the gut microbiota may contribute to the metabolic disturbances seen in PCOS. These correlations point toward the gut microbiome and its metabolic outputs as potential targets for further mechanistic and therapeutic investigation in PCOS.
This study examined the Spleen-strengthening and Liver-draining formula (SLF), a Traditional Chinese Medicine preparation based on the 'One Qi Circulation' theory, as a treatment for non-alcoholic fatty liver disease (NAFLD). Because intestinal flora disturbance is a known feature of NAFLD, the researchers focused on whether SLF works partly by altering the gut microbiome and glucolipid metabolism. The study used a prospective, randomized, controlled clinical design over 12 consecutive weeks to test this mechanism.
The abstract does not give an exact number of participants, but describes NAFLD patients who were randomly and evenly divided into a control group and an SLF treatment group. A healthy control (HC) group was also included for comparison of intestinal flora. Fecal samples from both NAFLD groups were collected before and after the 12-week treatment period and analyzed alongside samples from the healthy controls.
The abstract text provided is cut off before the results are fully described, so specific findings (such as taxa affected or magnitude of change) cannot be stated. What can be confirmed is that the study compared 16S rRNA gene sequencing profiles of intestinal flora across the SLF group, control group, and healthy controls before and after treatment. The design indicates the researchers intended to link any SLF-associated clinical improvement in NAFLD to detectable shifts in gut microbial composition.
If SLF reliably shifts intestinal flora alongside clinical improvement, it would support gut microbiome modulation as a mechanism behind a traditional herbal therapy for NAFLD. This kind of trial helps bridge Traditional Chinese Medicine practice with microbiome-based explanations that are testable by modern sequencing methods. It also underscores that lifestyle adjustment alone (the control group) is a comparator whose own microbiome effects need to be accounted for when evaluating add-on therapies like SLF.
This study examined the environmental drivers of gut microbiome composition and function in wild Ethiopian geladas. Researchers focused on how food availability, tracked using rainfall, and thermoregulatory stress, tracked using temperature, predicted shifts in gut microbial diversity. Geladas were chosen because they live in a cold, high-altitude environment and eat a low-quality, grass-based diet, creating both energetic and thermoregulatory pressures. The study looked beyond diet alone to ask whether other environmental factors also shape the gut microbiome in a natural setting.
The subjects were wild Ethiopian geladas (Theropithecus gelada), a nonhuman primate species living at high altitude in a cold climate. The dataset comprised 758 gut microbiome samples collected from these wild animals, making it the largest wild nonhuman primate gut microbiome dataset generated to date. The abstract does not specify the number of individual animals sampled or their sex or age distribution.
Gut microbiome composition in geladas covaried with both rainfall and temperature, but in patterns suggesting distinct responses to dietary versus thermoregulatory challenges. Seasonal microbial shifts tracked changes in the dominant components of the diet. During rainier periods, the gut was dominated by cellulolytic and fermentative bacteria specialized in digesting grass, while dry-period communities differed accordingly. This indicates that the gelada gut microbiome adjusts compositionally in step with seasonal food quality and availability.
The findings suggest that gut microbiome plasticity helps wild primates cope with seasonal swings in diet quality and possibly with thermoregulatory demands, not diet changes alone. By generating the largest wild nonhuman primate gut microbiome dataset to date, this work provides a foundation for studying how environmental variables beyond diet shape host-microbe relationships in natural settings. It also underscores the value of long-term, in-situ sampling for understanding adaptive microbiome responses to seasonal environmental stress.
This study used 16S rRNA gene sequencing on rectal swabs to characterize the gut microbiota of patients with COVID-19 pneumonia. It compared microbial composition and diversity across two COVID-19 patient groups of differing disease severity against non-infected controls. The aim was to detect whether SARS-CoV-2 infection is associated with a distinct, severity-linked shift in gut bacterial communities.
The abstract describes two COVID-19 patient groups: those with COVID-19 pneumonia admitted to an intensive care unit (i-COVID19) and those managed in infectious disease wards (w-COVID19). A separate control group (CTRL) without COVID-19 was also included for comparison. Exact sample sizes, ages, and other demographic details are not given in the abstract.
ICU patients (i-COVID19) showed a lower Chao1 index than both controls and ward patients, indicating reduced microbial richness in the more severe disease group, while Shannon diversity did not differ. At the phylum level, ward patients (w-COVID19) had increased Proteobacteria compared to controls. Fusobacteria and Spirochetes were decreased overall, with the Spirochetes decrease most pronounced in ICU patients compared to controls.
The findings show that gut microbial communities differ by COVID-19 disease severity, with the most pronounced richness loss occurring in the sickest, ICU-admitted patients. The authors suggest these preliminary compositional changes could serve as candidate biomarkers for diagnosis and severity stratification. They note this would need validation in larger cohorts before clinical application.
This study examined the gut microbiome of patients with Parkinson's disease (PD) using metagenomics paired with serum metabolomics. The researchers integrated these two data types through metabolic modeling and built a correlation network to connect microbial species with disease features. The goal was to clarify how gut bacteria relate to gastrointestinal dysfunction, an early and common nonmotor symptom of PD. Personalized, community-level metabolic models were used to estimate each patient's microbial metabolic contributions.
The abstract describes patients with Parkinson's disease whose gut metagenomes and serum metabolomes were profiled, but it does not give an exact sample size or demographic breakdown. The analysis draws on individual-level, personalized metabolic models, indicating the cohort was studied at the level of single patients rather than pooled averages. Disease severity, gastrointestinal dysfunction, and age were all tracked as patient-level variables linked to microbial findings.
The gut microbiome in PD patients showed an increased capacity to degrade mucin and host glycans, pointing to disruption of the gut mucus barrier. The integrative correlation network identified specific microbial species associated with disease severity, gastrointestinal dysfunction, and patient age. Personalized metabolic modeling further revealed that the gut microbiota contributes to folate deficiency and hyperhomocysteinemia observed in these patients. These results tie a specific microbial metabolic function, bacterial folate and homocysteine handling, to biochemical abnormalities already documented in PD.
By linking microbial mucin degradation and altered folate/homocysteine metabolism to PD, the study suggests the gut microbiome may actively contribute to disease-associated gastrointestinal and metabolic disturbances, not just reflect them. The personalized metabolic modeling approach offers a template for uncovering how gut microbes shape PD pathophysiology in individual patients. This framework could help identify microbial targets tied to folate and homocysteine handling for further investigation in PD management.
This study is a meta-analysis that re-analyzed ten previously published 16S rRNA gut microbiome datasets from Parkinson's disease (PD) research. The goal was to determine whether a consistent, PD-specific pattern of gut microbiota alterations could be identified across these independently collected cohorts. Prior individual studies had reported gut microbiome changes in PD, but no consensus had emerged on which features were reproducible. By pooling and re-analyzing the existing datasets together, the authors aimed to filter out study-specific technical noise and find robust, shared signals.
The analysis draws on ten already-published 16S microbiome datasets comparing Parkinson's disease patients to control subjects, rather than a single newly recruited cohort. The abstract does not specify the exact number of participants, their ages, or geographic locations within these combined datasets. What can be said is that this was a cross-cohort meta-analysis of existing PD-versus-control 16S sequencing data assembled from multiple prior studies.
The meta-analysis identified significant, reproducible alterations in the PD-associated gut microbiome that held up across the technical differences between the original studies, even though overall differences in microbiome structure between PD patients and controls were small. The most consistent changes were enrichment of the genera Lactobacillus, Akkermansia, and Bifidobacterium, paired with depletion of bacteria in the Lachnospiraceae family and the Faecalibacterium genus. Lachnospiraceae and Faecalibacterium are both important producers of short-chain fatty acids, so their depletion was a notable shared feature across cohorts.
The loss of short-chain fatty acid-producing bacteria such as Faecalibacterium and Lachnospiraceae members suggests that PD-associated gut dysbiosis may promote a pro-inflammatory intestinal environment. The authors propose this inflammatory shift could be linked to the gastrointestinal symptoms that commonly recur in PD patients. By establishing a reproducible cross-cohort microbiome signature, this meta-analysis strengthens the case that gut microbiota alterations are a real, consistent feature of PD rather than isolated findings, supporting further research into the gut-brain axis in neurodegeneration.
This study examined whether gut microbial dysbiosis differs between diabetic patients with and without retinopathy. Fecal samples were analyzed using 16S ribosomal RNA gene sequencing to characterize microbial structure and composition. The researchers compared microbial diversity and the abundance of specific bacterial genera across the three groups. They also sought to identify a bacterial biomarker set capable of distinguishing diabetic retinopathy from diabetes alone and from healthy controls.
The study included 75 participants divided into three groups of 25 each. One group consisted of diabetic patients without retinopathy (DM), one of diabetic patients with retinopathy (DR), and one of healthy controls (HC). Clinical information and fecal samples were collected from all participants for microbial analysis.
Microbial structure and composition differed across the three groups, with both the DM and DR groups showing reduced alpha and beta diversity compared with healthy controls. Blautia was the most abundant genus overall, particularly in the DM group. Bifidobacterium and Lactobacillus were increased, while Escherichia-Shigella, Faecalibacterium, Eubacterium_hallii_group, and Clostridium were decreased in the DM and DR groups relative to healthy controls. A biomarker set of 25 bacterial families distinguished DR patients from DM and HC groups, with area under the curve values ranging from 0.69 to 0.85.
The findings suggest that gut microbial dysbiosis is not uniform across diabetes and diabetic retinopathy, indicating a possible gut-eye axis specific to retinal complications. The identification of a distinguishing bacterial biomarker set raises the possibility of using gut microbiota profiles to help differentiate diabetic patients at risk for retinopathy. These results support further investigation into the gut microbiome as a factor in the pathogenesis of diabetic retinopathy, though the abstract does not establish causation.
This study examined whether gut microbiota composition is associated with high-grade (high-Gleason) prostate cancer in men undergoing prostate biopsy. The researchers had previously found in mouse models that intestinal bacteria and their short-chain fatty acid (SCFA) metabolites promote prostate cancer growth. Building on that finding, they used 16S rRNA gene sequencing to compare gut microbiota profiles between men with high-risk prostate cancer and men with negative or low-risk biopsy results. They then tested whether a microbiota-based index could help detect high-risk disease.
The study included 152 Japanese men undergoing prostate biopsies for suspected prostate cancer, of whom 96 had cancer and 56 did not. Participants were randomly split into a discovery cohort of 114 samples and a test cohort of 38 samples. Within these cohorts, men were grouped as high-risk (Grade group 2 or higher prostate cancer) versus negative or low-risk (negative biopsy or Grade group 1 cancer).
The relative abundances of Rikenellaceae, Alistipes, and Lachnospira, all SCFA-producing bacteria, were significantly increased in the high-risk group compared with the negative or low-risk group. Using least absolute shrinkage and selection operator (LASSO) regression, the researchers identified an index based on 18 bacterial genera that distinguished high-risk prostate cancer from lower-risk or negative cases. In the discovery cohort, this microbiota-based index detected high-risk disease more accurately than the prostate specific antigen (PSA) test, with an area under the curve of 0.85 versus 0.74.
These findings support a link between gut microbiota, particularly SCFA-producing bacteria, and more aggressive prostate cancer in humans, consistent with prior mouse model results. A gut microbiota based index may offer a noninvasive tool that outperforms PSA alone for identifying men with high-risk prostate cancer. This suggests the gut microbiome could eventually inform risk stratification and biopsy decision-making for men undergoing prostate cancer screening, pending further validation.
This study examined how gepotidacin, a first-in-class triazaacenaphthylene antibiotic with a novel mechanism of action, affects the human microbiome during treatment for uncomplicated urinary tract infections. It was conducted as part of a randomised Phase 2a clinical trial evaluating repeated oral doses of gepotidacin (GSK2140944). Researchers tracked microbiota composition across three body sites, the gastrointestinal tract, the pharyngeal cavity, and the vagina, using 16S rRNA gene sequencing. Samples were collected at three time points relative to dosing to capture both immediate effects and later recovery.
The study population consisted of 22 adult female patients with uncomplicated urinary tract infections who were enrolled in the gepotidacin Phase 2a trial (ClinicalTrials.gov NCT03568942). Each participant contributed microbiome samples from the gut, throat, and vagina. Samples were collected pre-dose on Day 1, at the end of dosing on Day 5, and at a Follow-up visit around Day 28. This design allowed within-subject comparison of microbiome changes over the course of treatment and recovery.
By Day 5, at the end of the gepotidacin dosing regimen, significant changes in microbiome diversity were observed relative to pre-dose baseline across all three tested body sites. These shifts indicate that gepotidacin measurably disrupted the gut, pharyngeal, and vaginal microbiota during active treatment. By the Follow-up visit approximately three weeks later, microbiome diversity had reverted to compositions comparable to Day 1 baseline. This pattern points to disruption during dosing followed by recovery after treatment ended, though the abstract does not specify which body site showed the greatest change.
The findings suggest that gepotidacin's effects on the microbiome are transient rather than persistent, with diversity returning to baseline within about a month of treatment completion. This supports the value of characterizing microbiome impacts early in antibiotic drug development, especially for agents with novel mechanisms of action. Demonstrating recovery across multiple body sites, not just the gut, offers reassurance about the drug's broader ecological footprint. The approach also illustrates a model for how future antibiotic trials might systematically monitor microbiome perturbation and recovery as part of safety evaluation.
This study characterized the skin and gut bacterial communities of the invasive Asian common toad, Duttaphrynus melanostictus, in Toamasina, Eastern Madagascar. The researchers compared these microbial communities to those of a co-occurring native frog species, Ptychadena mascareniensis. Sampling took place at three sites where the toad had established at different points in time, allowing the team to examine whether the toad's microbiome changed as its invasion expanded.
The subjects were individuals of the invasive Asian toad, Duttaphrynus melanostictus, sampled at three sites in Toamasina, Eastern Madagascar that the toad colonized in different years. A native, co-occurring amphibian, Ptychadena mascareniensis, was sampled at the same sites for comparison. The abstract does not give exact animal counts, so the population is best described as field-collected amphibians from these two species across the toad's Madagascar expansion range.
Microbial composition in the toad did not vary among the three sites, indicating that D. melanostictus maintains a stable skin and gut bacterial community as it spreads across its expansion range. However, significant differences emerged between the toad and the native frog species. The toad hosted richer and more diverse bacterial communities and carried a high percentage of unique taxa not found in the native frog, including 80 percent unique taxa on the skin and 52 percent in the gut.
The findings suggest that the invasive toad's microbiome is stable and distinct, potentially reflecting a combination of host-associated factors such as microhabitat selection, skin features, and dietary preferences rather than simple environmental convergence with the native species. This stability and distinctiveness may help explain the toad's resilience and adaptability as an invader. Understanding these host-microbe differences can inform how invasive amphibians establish and persist, and how they might affect native ecosystems in Madagascar.
This study examined the gut microbiota and fecal metabolome in children with systemic lupus erythematosus (SLE), an autoimmune connective tissue disease with unclear origins. Researchers used 16S rRNA sequencing to profile intestinal bacterial communities and gas chromatography-mass spectrometry (GC-MS) to characterize fecal metabolites. The goal was to correlate microbial composition changes with metabolite shifts to better understand SLE pathogenesis.
The abstract identifies the population as children with systemic lupus erythematosus, compared against healthy controls (referred to as HCs). No specific sample size, age range, or recruitment site is given in the abstract. The comparison design implies a case-control cohort of pediatric SLE patients and matched or unmatched healthy children.
Alpha diversity of the gut microbiota was unchanged in SLE patients, while beta diversity was partially altered compared to controls. Proteobacteria and Enterobacteriales increased and Ruminococcaceae decreased among SLE patients. Fecal metabolite analysis showed enrichment of amino acids and short-chain fatty acids alongside a decrease in long-chain fatty acids, with KEGG pathway analysis highlighting protein digestion and absorption, and association analysis pointing to 3-phenylpropanoic acid and Sphingomonas as key features. Sphingomonas was also found to be less abundant in healthy periodontal sites of SLE patients than in controls, suggesting possible oral-to-gut transmission of this taxon.
These findings suggest that gut microbial imbalance and altered fecal metabolites, particularly involving Ruminococcaceae, Proteobacteria, and short-chain and long-chain fatty acids, may contribute to SLE pathogenesis in children. The identification of Sphingomonas and 3-phenylpropanoic acid as correlated features points to a potential oral-gut microbial axis worth further investigation. This work provides a foundation for exploring microbiome-targeted approaches as potential treatments for pediatric SLE.
This study assessed whether the gut microbiota composition differs between children with autism spectrum disorder (ASD) and healthy children. Researchers used high-throughput sequencing of the V3-V4 region of the 16S rRNA gene to characterize fecal bacterial communities. They evaluated alpha diversity using the Shannon, Chao, and ACE indexes, and beta diversity using unweighted UniFrac analysis and PCA plots. LDA and LEfSe were applied to identify bacterial taxa that differed in abundance between groups.
The study included 25 children diagnosed with ASD and 20 healthy children serving as controls. Autistic symptoms were diagnosed using the Diagnostic and Statistical Manual for Mental Disorders and assessed for severity with the Autism Treatment Evaluation Checklist (ATEC). Gastrointestinal symptoms in the ASD group were further evaluated with a GI Severity Index (GSI) questionnaire.
Children with higher GSI scores had markedly higher ATEC Total scores than those with lower GSI scores, indicating that gastrointestinal symptoms were strongly associated with the severity of autism symptoms. There was no significant difference in overall bacterial diversity, as measured by the Chao, ACE, and Shannon indexes, between children with ASD and healthy controls. Despite similar diversity levels, both groups showed differences in the composition of specific bacterial taxa, based on the abstract provided.
The findings suggest that gastrointestinal symptoms in children with ASD are closely tied to the severity of their behavioral symptoms, reinforcing the relevance of the gut-brain axis in autism. The lack of difference in overall diversity but presence of compositional shifts implies that specific taxonomic imbalances, rather than overall community richness, may be more informative for understanding ASD-related gut disruption. These results support further investigation into targeted microbiota-based markers or interventions tied to GI symptom severity in ASD.
This study examined the gut microbiome of patients with young-onset colorectal cancer (yCRC) using 16S rRNA gene sequencing across a discovery and a validation cohort. Metagenome sequencing was additionally used to characterize species-level composition and bacterial functional pathways. The researchers then built a random forest classifier to test whether microbial signatures could distinguish yCRC from other groups. The overall goal was to close a knowledge gap around gut microbiota and its diagnostic value in yCRC.
The analysis drew on 728 samples for microbial marker discovery via 16S rRNA sequencing, with an independent cohort of 310 samples used for validation. A further 200 samples underwent metagenome sequencing for species-level and functional analysis. The abstract does not specify age ranges, sex distribution, or geographic origin of participants, so no further demographic detail can be stated.
Gut microbial diversity was increased in young-onset colorectal cancer compared to controls. Flavonifractor plautii emerged as an important bacterial species associated with yCRC, while the genus Streptococcus contained the key phylotype associated with old-onset colorectal cancer instead. Functional analysis showed yCRC was characterized by distinct bacterial metabolic activity, dominated by DNA binding and RNA-dependent DNA biosynthetic processes. The random forest classifier built from these microbial features achieved strong classification performance.
The findings suggest gut microbiota biomarkers, particularly Flavonifractor plautii, could serve as a non-invasive tool for detecting young-onset colorectal cancer. Because the microbial and functional signatures differ between young-onset and old-onset disease, diagnostic approaches may need to be age-stratified rather than applied uniformly. This supports further development of microbiome-based screening as sporadic yCRC incidence continues to rise.
This study examined whether fecal microbiota transplantation (FMT) improves slow transit constipation (STC) and investigated the underlying mechanism, with a focus on the protein digestion and absorption pathway. Researchers combined 16S rRNA microbiome sequencing with metabolomic analysis of feces and serum collected after each of three FMT treatments. The aim was to connect clinical outcomes with measurable shifts in gut bacteria and metabolites.
Eight patients diagnosed with slow transit constipation were selected according to defined inclusion and exclusion criteria. Each patient received three rounds of FMT treatment. Feces and serum samples were collected from these same patients after each treatment for microbiome and metabolomic analysis.
After the third FMT treatment, 62.5 percent of patients showed clinical improvement and 75 percent achieved clinical remission, with better scores on the Wexner constipation scale, the Gastrointestinal Quality-of-Life Index, and the Hamilton Depression Scale. Fecal microbiome alpha and beta diversity changed significantly following FMT. Bacteroidetes (Prevotella and Bacteroides) and certain Firmicutes (Roseburia and Blautia) decreased, while Actinobacteria (Bifidobacterium), Proteobacteria (Escherichia), and Lactobacillus (Firmicutes) increased. Metabolomic analysis showed FMT treated patients had relatively high levels of N-Acetyl-L-glutamate among other metabolite changes linked to the protein digestion and absorption pathway.
The findings support FMT as an effective treatment for slow transit constipation, improving not only bowel symptoms but also quality of life and depressive symptoms. The paired shifts in specific bacterial taxa and metabolites such as N-Acetyl-L-glutamate suggest a mechanistic link between microbiome remodeling and the protein digestion and absorption pathway. This points toward specific bacterial and metabolic targets that could be explored to refine or monitor FMT based therapies for constipation.
This study examined how childhood obesity relates to alterations in the gut microbiota. Researchers extracted genomic DNA from fecal samples and sequenced the V4 region of the bacterial 16S rDNA gene using the Illumina HiSeq 2500 platform. This approach allowed them to characterize the diversity and taxonomic composition of the gut microbiota in obese versus normal weight children.
The study recruited twenty three normal weight children and twenty eight obese children from Nanjing, China, based on defined inclusion and exclusion criteria. Fecal samples from these fifty one children served as the basis for the microbiota analysis. No further demographic details are given in the abstract.
The number of operational taxonomic units (OTUs) decreased as body weight increased, indicating lower gut microbiota diversity in heavier children. Alpha diversity measures, including Chao1, observed species, PD whole tree, and the Shannon index, were all significantly higher in the normal weight group than in the obese group (P values ranging from 0.008 to less than 0.001). Principal coordinate analysis was also used to assess differences in microbial community composition between the two groups, though the abstract text is cut off before further compositional details are given.
The findings support the idea that reduced gut microbiota diversity is associated with childhood obesity, reinforcing the concept that dysbiosis may contribute to excess body weight in children. Because the microbiota continues developing throughout childhood, this period may represent a key window for interventions aimed at restoring microbial diversity to promote health or prevent disease. These results underscore the importance of characterizing pediatric gut microbiota structure and function as a foundation for future obesity prevention strategies.
This study examined whether the gut microbiome is altered in schizophrenia (SCZ) and whether such alterations relate to brain structure. Researchers used 16S rRNA gene sequencing of faecal samples to profile gut microbial composition. They also acquired T1-weighted structural MRI brain imaging data to test for correlations between microbial composition and structural brain signatures. The goal was to determine whether microbiome changes were linked to SCZ itself or to antipsychotic treatment.
The study included 40 first-episode drug-naive schizophrenia (FSCZ) patients, 85 chronically antipsychotic-treated schizophrenia (TSCZ) patients, and 69 healthy controls (HCs). Faecal samples were collected from all participants for microbiome analysis. A subset also underwent structural brain MRI to allow correlation with microbial composition.
TSCZ patients showed lower microbiome alpha-diversity compared to healthy controls, but this reduction was not seen in FSCZ patients. Both FSCZ and TSCZ patients had distinct changes in gut microbial composition compared to healthy controls, including alterations in Christensenellaceae, Enterobacteriaceae, Pasteurellaceae, and Turicibacteraceae at the family level, and Escherichia at the genus level. The abstract also indicates significant disturbances in gut microbial composition when comparing TSCZ to FSCZ patients directly.
The findings suggest gut microbiome alterations, including in Christensenellaceae, are present from the earliest, treatment-naive stage of schizophrenia and are further altered with chronic antipsychotic treatment. Linking microbial composition to regional brain volumes supports a potential gut-brain connection in the pathogenesis of schizophrenia. This distinguishes disease-associated microbial changes from those attributable to medication, informing future work on the gut microbiome as a biomarker or target in psychiatric illness.
This study examined whether fecal gut microbiota composition differs between patients with Parkinson's disease (PD) who have mild cognitive impairment (PD-MCI) and those with normal cognition (PD-NC), as well as healthy controls (HC). Researchers analyzed fecal bacterial composition using 16S ribosomal RNA sequencing alongside short-chain fatty acid levels measured by gas chromatography-mass spectrometry. The study also investigated whether specific microbiota alterations were associated with cognitive ability in PD patients.
The study included 13 patients with PD-MCI, 14 patients with PD-NC, and 13 healthy spouses serving as controls. Using spouses as the healthy control group suggests an effort to account for shared household and dietary environment. Statistical adjustments were made for age, sex, body mass index, education, and constipation to isolate microbiota differences related to cognitive status.
Fecal microbial diversity was higher in both the PD-MCI and PD-NC groups compared with healthy controls. After adjusting for confounders, the PD-MCI group showed higher relative abundances of the families Rikenellaceae and Ruminococcaceae and the genera Alistipes, Barnesiella, Butyricimonas, and Odoribacter compared with the other two groups. The abundance of the genera Blautia and Ruminococcus decreased in association with cognitive impairment, indicating a distinct microbial signature linked to PD-MCI.
These findings suggest that gut microbiota alterations may be linked specifically to cognitive impairment in Parkinson's disease, not just to PD status itself. Identifying distinct bacterial taxa associated with PD-MCI raises the possibility that fecal microbiota could serve as a biomarker for cognitive decline in PD patients. This work supports further investigation into the gut-brain axis as a factor in PD-related cognitive outcomes, though the small sample size means findings require validation in larger cohorts.
This study examined the structure of the gut microbiota in children with Autism Spectrum Disorder (ASD) across different ages, and how that microbial structure relates to fecal metabolites. Researchers used 16S rRNA sequencing to characterize the gut microbial population, then applied metagenomics and liquid chromatography-mass spectrometry to a subset of children with constipation to probe microbiota-metabolite interactions. The work specifically targeted the overlap between ASD core symptoms and chronic gastrointestinal (GI) symptoms, particularly constipation.
The primary cohort consisted of 143 children aged 2 to 13 years old, compared against a typically developing (TD) group of the same age range. From this cohort, a subset of 30 children with ASD and constipation (C-ASD) were selected along with age-matched TD controls for deeper metagenomic and metabolomic analysis. The abstract does not specify additional demographic details such as sex distribution or geographic origin.
The ASD group showed no significant increase in gut microbial alpha-diversity with age, whereas the TD group's alpha-diversity increased with age, indicating a divergent developmental trajectory in ASD. In the C-ASD subgroup, metagenomic analysis revealed decreased microbial diversity and depletion of Sutterella, Prevotella, and Bacteroides, accompanied by dysregulated metabolic activity. Metabolomic analysis using liquid chromatography-mass spectrometry was consistent with these metagenomic findings, reinforcing a link between altered microbiota composition and abnormal metabolism in C-ASD.
The findings suggest that gut microbiota development in ASD does not follow the same age-related maturation pattern seen in typically developing children, which may have relevance to understanding ASD pathophysiology over time. The depletion of specific genera and disrupted metabolic activity in children with both ASD and constipation points to a potential microbiota-metabolite mechanism underlying comorbid GI symptoms. These results support further investigation into gut microbiota and its metabolic outputs as contributors to, or biomarkers of, ASD-associated gastrointestinal dysfunction.
This study examined gut microbiota dysbiosis in Parkinson's disease (PD) using 16S ribosomal RNA gene sequencing. The researchers combined their own dataset with four previously reported datasets from other countries to meta-analyze shared patterns of gut dysbiosis in PD. They also developed a new pathway-analysis method, the Kyoto Encyclopedia of Genes and Genomes orthology set enrichment analysis, to interpret functional changes in the microbiota. The goal was to identify gut dysbiosis signatures in PD that hold across different national populations, since microbiota variability across countries had previously obscured shared findings.
The primary cohort consisted of 223 patients with PD and 137 controls. This dataset was then meta-analyzed together with four previously published datasets from the United States, Finland, Russia, and Germany. An additional 12 datasets not included in the meta-analysis were used afterward to inspect and cross-check specific bacterial findings.
After adjusting for confounders including body mass index, constipation, sex, age, and catechol-O-methyl transferase inhibitor use, the genera Akkermansia and Catabacter, and the family Akkermansiaceae, were increased in PD, while the genera Roseburia and Faecalibacterium and the family Lachnospiraceae ND3007 group were decreased. Catechol-O-methyl transferase inhibitor intake was separately associated with a marked increase in the family Lactobacillaceae. Checking these results against 12 additional independent datasets confirmed that the increase in Akkermansia was a consistent finding.
By combining datasets across the United States, Finland, Russia, Germany, and the authors' own cohort, the study identifies gut dysbiosis features in PD that are shared across countries rather than population-specific artifacts. The consistent increase in Akkermansia and Akkermansiaceae, alongside depletion of short-chain-fatty-acid-associated taxa like Roseburia and Faecalibacterium, points to reproducible microbial targets for further mechanistic study in PD. The finding that a PD medication itself alters the microbiome (increasing Lactobacillaceae) also underscores the need to account for medication effects when interpreting gut-brain axis research in PD.
This cohort study examined the composition of the gut microbiome in patients with schizophrenia (SCZ), comparing samples taken during acute illness and during remission. Researchers used 16S rRNA MiSeq sequencing to characterize fecal microbial communities and identify differences relative to healthy controls. They then built a random forest model to test whether genus-level and OTU-level microbial features could serve as diagnostic biomarkers for SCZ status.
The study included 29 patients with schizophrenia who each contributed two fecal samples, one from the acute onset period and one from the remission period, for a total of 58 patient samples. An additional 29 fecal samples were collected from a healthy control (HC) group, bringing the total to 87 fecal samples analyzed. The abstract does not report ages, sex distribution, geographic origin, or other demographic details.
A random forest model using three optimal genus-level biomarkers distinguished acute SCZ patients from healthy controls with an AUC of 0.76 (95% CI 0.63 to 0.89). Eleven OTU-level biomarkers were identified separating remission-phase SCZ patients from controls, yielding an AUC of 0.7 (95% CI 0.56 to 0.84) as a disease status marker. Gut microbiota composition differed both between SCZ patients and healthy controls and between the acute and remission phases of illness within patients.
The findings support the potential of gut microbiota profiling as a non-invasive diagnostic tool for schizophrenia. Because microbial signatures differed between acute and remission states, the gut microbiome may also offer clues for assessing disease prognosis and monitoring illness phase. The authors suggest these microbial features could help guide targeted, microbiome-informed intervention in schizophrenia care.
This pilot study examined the bacterial microbiota composition of human breast tissue, comparing bilateral normal breast tissue within the same women and comparing normal tissue to breast tumor tissue between women. The researchers extracted, amplified, and sequenced bacterial DNA from these samples and analyzed the data using QIIME and RStudio. They aimed to determine whether microbiota composition differs by breast side and between normal and tumor tissue, and whether specific bacterial taxa are associated with breast tumors.
Bilateral normal breast tissue samples (n = 36) were collected from ten women who underwent routine mammoplasty procedures. Archived breast tumor samples (n = 10) were obtained separately from a biorepository. The abstract does not specify additional demographic details such as age or health status of the tumor-sample source patients.
Bacteroidetes, Firmicutes, Proteobacteria, and Actinobacteria were the most abundant phyla in both normal and tumor breast tissue. Statistically significant differences in the relative abundance of various bacterial taxa were found between the tissue groups. Alpha diversity, measured by Simpson's index, was significantly higher in normal tissue than in tumor tissue (0.968 versus 0.957, p = 0.022). Unweighted UniFrac analysis showed that breast tumor samples clustered distinctly from normal samples, indicating an overall difference in community composition.
The findings support the existence of a distinct microbiota within breast tumor tissue that differs from normal breast tissue in both diversity and composition. Reduced microbial diversity in tumors and distinct clustering patterns suggest the breast microbiome could play a role in breast cancer biology or serve as a marker of tumor status. As a pilot study with a small sample size, these results point to the need for larger studies to confirm which bacterial taxa are consistently associated with breast tumors and to clarify any causal relationship to breast cancer etiology.
This prospective observational study examined whether patients with encephalitis, brain inflammation caused by infection or autoimmune reactions, show altered gut microbiome composition compared to healthy individuals. Researchers used 16S rRNA sequencing of fecal samples to assess microbial diversity and composition. They also measured short-chain fatty acids (SCFAs) in stool by gas chromatography-mass spectrometry and serum markers of intestinal barrier integrity, including D-lactate, intestinal fatty acid-binding protein, lipopolysaccharide, and lipopolysaccharide-binding protein. Clinical severity was assessed using standard scales including the Glasgow Coma Scale, SOFA, and APACHE-II.
The study enrolled patients with encephalitis recruited from an academic hospital in Guangzhou, China, between February 2017 and February 2018. Healthy volunteers from the surrounding community served as a comparison group. The abstract indicates a total of twenty-eight participants were involved, though the exact breakdown between patients and healthy controls is cut off in the provided text.
The study evaluated gut microbial diversity (alpha and beta diversity) alongside fecal SCFA levels and serum markers of gut barrier disruption in encephalitis patients versus healthy controls. Spearman correlation analysis was used to relate microbial features to clinical severity scores and serum biomarkers, suggesting the investigators found associations linking gut dysbiosis to disease severity and barrier dysfunction. The abstract text provided is truncated before the specific results are detailed, so exact findings on direction or magnitude of these associations cannot be confirmed here.
This pilot work suggests the gut microbiome and its metabolic byproducts, particularly SCFAs, may be altered in encephalitis and linked to intestinal barrier integrity and clinical severity. If confirmed in larger cohorts, this gut-brain axis relationship could point toward microbiome-derived biomarkers for monitoring disease severity in encephalitis. It may also open avenues for investigating whether restoring gut barrier function or SCFA-producing bacteria could support recovery, though this remains speculative given the small, single-center pilot design.
This study explored the relationship between fecal metabolites and gut microbiota composition in obese women with polycystic ovary syndrome (PCOS). Researchers used 16S rRNA gene sequencing alongside untargeted metabolomics to profile fecal samples from the two groups. They also collected peripheral venous blood to measure serum sex hormones and used these to look for associations among gut microbes, fecal metabolites, and hormone levels. The goal was to clarify the pathological mechanisms linking obesity and PCOS.
The study included 18 obese patients with PCOS and 15 obese women without PCOS, serving as a control group. Fecal samples from both groups underwent 16S rRNA sequencing and metabolomic analysis. Peripheral venous blood was also drawn from all subjects to measure serum sex hormone levels.
The analysis identified 122 named differential fecal metabolites and 18 enriched KEGG pathways distinguishing the obese PCOS group from controls, including seven characteristic metabolites such as DHEA sulfate. Gut microbiota richness and diversity were lower in the obese PCOS group than in the control group. Lachnoclostridium, Fusobacterium, Coprococcus_2, and Tyzzerella 4 emerged as characteristic genera in obese women with PCOS. Serum testosterone correlated positively with fecal DHEA sulfate, while serum DHEAS correlated negatively with fecal teasterone.
The findings suggest that altered gut microbiota and fecal metabolite profiles are linked to hormonal disturbances in obese women with PCOS. Specific metabolites like DHEA sulfate and specific bacterial genera may serve as markers connecting gut dysbiosis to androgen excess in this population. This integrated microbiome-metabolome-hormone approach offers a new strategy for investigating the pathological mechanisms underlying obesity and PCOS.
This pilot study examined whether gut microbiota composition relates to unintended weight loss in Parkinson's disease (PD). Researchers used 16S rRNA gene sequencing to profile gut bacteria and applied KEGG functional predictions to infer the metabolic pathways associated with those bacterial communities. The comparison centered on weight loss (WL) patients versus non-weight-loss (NWL) patients versus normal subjects.
The study compared PD patients experiencing unintended weight loss (WL) against PD patients with steady weight (NWL), alongside matched normal control subjects. The abstract does not report specific sample sizes, ages, or other demographic details for these groups. Gut microbiota data came from fecal or related samples profiled by 16S rRNA sequencing in this pilot cohort.
Microbiota profiles were dissimilar between the WL and NWL patient groups. Predicted functional pathways also diverged: WL patients showed enrichment in fatty acid biosynthesis pathways, while NWL patients showed enrichment in inflammation-related pathways. This suggests the two clinical presentations of PD are linked to distinct microbial community functions.
The findings suggest gut microbiota may actively participate in the weight alterations seen in PD, through bacteria tied to weight gain and inflammation on one hand, or to energy expenditure on the other. This raises the possibility that microbiome profiling could help identify PD patients at risk of unintended weight loss. As a pilot study, these results point toward a mechanistic hypothesis that would need confirmation in larger, more detailed cohorts.
This study characterized the gut microbiome in chronic kidney disease (CKD) using fecal samples and built microbial-marker-based classifiers to distinguish CKD from healthy states. Researchers compared microbial diversity, community composition, and predicted functional pathways between CKD patients and healthy controls. They then used a random forest model to identify optimal microbial markers and tested those markers as non-invasive diagnostic tools across multiple cohorts.
The study drew on 520 fecal samples collected from different regions of China. This included 210 healthy controls and 110 CKD patients in the primary comparison, plus a separate validation cohort of 49 CKD cases versus 63 healthy controls and an additional diagnosis cohort from Hangzhou. The population was therefore a multi-region Chinese cohort spanning discovery, validation, and extra diagnostic testing groups.
Gut microbial diversity was significantly decreased in CKD, and the overall microbial community was clearly distinguished from healthy controls. The genera Klebsiella and Enterobacteriaceae were enriched while Blautia and Roseburia were reduced in CKD, alongside broad shifts in predicted metabolic functions such as increased tryptophan and phenylalanine metabolism and decreased arginine and proline metabolism. Five optimal microbial markers achieved an AUC of 0.9887 in the discovery cohort, 0.9512 in validation, and 0.8986 in the extra Hangzhou cohort, and Thalassospira and Akkermansia increased with CKD progression while thirteen operational taxonomic units correlated with six clinical indicators.
The findings suggest gut microbiome alterations are closely tied to CKD and its progression, extending beyond a single organ system to reflect broader metabolic disruption. The high diagnostic accuracy of the identified microbial markers across discovery, validation, and independent regional cohorts supports their potential as non-invasive tools for detecting non-dialysis CKD. This points toward stool-based microbial signatures as a practical complement to existing kidney function testing in diverse populations.
This study examined a self-extracted traditional Chinese medicine formulation developed to treat constipation. The researchers used 16S rRNA sequencing and qRT-PCR to characterize how this treatment altered the intestinal flora of constipated rats. The goal was to explore the mechanism and role of the Chinese medicine in relieving constipation through its effects on gut microbiota.
The subjects were rats with experimentally induced constipation, treated with a certain dose of the traditional Chinese medicine extract. The abstract does not specify the exact number of animals, strain, sex, or age used in the experiment. This was an animal model study rather than a human cohort.
Before treatment, constipated rats showed a significantly elevated relative abundance of Firmicutes, accounting for 86.7% of the flora. After treatment with the Chinese medicine, the gut microbiota changed significantly, with Lactobacillus abundance rising to 23.1% and its symbiotic relationships with other intestinal flora becoming enhanced. The total copies of intestinal bacteria in the constipated rats decreased following treatment.
The findings provide a theoretical basis for understanding how this traditional Chinese medicine formulation acts on the gut microbiome to relieve constipation. The shift toward increased Lactobacillus and reduced overall bacterial load suggests a microbiota-mediated mechanism of action for the treatment. This supports further investigation into traditional Chinese medicine as a microbiome-targeted approach to constipation management.
This study investigated the composition of the intestinal (gut) microbiota in patients with gastric cancer compared with healthy individuals. The researchers used 16S rRNA gene sequencing on fecal samples to characterize microbial community differences. They also examined correlations between the intestinal microbiota and cellular immunity, including peripheral T lymphocyte subpopulations and NK cells, measured by flow cytometry.
The study included 116 gastric cancer patients and 88 healthy controls from Shanxi Province, China, who provided fecal samples for microbiota analysis. A subset of this group, 66 gastric cancer patients and 46 healthy controls, also provided peripheral blood samples for immune cell profiling. All participants were drawn from a single geographic region in China.
Gastric cancer patients showed increased intestinal species richness compared with healthy controls. Butyrate-producing bacteria were decreased, while other symbiotic bacteria were enriched, particularly Lactobacillus, Escherichia, and Klebsiella. Lactobacillus and Lachnospira emerged as key species within the network of gastric cancer associated bacterial genera, and a combination of five genera, Lachnospira, Lactobacillus, Streptococcus, Veillonella, and Tyzzerella_3, performed well in distinguishing gastric cancer patients from controls based on the information provided.
These findings suggest that gastric cancer is associated with a distinct pattern of intestinal dysbiosis, marked by loss of butyrate producers and enrichment of specific symbiotic genera. The identified microbial signature, especially the five-genus combination, points toward potential use of gut microbiota profiling as a non-invasive tool to help distinguish gastric cancer patients from healthy individuals. The proposed links to cellular immunity also support the broader concept that host-microbial interactions may influence immune regulation relevant to gastric cancer development.
The study examined how Zengye decoction (ZYD), a traditional Chinese medicinal formula, affects the gut microbiota and host metabolites in aged constipated rats. Researchers used 16s rRNA gene sequencing to profile faecal microbial composition and predicted the metabolic function of the altered microbiota. They also applied 1H NMR profiling of urine and faecal samples to verify these metabolic changes at the host level. The overall aim was to clarify the mechanisms by which ZYD acts on constipation through the gut microbiota and its relationship with the host.
The subjects were aged rats divided randomly into three groups of ten animals each: a control group, a recovery group, and a ZYD-treated group. An aged constipation model was established in both the recovery group and the ZYD group before treatment began. Urinary and faecal samples were collected from each animal for microbiome and metabolomic analysis, so no human cohort was involved, this was an animal model study.
ZYD treatment reduced the levels of harmful bacteria in the gut, including Desulfovibrio, Ruminococcus, and Prevotella. These shifts in the microbiota were accompanied by predicted changes in metabolic function, which were corroborated by alterations detected in host urinary and faecal metabolites via 1H NMR. Together, the sequencing and metabolomic data point to a coordinated, metabolically active change in the gut microbiome following ZYD administration.
The findings suggest that ZYD may relieve aged constipation in part by reshaping the gut microbiota and reducing populations of harmful, metabolically active bacteria. This supports a microbiome-mediated mechanism for a traditional Chinese medicine whose clinical mechanisms had previously been unclear. The combined sequencing and metabolomic approach offers a model for investigating how other herbal formulas act through the gut-microbiota-host axis in chronic disease.
This study investigated the relationship between gut microbiota composition, microbial metabolic pathways, and metabolite profiles in thyroid carcinoma (TC). Researchers used 16S rRNA gene sequencing to characterize fecal microbial communities and applied PICRUSt to predict functional metabolic pathways. In a subset of participants, liquid chromatography mass spectrometry was also performed to characterize circulating or fecal metabolite profiles and correlate them with microbial genera.
The primary comparison included 30 patients with thyroid carcinoma and 35 healthy controls, whose fecal samples were used for 16S rRNA sequencing. A smaller, matched subset of the same population, 15 TC patients and 15 healthy controls, was then analyzed in more depth for combined microbiota and metabolite profiling. All participants were human subjects recruited for direct comparison between disease and healthy states.
Gut microbiota composition differed significantly between TC patients and healthy controls, with 19 genera enriched and 8 genera depleted in TC samples. Six differentially abundant genera distinguished TC patients from healthy controls with an area under the curve of 0.94, indicating strong discriminatory potential. Twelve metabolic pathways predicted by PICRUSt were significantly altered, and in the smaller matched subset, 21 differential genera and 72 significantly changed metabolites were identified and found to correlate with one another. Several genera also correlated with clinical parameters such as lipoprotein A and apolipoprotein B.
The findings suggest that gut microbiota alterations and their associated metabolite changes are linked to thyroid carcinoma and may reflect or contribute to underlying metabolic disturbances in these patients. The high discriminatory accuracy of the six-genus panel raises the possibility that gut microbiota signatures could serve as non-invasive biomarkers for thyroid carcinoma. The correlations between specific genera, metabolites, and clinical lipid parameters point toward a potential mechanistic link between the gut microbiome and host lipid metabolism in thyroid carcinoma that warrants further investigation.
This study examined whether abnormalities in gut microbiota composition are associated with Parkinson's disease (PD) and atypical parkinsonism. Researchers performed 16S ribosomal RNA gene sequencing on fecal samples to characterize gut bacterial taxa across disease groups. They compared unadjusted results with confounder-adjusted analyses, accounting for factors including dietary habits, to see which microbial differences held up. The design also compared PD to two atypical parkinsonian syndromes, progressive supranuclear palsy (PSP) and multiple system atrophy (MSA), to test how their microbiota profiles relate to PD.
The cohort included 350 individuals total. This comprised 193 people with idiopathic PD, of whom 39 were drug naive, stratified by disease duration, along with 22 patients with progressive supranuclear palsy (PSP), 22 patients with multiple system atrophy (MSA), and 113 healthy controls. Fecal samples from all 350 participants underwent 16S rRNA gene sequencing, and dietary habits and other confounders were recorded and adjusted for in the analysis.
Unadjusted comparisons between PD and healthy controls showed several differences in taxa abundance, but most of these differences shrank substantially after adjusting for confounders. Lower abundance of Lachnospiraceae was the one difference that held between de novo PD and healthy controls, and it remained lower across nearly all PD duration strata. Decreased Lachnospiraceae together with increased Lactobacillaceae and Christensenellaceae was associated with a worse clinical profile, including higher frequencies of cognitive impairment, gait disturbances, and postural instability. MSA and PSP patients largely shared the microbial changes seen in PD, though MSA did not show the same reduction in Lachnospiraceae.
The findings suggest that many previously reported gut microbiota differences in PD are confounded by factors such as diet rather than reflecting disease-specific biology. Lachnospiraceae depletion emerges as a more robust, duration-independent signal that may relate directly to PD pathophysiology rather than disease progression. The association of Lachnospiraceae, Lactobacillaceae, and Christensenellaceae shifts with clinical severity, including cognitive and motor decline, points to a possible link between specific gut taxa and disease phenotype. The overlap in microbial changes between PD and the atypical parkinsonian syndromes MSA and PSP suggests some gut microbiota alterations may reflect shared neurodegenerative processes rather than being unique to PD.
This study examined how daily consumption of orange juice from two Citrus sinensis cv. cultivars, Cara Cara and Bahia, affects the gut microbiota and faecal metabolome. Researchers used a randomized crossover design comparing each juice against an isocaloric control drink. Faecal samples were analyzed with an integrated meta-omics approach, combining 16S rRNA pyrosequencing of microbial operational taxonomic units (OTUs) with untargeted metabolomics based on 1H NMR spectroscopy. Samples were collected at baseline and after one week of each intervention to capture short-term shifts in microbial composition and metabolite output.
The abstract describes healthy subjects who consumed 500 mL per day of either Cara Cara orange juice, Bahia orange juice, or an isocaloric control drink in a crossover design. No specific sample size, age range, or other demographic details are given in the abstract. The population can be described only as healthy adult volunteers participating in a controlled dietary intervention trial.
Orange juice intake increased the abundance of a network of Clostridia OTUs drawn from the Mogibacteriaceae, Tissierellaceae, Veillonellaceae, Odoribacteraceae, and Ruminococcaceae families. The specific members of this network responded differently depending on whether subjects drank Cara Cara or Bahia juice, indicating cultivar-specific microbial effects. Metabolomic analysis also identified a core set of six faecal metabolites, inositol, choline, lysine, arginine, urocanic acid, and formate, that rose significantly more after Cara Cara consumption than after Bahia consumption.
The findings suggest that even closely related citrus cultivars can exert distinct effects on gut microbial communities and their metabolic output, meaning food source and variety may matter for microbiome-targeted dietary strategies. The consistent rise in specific Clostridia taxa points to a reproducible short-term dietary effect on the gut ecosystem worth further mechanistic study. The identified metabolite shifts offer candidate biomarkers for tracking individualized responses to citrus juice intake in future microbiome research.
The study tested whether Gegen Qinlian decoction (GQD), a traditional Chinese medicine formula already used for ulcerative colitis and type 2 diabetes, could improve the effectiveness of anti-PD-1 immunotherapy in microsatellite stable (MSS) colorectal cancer. MSS colorectal cancer typically does not respond to anti-PD-1-based immunotherapy, so the researchers examined combination therapy as a strategy to overcome this resistance. A systemic pharmacological analysis first mapped the multiple targets and pathways through which GQD may act in the body. The researchers then evaluated tumor growth, gut microbiota composition, and metabolomic changes under combination treatment.
The work used a CT26 tumour xenograft mouse model rather than a human patient cohort. Mice bearing CT26 tumours, a model of microsatellite stable colorectal cancer, were treated with combination therapy consisting of GQD and anti-mouse PD-1 antibody. Gut microbiota and metabolomic analyses were performed on samples from these treated animals.
Combination therapy with GQD and anti-mouse PD-1 potently inhibited CT26 tumour growth compared to what would be expected without this combined approach. Gut microbiota analysis showed the combination therapy significantly enriched Bacteroides acidifaciens and an uncultured organism from the norank Bacteroidales S24-7 group. Metabolomic analysis revealed profoundly altered metabolites in the combination therapy group, with glycerophospholipid metabolism and sphingolipid metabolism identified as key affected signalling pathways. The combination also significantly increased the proportion of certain immune-related cells, though the specific cell type is cut off in the provided abstract.
The findings suggest that a traditional Chinese medicine formula can enhance anti-PD-1 efficacy in an immunotherapy-resistant cancer subtype by remodelling both the gut microbiota and the tumour microenvironment. This points to specific gut bacteria, such as Bacteroides acidifaciens, and specific lipid metabolic pathways as potential mechanistic links between TCM formulas and improved immunotherapy response. The results support further investigation of GQD combined with PD-1 blockade as a strategy to convert microsatellite stable colorectal cancer into a more immunotherapy-responsive state. Because this evidence comes from a mouse xenograft model, clinical translation to human patients would require further study.
This study examined how the oral microbiome influences the development of oral squamous cell carcinoma (OSCC), the most common head and neck malignancy worldwide. Using 16S rRNA gene sequencing and metatranscriptomic analysis, researchers tracked longitudinal changes in oral microbiome composition and function in a 4-nitroquinoline-1-oxide (4-NQO)-induced mouse model of OSCC. The work compared gnotobiotic mice colonized with different oral microbiome inocula to mice exposed to 4-NQO without any microbiome present.
The subjects were gnotobiotic (germ-free) mice experimentally colonized with one of two oral microbiome inocula, one sourced from healthy mice and the other from mice bearing a 4-NQO-induced tumor. Controls consisted of mice exposed to 4-NQO but lacking any microbiome colonization. This was an animal model study, not a human cohort, designed to isolate the microbiome's contribution to tumorigenesis.
Mice colonized with an oral microbiome and exposed to 4-NQO developed more tumors and larger tumors than 4-NQO-exposed controls with no microbiome, indicating the microbiome actively promoted tumorigenesis rather than merely accompanying it. Tumorigenic samples showed an overall increase in microbial diversity compared to non-tumor, non-4-NQO-exposed samples. Despite variable community dynamics across groups, consistent patterns emerged during disease progression, including opposite abundance trends for Parabacteroides and Corynebacterium in the two groups inoculated with the OSCC-associated microbiome, with Parabacteroides decreasing in the control group.
The findings suggest the oral microbiome is not a passive bystander in OSCC but an active promoter of tumor initiation and growth, supporting a causal rather than merely correlative role for oral dysbiosis in this cancer. The divergent Parabacteroides and Corynebacterium dynamics point to specific taxa that could serve as markers of tumorigenic risk or as targets for future mechanistic study. Because the model used gnotobiotic mice with defined inocula, it offers a controlled system for further dissecting which microbial functions drive carcinogenesis in the oral cavity.
This study characterized the gut microbiome of women with locally advanced cervical cancer using 16S rDNA sequencing of fecal samples. Researchers measured alpha diversity (within-sample diversity, via the Shannon diversity index) and beta diversity (between-sample diversity, via unweighted Unifrac distances and principal coordinate analysis). They then compared relative abundance of microbial taxa between groups using LEfSe (Linear Discriminant Analysis Effect Size), adjusting for age and race.
The study included 42 women with locally advanced cervical cancer and 46 healthy female controls. Fecal samples from these two groups were profiled and compared directly. The abstract does not provide further demographic detail beyond the age- and race-adjusted analysis used in the statistical comparisons.
Alpha diversity was significantly higher in cervical cancer patients than in controls, though this difference was driven mainly by older women (over 50 years). Notably, alpha diversity correlated positively with age in cancer patients but inversely with age in controls, suggesting opposite age-related diversity trends between the two groups. Beta diversity also differed significantly between cervical cancer patients and controls, and age- and race-adjusted LEfSe analysis identified multiple taxa that differed between groups, including Prevotella and Porphyromonas.
The findings suggest that cervical cancer is associated with detectable, age-dependent shifts in gut microbial community structure and composition. The identification of specific differentially abundant genera, such as Prevotella and Porphyromonas, points to candidate taxa that could be further investigated for mechanistic links to cervical cancer. These results support continued investigation of the gut microbiome as a potential factor in cervical cancer biology, though the abstract does not describe causal mechanisms or clinical applications.
This study examined how feeding fermented corn-soybean meal (FF), compared with unfermented feed (UF), affects gut and immune health in pigs. The researchers measured serum immune markers, the mRNA expression of antimicrobial peptides and Toll-like receptors (TLR1-9) related to gut immunity, and bacterial abundance in the duodenum and colon. They also profiled colonic metabolic phenotypes using LC-MS based metabolomics, and used Spearman's correlation analysis to link gut bacteria, gut immunity gene expression, and colonic metabolites.
The subjects were crossbred barrows (Duroc x Landrace x Large White) at the grower-finisher stage of swine production. Pigs were divided into two feeding groups, fermented feed and unfermented feed, with six animals per group (n = 6). This was an animal husbandry study in pigs, not a human or human-microbiome cohort.
Pigs fed fermented feed had significantly higher serum IgG and IgM levels than pigs fed unfermented feed. FF also significantly decreased Bacteroides and Verrucomicrobia in the duodenum, and decreased Bacteroides, Proteobacteria, and Verrucomicrobia in the colon, while increasing Firmicutes and Actinobacteria. Serum immunity and gut immunity gene expression correlated with specific bacterial families, and differentially abundant colonic microbiota correlated with colonic metabolites, of which 1,351 metabolites differed between the two groups (including C5-branched dibasic acid).
The findings suggest that fermented corn-soybean meal can enhance systemic immunity and reshape gut bacterial composition and metabolic output in grower-finisher pigs. The correlations found between specific bacterial taxa, gut immune gene expression, and colonic metabolites point to a mechanistic link between fermented feed, the gut microbiota, and host immune function. This supports the use of fermented feed as a dietary strategy to support gut and immune health in swine production, though it does not directly establish human microbiome relevance.
This study examined whether the composition of the human gut microbiota is associated with antibody responses to an HIV vaccine. The researchers focused on antibodies that recognize commensal microbial antigens and may cross react with the gp41 envelope glycoprotein of HIV. They analyzed gut microbiota composition alongside HIV-specific IgG responses generated by a DNA-prime, pox virus boost vaccination strategy designed to recapitulate the RV144 trial, the only HIV vaccine trial shown to be efficacious.
The participants were enrolled in the HIV Vaccine Trials Network 096 clinical trial, a study of an HIV vaccine regimen combining a DNA prime and a pox virus boost. The abstract does not give an exact number of participants or demographic details beyond their status as HIV Vaccine Trials Network 096 trial subjects. Gut microbiota composition was assessed at the family level in this vaccinated cohort.
Baseline IgG antibodies to gp41 and post-vaccination IgG antibodies to Con.6.gp120.B, ZM96.gp140, and gp70 B.CaseA V1-V2 antigens were each associated with three co-occurring clusters of family-level gut microbial taxa. One cluster of families was positively associated with gp41-specific IgG but negatively associated with vaccine-matched gp120, gp140, and V1-V2-specific IgG responses. A second cluster showed the opposite pattern, negatively associating with gp41 and positively associating with the vaccine-matched responses, while a third cluster of microbial groups did not correlate with any of the immune responses measured.
The findings suggest that specific gut microbial taxa may help shape whether the immune system directs antibody responses toward the non-protective gp41 target or toward vaccine-matched targets linked to protection. This raises the possibility that gut microbiota composition could be a modifiable factor influencing the quality of immune responses to HIV vaccination. Understanding these microbiota-immune associations could inform strategies to improve the design or delivery of future HIV vaccines.
This study examined how psychological stress affects the gut microbiota and the structural integrity of the intestinal barrier and blood-brain barrier. Researchers used an improved communication box to create a psychological stress model and measured tight junction protein expression across multiple gut regions (duodenum, jejunum, ileum) and brain regions (amygdala, hippocampus). They also profiled fecal microbiota using 16S rRNA gene sequencing and measured stress-related hormonal indicators. The goal was to clarify how gut bacteria relate to stress-induced breakdown of these two barriers.
The subjects were rats divided into a psychological stress model group and a control group. The abstract does not give an exact sample size, so the specific number of animals cannot be stated. This was an animal model study, not a human cohort, and findings are based on comparisons between the two rat groups.
Stressed rats showed elevated levels of the stress indicators adrenocorticotropic hormone, NR3C1,2, and norepinephrine compared to controls. Psychological stress reduced tight junction proteins, including claudin5, occludin, alpha-actin, and ZO-1, in both intestinal and brain barrier regions. Microbiota analysis found increased microbial diversity and higher fecal proportions of Intestinimonas, Catenisphaera, and Globicatella in the stressed group. The abstract indicates further analysis found a correlation between these microbial shifts and barrier changes, though the specific correlation direction and strain-level detail are cut off in the provided text.
The findings suggest psychological stress can simultaneously disrupt gut and blood-brain barrier integrity while reshaping the gut microbiota. This supports a model in which specific bacterial taxa are linked to barrier weakening under stress, potentially allowing altered bacterial translocation and gut-brain signaling. The results point to gut microbiota and tight junction proteins as possible targets for understanding or mitigating stress-related health issues, though further work is needed to establish causal mechanisms.
This study examined whether gut microbiome composition differs in people with kidney stones (nephrolithiasis) compared to healthy people. Researchers used 16S ribosomal RNA (rRNA) gene sequencing to characterize the gut microbiota of both groups. They assessed diversity, overall community structure, and genus-level abundance differences, and examined correlations between specific bacterial genera and blood trace-element concentrations.
The study included 13 patients with multiple kidney stones and 13 matched healthy controls. This is a small, case-control cohort rather than a large population sample. Matching between the two groups was used to help isolate microbiome differences associated with nephrolithiasis.
Beta diversity analysis showed a clear separation in gut microbial community structure between nephrolithiasis patients and healthy controls. Twenty genera differed significantly in relative abundance between the two groups. Among these, Phascolarctobacterium, Parasutterella, Ruminiclostridium_5, Erysipelatoclostridium, Fusicatenibacter, and Dorea were correlated with blood concentrations of trace elements including potassium, sodium, calcium, and chlorinum. A decreasing trend in observed species richness was seen in patients, though it did not reach statistical significance (p = 0.086).
These findings suggest a distinct gut microbiome signature is associated with nephrolithiasis and may link to blood trace-element balance. This raises the possibility that specific gut genera could serve as biomarkers or contribute mechanistically to kidney stone risk. Given the small sample size, larger studies are needed to confirm these associations and clarify causality.
This study used a meta-analysis to examine structural and functional changes in the gut microbiota of diet-induced obese rodents. Researchers reprocessed raw sequencing data from nine separate high-fat diet (HFD)-induced obesity studies using a standardized pipeline (QIIME) to derive comparable gut microbiota compositions. They also used PICRUSt to predict biological functions and annotate them against KEGG pathways. The goal was to resolve inconsistent findings across individual obesity-microbiome studies by pooling data for an unbiased evaluation.
The subjects were diet-induced obese rodents compared against lean rodent controls, drawn from nine previously published high-fat diet studies. The abstract does not give a total animal count, species breakdown, or the specific rodent strains used across the pooled studies. This was therefore a secondary, dataset-level analysis of existing rodent microbiome sequencing data rather than a new primary animal experiment.
Alpha diversity and the Bacteroidetes-to-Firmicutes ratio did not differ significantly between obese and lean rodents, despite this ratio being a commonly cited obesity marker. Bacteroidia, Clostridia, Bacilli, and Erysipelotrichi were the dominant classes overall, though compositions varied notably across the nine studies. The meta-analysis identified 15 differential taxa and 57 differential functional pathways distinguishing obese from lean rodents. Obese rodents showed increased Dorea, Oscillospira, and Ruminococcus, genera known for fermenting polysaccharides into short chain fatty acids, alongside decreased Turicibacter and increased Lactococcus, a pattern consistent with elevated inflammation in obesity.
The findings suggest that a simple Bacteroidetes-to-Firmicutes ratio is not a reliable, reproducible signature of obesity when data are pooled across independent rodent studies. Instead, obesity appears to be more consistently characterized by specific differential taxa and functional pathway shifts, including changes tied to short chain fatty acid fermentation and inflammatory processes. This supports a shift toward function-based and multi-taxon analyses, rather than single ratio metrics, when using rodent models to understand gut microbiota contributions to obesity-related insulin resistance and inflammation.
This study examined gut microbiota composition in school-age children using 16S rRNA sequencing, comparing obese and normal-weight groups. Researchers looked for differences in bacterial taxa abundance and tested whether microbiota profiles were associated with serum amino acid levels and other obesity-related metabolic traits. Serum amino acids were measured by mass spectrometry to allow these correlations.
The study included 67 normal-weight and 71 obese children aged 6 to 12 years in Mexico. This population was relevant given that childhood obesity is described as a serious public health problem in the country. The sample allowed direct comparison of gut microbiota and metabolic traits between weight groups within the same age range.
Overall phyla abundances and Firmicutes/Bacteroidetes ratios did not differ significantly between obese and normal-weight children. However, Bacteroides eggerthii was significantly more abundant in obese children and correlated positively with body fat percentage and negatively with insoluble fibre intake. Bacteroides plebeius and unclassified Christensenellaceae were both significantly higher in normal-weight children, and abundance of these taxa correlated negatively with phenylalanine serum levels.
The findings suggest that in children, obesity-associated microbiota shifts may be more evident at the species level than through broad phylum ratios like Firmicutes/Bacteroidetes. The association of Christensenellaceae and Bacteroides plebeius with normal weight and lower phenylalanine levels points to a possible link between specific gut taxa, amino acid metabolism, and leanness in children. These results support further investigation into specific bacterial species and their metabolic byproducts as potential markers or targets related to childhood obesity.
This study examined whether alterations in the gut microbiota are associated with Henoch-Schonlein Purpura (HSP), an allergic-type vasculitis in children. The researchers profiled fecal microbial composition using 16S rRNA gene-based pyrosequencing. They compared microbial diversity, richness, and community composition between children with HSP and healthy controls.
The study included 85 children diagnosed with HSP and 70 healthy children as controls, for a total of 155 subjects. Fecal samples from these children were analyzed to characterize their gut bacterial communities. No further demographic details are given in the abstract.
Children with HSP had lower gut microbial diversity and richness than healthy controls, and their overall microbiota composition differed significantly from controls (r = 0.306, P = 0.001). The genera Dialister, Roseburia, and Parasutterella were significantly decreased in HSP children (all P < 0.0001), while Parabacteroides (P < 0.006) and Enterococcus (P < 0.0001) were significantly increased. A Spearman correlation analysis also found a significant negative relationship involving LOS, though the abstract is truncated before fully describing this association.
The findings support a link between gut microbial dysbiosis and HSP in children, adding this condition to the list of allergic-type diseases associated with intestinal microbiota alterations. The depletion of short-chain-fatty-acid-associated genera like Roseburia alongside enrichment of Parabacteroides and Enterococcus suggests a shift toward a less protective, more pro-inflammatory microbial community. These results point to the gut microbiota as a potential factor in HSP pathogenesis and a possible avenue for future diagnostic or therapeutic exploration, though causality cannot be established from this abstract alone.
The study examined the gut (stool) microbiome of Moroccan colorectal cancer (CRC) patients compared with healthy individuals, since no prior microbiome research existed for CRC in this population despite it being the third leading cause of death in Morocco. Researchers used 16S rRNA amplicon sequencing to characterize bacterial community composition and used principal coordinate analysis to see whether cancer and healthy samples formed distinct clusters. They also used predicted functional profiling to infer which bacterial metabolic pathways were enriched in each group.
The cohort consisted of stool samples from 11 Moroccan colorectal cancer patients and 12 healthy Moroccan individuals. This is a small, population-specific case-control comparison rather than a large multi-cohort study. The abstract does not provide further demographic details such as age or sex distribution.
Cancer samples had significantly higher proportions of Firmicutes (50.5% vs 28.4%, p = 0.04), particularly Clostridia (48.3% vs 19.0%, p = 0.002), and Fusobacteria (0.1% vs 0.0%, p = 0.02), especially Fusobacteriia. Bacteroidetes, and specifically Bacteroidia, were enriched in healthy samples (35.1% vs 62.8% and 35.1% vs 62.6%, respectively, both p = 0.06). Porphyromonas, Clostridium, Ruminococcus, Selenomonas, and Fusobacterium were significantly overrepresented in diseased patients, consistent with findings from other populations. Predicted functional analysis showed cancer samples were enriched for bacterial motility proteins, flagellar assembly, and fatty acid biosynthesis pathways.
This is the first characterization of CRC-associated microbiome shifts in a Moroccan population, and the taxonomic patterns (elevated Firmicutes/Clostridia/Fusobacteria, depleted Bacteroidetes) largely mirror findings reported in other populations, suggesting some shared microbial signatures of CRC across geographies. The enrichment of motility and flagellar assembly functions alongside known pro-inflammatory and pro-carcinogenic genera such as Fusobacterium and Porphyromonas points to potential mechanistic contributors to tumorigenesis worth further investigation. Because the sample size is small (11 vs 12), these findings should be viewed as preliminary and hypothesis-generating rather than definitive, warranting larger studies to confirm population-specific and cross-population microbial biomarkers for CRC.
This study examined how pectin, a complex dietary fiber and prebiotic, is fermented by the human gut microbiome. The researchers performed in vitro pectin fermentation using human fecal samples to track changes in bacterial composition. They also measured how this fermentation affected production of short chain fatty acids (SCFAs), specifically acetate and butyrate, over the incubation period.
The study used fecal samples from three Korean donors as the source material for the in vitro fermentation experiments. No further demographic details, such as age, sex, or health status, are given in the abstract. The donors showed differences in their baseline gut microbiota composition before pectin was introduced.
Pectin was degraded in the fecal samples from all three donors despite their differing baseline microbiota. Fermentation commonly increased Lachnospira, Dorea, Clostridium, and Sutterella across donors, with Lachnospira showing the greatest increase, and these findings point to enrichment of bacteria within Clostridium cluster XIV. Acetate levels rose rapidly upon incubation with pectin, and butyrate levels also increased after 6 hours of incubation.
The findings suggest that pectin fermentation reliably promotes Clostridium cluster XIV bacteria, particularly Lachnospira, along with acetate and butyrate production, even across individuals with different starting microbiota. This supports pectin's role as a prebiotic capable of shifting gut bacterial composition toward SCFA producing groups. Because butyrate and acetate are linked to gut health, these results reinforce the rationale for using pectin to encourage beneficial fermentation in the colon.
This study examined whether a consistent taxonomic signature of obesity exists in the human gut microbiome. Researchers compared gut microbiome diversity, overall community composition, and individual taxon abundance across obese, overweight, and healthy-weight adults. Gut microbiome was profiled from stool using 16S rRNA gene sequencing, and findings were tested across two independent study populations to check for reproducibility.
The analysis drew on 599 adults whose gut microbiome was assessed from stool samples. Participants were classified by body mass index into obese (BMI of 30 kg/m2 or higher), overweight (BMI 25 to under 30), and healthy-weight (BMI 18.5 to under 25) groups. The findings were then validated across two independent study populations, and prediction models were additionally tested against a previously published external dataset.
Obese participants showed reduced gut species richness (p = 0.04) and altered overall microbiome composition (p = 0.04) compared to healthy-weight participants, while overweight participants did not differ significantly from healthy-weight participants. Obesity was characterized by increased abundance of class Bacilli, including the families Streptococcaceae and Lactobacillaceae, and decreased abundance of several groups within class Clostridia, including Christensenellaceae, Clostridiaceae, and Dehalobacteriaceae (q < 0.05). These compositional differences were consistent across both independent study populations. Random forest models trained on one population predicted obesity status in the other population and in a previously published dataset with roughly 70 percent accuracy.
By identifying a taxonomic signature of obesity that reproduced across independent populations, this study strengthens the case that specific gut bacterial groups, including the depletion of Christensenellaceae and other Clostridia, are reliably associated with obesity in humans rather than being population-specific noise. The roughly 70 percent prediction accuracy of the random forest models suggests gut microbiome composition could eventually support obesity risk classification tools. The consistent decrease in Clostridia groups alongside increased Bacilli points to specific bacterial targets for future mechanistic and intervention research.
This study performed a systematic comparative analysis of the gut microbiome in people with generalized anxiety disorder (GAD) versus healthy controls. Researchers examined microbial richness, diversity, and taxonomic composition using metagenomic profiling. They also tested whether an antidepressant-naive subgroup showed the same pattern, and whether microbial changes reversed once anxiety went into remission.
The primary cross-sectional cohort included 40 patients with GAD in an active anxious state and 36 healthy controls. A validation subgroup analysis was performed in 12 antidepressant-naive patients and 22 controls. A prospective subgroup of nine GAD patients was followed longitudinally, comparing their microbiome during active anxiety and again after remission.
Patients with GAD had markedly decreased microbial richness and diversity compared with healthy controls, along with a distinct metagenomic composition. Short-chain fatty acid (SCFA)-producing bacteria, which are associated with a healthy gut status, were reduced in GAD patients. There was overgrowth of Escherichia-Shigella, Fusobacterium, and Ruminococcus gnavus. Unexpectedly, these genus-level changes did not reverse when patients achieved remission from anxiety.
The findings identify a distinct gut microbiota dysbiosis signature associated with GAD, marked by loss of SCFA producers and overgrowth of specific pathobionts. The persistence of dysbiosis into remission suggests the microbiome alteration is not simply a transient marker of active anxiety symptoms. This raises the possibility that the microbiome itself could be a therapeutic and preventive target for GAD, rather than only a downstream consequence of the disorder.
This study examined whether ethnicity is associated with reproducible differences in the composition of the human gut microbiota. The researchers analyzed two US-based 16S rRNA gut microbiota data sets to look for microbial genera and families that consistently varied across ethnic groups. They also examined whether these ethnicity-associated taxa overlapped with taxa previously linked to host genetics and whether such taxa clustered by shared metabolic function.
The analysis drew on two US-based 16S gut microbiota data sets comprising a combined total of 1,673 individuals. The abstract does not specify additional demographic breakdowns, recruitment sites, or age ranges beyond identifying the cohorts as US-based and multi-ethnic. This population allowed the authors to compare microbiota composition across ethnic groups within the United States.
The study identified 12 microbial genera and families that reproducibly differed by ethnicity across both data sets. Notably, most of these taxa, including Christensenellaceae, the most heritable bacterial family described in the gut microbiota, overlapped with taxa previously shown to be genetically associated. These ethnicity-linked, genetically associated taxa also formed co-occurring clusters connected by similar fermentative and methanogenic metabolic processes.
These findings demonstrate that specific gut microbiota taxa show recurrent, reproducible associations with ethnicity rather than one-off, study-specific patterns. Because many of these taxa are also heritable, including Christensenellaceae, the results suggest a genetic contribution to ethnicity-linked microbiome variation. This work provides testable hypotheses for investigating specific gut microbes as potential mediators of health disparities affecting ethnic minorities.
This study investigated whether the composition of a child's gut microbiome could help predict the later onset of obesity. Researchers characterized the faecal microbiota of children at two time points across a four-year window. They analyzed the microbiome data alongside each child's diet, physical activity levels, and inflammatory markers to look for a microbiome-host-diet configuration linked to weight gain.
The study followed 70 children in a prospective, two-time-point design over four years. All children had normal body weight at the start of the study. By the follow-up check-up, 36 of the 70 children had gone on to gain excessive weight, while the rest remained at a healthy weight.
The children's gut microbiota structures sorted into a discrete number of distinct groups, each defined by a different level of biodiversity. This biodiversity pattern correlated with inflammatory markers and dietary habits. Notably, these microbiome groupings were independent of the children's age, gender, and starting body weight, suggesting the microbiome signal was not simply a byproduct of these factors.
The findings support the idea that gut microbiome configuration, considered together with diet, may serve as an early predictor of which normal-weight children are at risk of developing obesity. Because the microbiome differences were detectable independent of body weight at baseline, this approach could potentially flag risk before excess weight ever appears. This underscores the value of monitoring the microbiome-host-diet relationship as a tool for early identification and possible prevention efforts in pediatric obesity.
This study examined whether Parkinson's disease (PD) is associated with dysbiosis of the gut microbiome. Researchers used 16S rRNA gene sequencing of stool DNA to characterize microbial composition and function. They collected detailed metadata on 39 potential confounders, including medications, diet, gastrointestinal symptoms, and demographics, so they could statistically separate disease effects from these other factors. The goal was to identify candidate taxa and functional pathways specifically linked to PD, distinct from its treatments and other covariates.
The study included 197 people with Parkinson's disease and 130 control participants. Stool samples were collected from these individuals for microbial DNA sequencing. Extensive metadata on medication use, diet, gastrointestinal symptoms, region of residence, age, and sex were gathered from the same participants to allow adjustment for confounding.
An independent microbial signature was detected for Parkinson's disease itself (P = 4E-5), distinct from signatures associated with region of residence, age, sex, and dietary fruit and vegetable intake. Among PD patients, separate microbial signals were linked to specific medication classes, including catechol-O-methyltransferase inhibitors (P = 4E-4), anticholinergics (P = 5E-3), and possibly carbidopa/levodopa (P = 0.05). This indicates that both the disease state and the drugs used to treat it independently reshape the gut microbiome.
By statistically disentangling PD-related dysbiosis from medication effects and other confounders, this study clarifies that prior microbiome findings in PD cohorts could reflect drug exposure rather than disease biology alone. This distinction is important for designing future microbiome studies in PD, since failing to control for medications could produce misleading conclusions. The identified taxa and pathways offer candidate targets for further research into the gut's role in PD pathophysiology and treatment response.
This study tested whether melatonin's known ability to reduce body weight and improve energy balance works through changes in the gut microbiota. Mice were fed a high fat diet (HFD) to induce obesity, with or without melatonin supplementation, and compared to mice on a normal chow diet (NCD). Researchers measured body weight, liver steatosis, low-grade inflammation, and insulin resistance, and used high-throughput pyrosequencing of the 16S rRNA gene to profile the gut microbiota. The goal was to link melatonin's metabolic benefits to specific shifts in microbial composition.
The subjects were mice fed a high fat diet to model diet-induced obesity, compared against mice fed a normal chow diet. The abstract does not specify the number of animals, their strain, sex, or age. This was an animal (mouse) model study rather than a human cohort.
Melatonin reduced body weight, liver steatosis, and low-grade inflammation, and improved insulin resistance in HFD-fed mice. It significantly altered gut microbiota composition, notably decreasing overall richness and diversity. HFD feeding altered 69 operational taxonomic units (OTUs) relative to the NCD group, and melatonin reversed 14 of these OTUs back toward the NCD-like configuration. Melatonin also decreased the Firmicutes-to-Bacteroidetes ratio and increased the abundance of the mucin-degrading bacterium Akkermansia, which is associated with healthy mucosa.
The findings suggest that melatonin's protective effects against diet-induced obesity and its metabolic complications may be mediated in part through remodeling of the gut microbiota. The reversal of specific HFD-induced OTUs and the enrichment of Akkermansia point to a plausible microbiota-mediated mechanism linking melatonin to improved metabolic and mucosal health. This positions gut microbiota modulation as a potential therapeutic pathway for melatonin-based interventions in obesity, though the mouse-model nature of the work means further study would be needed before extending these conclusions to humans.
This study characterized the enteric virome and bacterial microbiome in people with HIV infection to determine whether virome alterations contribute to HIV-associated immunodeficiency and enteropathy. Researchers examined how these microbial communities differed across HIV infection status and CD4 T cell count, and whether antiretroviral therapy (ART) influenced any virome changes. The goal was to test whether enteric virome alterations track with immune decline independent of treatment.
The cohort consisted of Ugandan patients, including individuals without HIV infection and individuals with HIV infection who were either treated with ART or untreated. The abstract does not give an exact sample size, but the design compared these groups by HIV status, treatment status, and peripheral CD4 T cell count.
Low peripheral CD4 T cell counts were associated with an expansion of enteric adenovirus sequences, and this increase occurred independent of ART treatment. Patients with lower CD4 T counts also had an enteric bacterial microbiome with reduced phylogenetic diversity and richness. Specific bacteria showed differential abundance in these patients, including increases in Enterobacteriaceae, a family previously linked to inflammation.
The findings suggest that immunodeficiency in progressive HIV infection is accompanied by coordinated alterations in both the enteric virome and bacterial microbiome, not bacterial changes alone. These combined microbial shifts, including adenovirus expansion and Enterobacteriaceae enrichment, may contribute to AIDS-associated enteropathy and disease progression. This points to the enteric virome as a previously underappreciated factor worth considering alongside bacterial microbiome changes in HIV pathogenesis.
This study compared the fecal bacterial community composition and predicted microbial gene function of children with early onset pediatric multiple sclerosis (MS) against control children matched for age and sex. Researchers used 16S ribosomal RNA sequencing along with PICRUSt (phylogenetic reconstruction of unobserved states) analysis to characterize the gut microbiota and infer its functional potential. They examined associations between subject characteristics, including immunomodulatory drug (IMD) exposure, and measures of gut bacterial community structure such as beta diversity and taxa abundance.
The study included eighteen children with relapsing-remitting MS and seventeen control children, with a mean age of 13 years (range 4 to 18), recruited from a pediatric clinic at the University of California, San Francisco. The MS cases had a short disease duration, averaging 11 months since onset (range 2 to 24 months), and about half of them had never been exposed to immunomodulatory drugs. Controls were selected to be similar in age and sex to the cases and had no autoimmune disorders.
Overall gut bacterial beta diversity was not significantly associated with MS status, but it was significantly associated with immunomodulatory drug exposure. Compared to controls, MS cases showed significant enrichment of Desulfovibrionaceae family members, including Bilophila, Desulfovibrio, and Christensenellaceae, alongside a depletion of Lachnospiraceae and Ruminococcaceae. Predicted microbial genes involved in glutathione metabolism were also enriched in MS cases relative to controls, and these findings held regardless of immunomodulatory drug exposure.
The findings suggest that perturbations in gut microbiome composition occur early in the course of pediatric MS, alongside predicted enrichment of metabolic pathways linked to neurodegeneration. Together, these shifts point toward a pro-inflammatory gut milieu that may be relevant to MS pathophysiology in children. Because the disease duration in cases was short, these microbial differences appear close to disease onset rather than as a late consequence of prolonged illness or treatment.
This study examined how the gut microbiota relates to the two major precursor lesions of colorectal cancer: conventional adenomas and serrated polyps. Colorectal cancer is a heterogeneous disease, and the authors tested for the first time whether the gut microbiota's relationship to colorectal cancer differs by the specific type of precursor polyp. Gut microbiota were assessed using 16S rRNA gene sequencing of stool samples, allowing comparison of diversity, overall composition, and taxon abundance across groups.
The study included 540 adults who underwent colonoscopy screening. Participants were categorized as conventional adenoma cases (n = 144), serrated polyp cases (n = 73), or polyp-free controls (n = 323). Conventional adenoma cases were further divided by location (proximal, n = 87; distal, n = 55) and stage (non-advanced, n = 121; advanced, n = 22), and serrated polyp cases were subdivided into hyperplastic polyp (n = 40) and sessile serrated adenoma (n = 33).
Conventional adenoma cases had lower gut microbial species richness in stool than polyp-free controls, and this association was strongest among advanced conventional adenoma cases. In terms of overall microbiota composition, differences from controls were seen specifically among distal or advanced conventional adenoma cases. These patterns indicate that the gut microbiota relationship to colorectal cancer precursors is not uniform but varies by polyp type, location, and severity.
By distinguishing microbiota associations between conventional adenomas and serrated polyps, this study suggests that colorectal cancer's different developmental pathways may have distinct microbial signatures. The stronger association with advanced and distal conventional adenomas points to species richness and composition as potentially useful features for identifying higher-risk precursor lesions. These findings support future research treating colorectal cancer precursors as biologically distinct subtypes rather than a single category when studying the gut microbiota.
This study investigated the fecal microbiome of patients with irritable bowel syndrome (IBS) to identify signatures specific to IBS subtypes. Researchers analyzed 273 fecal samples using 16S rRNA sequencing, generating more than 20 million sequences. They examined microbial diversity and the relative abundance of specific bacterial and archaeal groups, including butyrate producers and methane producers, and correlated taxa with symptoms like flatulence and abdominal pain.
The cohort consisted of 113 patients with IBS and 66 healthy controls, for a total of 179 participants. A subset of these participants provided two fecal samples one month apart, allowing some assessment of stability over time. The abstract does not specify age, sex, or geographic location of the cohort.
IBS patients had significantly lower microbial diversity, which was associated with a lower relative abundance of butyrate-producing bacteria (P = 0.002; q < 0.06), particularly in those with IBS-D and IBS-M subtypes. Untreated IBS patients also had a lower abundance of Methanobacteria compared to healthy controls (P = 0.005; q = 0.05). Several bacterial taxa were significantly correlated with sensations of flatulence and abdominal pain (P < 0.05).
The findings suggest that reduced butyrate producers may impair intestinal barrier function in IBS-D and IBS-M patients, since butyrate is known to support gut barrier integrity. Lower methane-producing microorganisms may reduce hydrogen disposal in the colon, potentially explaining the excess abdominal gas reported in IBS. Together these microbial signatures point toward specific, subtype-linked mechanisms that could inform future diagnostic or therapeutic approaches for IBS.
This study examined the gut microbiome in new-onset, treatment-naive Crohn's disease (CD), a form of inflammatory bowel disease genetically linked to aberrant immune responses to intestinal microbiota. Samples were collected from multiple gastrointestinal locations before any treatment began. The researchers compared microbial community patterns across the ileum, rectum, and fecal samples to identify a consistent dysbiosis signature, since prior studies had produced inconsistent results. They also examined whether antibiotic exposure altered the microbial signature associated with disease.
The study drew on the largest pediatric Crohn's disease cohort assembled to date, though the abstract does not give an exact sample size. Participants were newly diagnosed children with CD who had not yet started treatment, allowing the microbiome to be assessed before medications could confound the results. Comparisons were made between patients with and without prior antibiotic exposure within this cohort.
An axis of dysbiosis emerged that correlated strongly with disease status: increased Enterobacteriaceae, Pasteurellaceae, Veillonellaceae, and Fusobacteriaceae, alongside decreased Erysipelotrichales, Bacteroidales, and Clostridiales. Antibiotic exposure amplified this dysbiosis signature in patients with CD, indicating that antibiotics compound the microbial disruption seen in the disease. Comparing sample sites showed that the rectal mucosal-associated microbiome captured the disease-associated signature distinctly from ileal or fecal samples.
The rectal mucosal microbiome offers a convenient, minimally invasive sampling site with unique potential for early diagnosis of Crohn's disease, even before treatment begins. The finding that antibiotics amplify CD-associated dysbiosis suggests antibiotic exposure should be considered when interpreting microbiome data in IBD research and clinical care. Together, these results support the microbiome as both a diagnostic signal and a modifiable factor in new-onset pediatric Crohn's disease.
2026-07-04
Christensenellaceae majorTaxon page created: biology (morphology, metabolism, heritability and health associations), the beneficial role and the limits on modulating it, exploratory interventions, the data-derived Conditions table across 82 conditions, and the full research feed.
Waters JL, Ley RE.
The human gut bacteria Christensenellaceae are widespread, heritable, and associated with health.BMC Biol. 2019
Goodrich JK, Waters JL, Poole AC, et al. (Ley RE).
Human genetics shape the gut microbiome.Cell. 2014
Overview
Interventions
FAQs
Research Feed
Update History
References