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Blautia wexlerae is one of the gut commensals most consistently found at lower levels in people with obesity and type 2 diabetes. In mice, feeding it reduced both.
Blautia wexlerae is a beneficial anaerobic gut commensal that is inversely correlated with obesity and type 2 diabetes. Its distinctive amino-acid and carbohydrate metabolism produces anti-inflammatory metabolites, and oral administration reduced diet-induced obesity and diabetes in mice, marking it as a promising next-generation probiotic.
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 MoreBlautia wexlerae is a Gram-positive, anaerobic commensal of the human gut and one of the species most consistently found at reduced abundance in people with obesity and type 2 diabetes.[1] A cross-sectional study of adults identified it as inversely correlated with both conditions, and it appears across this database as a differentially abundant taxon in many human microbiome studies.
In mice, oral administration of B. wexlerae reduced high-fat-diet obesity and diabetes and produced anti-inflammatory effects through a distinctive metabolism, accumulating amino-acid metabolites such as S-adenosylmethionine, acetylcholine, and L-ornithine and carbohydrate products including succinate, lactate, and acetate, while remodeling the surrounding microbiota.[1] In this database's framework it is not a metal-weaponizing pathogen but a beneficial commensal whose presence marks the healthy gut in which nutritional immunity keeps opportunists suppressed.[2]
B. wexlerae is a Gram-positive, strictly anaerobic, coccobacillus-shaped member of the Lachnospiraceae family, a group of core fiber-fermenting gut commensals.[1] Its beneficial profile comes from its metabolism rather than any structural virulence trait.
B. wexlerae is a beneficial commensal. Its unique amino-acid and carbohydrate metabolism yields metabolites with anti-inflammatory and metabolic benefits, and in animal models it decreased fat accumulation and improved glucose handling while shifting the wider microbiota toward a healthier composition.[1] Its abundance is inversely associated with metabolic disease in humans.[1]
Its useful features are metabolic and immunological.
| Factor | Description and role |
|---|---|
| Anti-obesity, anti-diabetic effect | Oral administration reduced high-fat-diet obesity and diabetes in mice, mirroring its inverse correlation with these conditions in humans.[1] |
| Distinctive amino-acid metabolism | Accumulates S-adenosylmethionine, acetylcholine, and L-ornithine, metabolites linked to its anti-inflammatory and metabolic effects.[1] |
| Short-chain fatty acid and organic-acid output | Produces succinate, lactate, and acetate that support the epithelium and cross-feeding microbes.[1] |
| Microbiota remodeling | Shifts the surrounding community toward a healthier composition, amplifying its host benefits.[1] |
B. wexlerae is a fiber-fermenting commensal, not a metal scavenger. Its metabolites and microbiota-remodeling activity support a healthy, anaerobic gut that resists the shift toward oxygen-tolerant, lipopolysaccharide-rich Enterobacteriaceae, the metal-weaponizing opportunists this database tracks.[2] Its depletion in metabolic disease marks that less protective state.
Several pressures reduce B. wexlerae, given its dependence on diet and an anaerobic niche.
| Pressure | Effect |
|---|---|
| Obesity and type 2 diabetes | Its abundance is inversely correlated with both, so metabolic disease accompanies its depletion.[1] |
| Low-fiber, high-fat diet | Western-style diets are associated with reduced Lachnospiraceae commensals like B. wexlerae.[1] |
| Dysbiosis and antibiotics | Loss of anaerobic commensals during dysbiosis accompanies the Enterobacteriaceae shift.[2] |
The entries below are supportive strategies classified by our validation method and are not medical advice. The goal is to sustain this beneficial commensal.
| Intervention | Class | Status |
|---|---|---|
| B. wexlerae as a next-generation probiotic | Probiotic | Validation In Progress |
| Dietary fiber and resistant starch | Diet | Validation In Progress |
| Metabolic-health support | Practice | Validation In Progress |
| Intervention | Mechanism |
| B. wexlerae probiotic | Oral administration reduced obesity and diabetes in mice, the basis for its next-generation probiotic development.[1] |
| Fiber and resistant starch | Feed Lachnospiraceae commensals like B. wexlerae and favor their growth.[1] |
| Metabolic-health support | Sustaining beneficial commensals supports the anti-inflammatory, anaerobic gut that resists opportunist expansion.[2] |
Where Blautia wexlerae (NCBI:txid418240) appears as a differentially abundant taxon across the Microbiome Medicine corpus. Each row aggregates every experiment in which the organism moved in a given condition; direction is its change in the case/exposure group, and grade is the strongest single study's methodology weight (A·D·S·C·R), the same engine that grades every signature on this site.
Across 39 conditions and 42 studies, the signal is genuinely mixed: enriched in 14, depleted in 17, and direction-conflicting in 8 (directional agreement 0.57). Because B. wexlerae is a health-associated commensal inversely tied to metabolic disease, depletion in a disease group is the more mechanistically interpretable direction, so the aggregate evidence tier is Low.
How to read these. B. wexlerae behaves as a marker of metabolic health, so a drop in an obesity or diabetes cohort is the expected, interpretable signal. Species-level resolution within Blautia can be imperfect, and direction can vary by cohort, which is why the aggregate tier stays Low.
Internal summaries of the 42 studies we reviewed in which B. wexlerae was a differential taxon across this corpus.
Extranodal natural killer/T-cell lymphoma (ENKTL) predominantly manifests in East Asia and Latin America. Despite shared intrinsic factors, such as ethnic and genetic backgrounds, the progression of ENKTL can be influenced by extrinsic factors related to changing lifestyle patterns.
This study collected stool samples from newly diagnosed (ND)-ENKTL patients (n=40) and conducted whole genome shotgun sequencing.
ND-ENKTL revealed reduced alpha diversity in ND-ENKTL compared to healthy controls (HCs) (p=0.008), with Enterobacteriaceae abundance significantly contributing to the beta diversity difference between ENKTL and HCs (p < 0.001). Functional analysis indicated upregulated aerobic metabolism and degradation of aromatic compounds in ND-ENKTL. Enterobacteriaceae were associated not only with clinical data explaining disease status (serum C-reactive protein, stage, prognosis index of natural killer cell lymphoma [PINK], and PINK-E) but also with clinical outcomes (early relapse and short progression-free survival). The relative abundance of Enterobacteriaceae at the family level was similar between ENKTL and diffuse large B-cell lymphoma (DLBCL) (p=0.140). However, the ENKTL exhibited a higher abundance of Escherichia, in contrast to the prevalence of Enterobacter and Citrobacter in DLBCL. Linear regression analysis demonstrated a significant association between Escherichia abundance and programmed cell death-ligand-1 (PD-L1) levels in tissue samples (p=0.025), whereas no correlation with PD-L1 was observed for Enterobacteriaceae at the family level (p=0.571).
ND-ENKTL exhibited an abundance of Enterobacteriaceae and a dominant presence of Escherichia. These microbial characteristics correlated with disease status, treatment outcomes, and PD-L1 expression, suggesting the potential of the ENKTL microbiome as a biomarker and cause of lymphomagenesis, which warrants further exploration.
Only the title of this study was available, not an abstract, so this summary is based solely on that title. The title indicates the researchers examined how diet exerts selective pressure on the human gut microbiota. The scope appears to span two levels of biological organization: which bacterial species are present (species composition) and the genetic makeup within individual bacterial strains (strain-level variation). No specific methods, sequencing approach, or statistical analyses can be confirmed from the title alone.
The abstract was not available, so no cohort size, demographic details, or recruitment setting can be stated. The title's reference to "the human gut microbiota" indicates the subjects were humans, most plausibly a study population or public dataset with dietary and gut metagenomic data. Without further detail, the sample should be understood only as human gut microbiome data linked to dietary information, not a defined patient group. No age, sex, geography, or health status can be honestly inferred.
Because no abstract text was provided, no specific results, effect sizes, or organism names can be reported. The title itself is the only available signal, and it asserts that dietary selective effects are detectable at multiple levels of microbial organization. This implies the study found diet-associated differences both in which species are present and in the genetic variants carried by strains within those species. Beyond this general claim embedded in the title, no further findings can be stated without fabricating detail.
If diet shapes the gut microbiota down to the strain-genetic level, dietary interventions could in principle drive evolutionary or selective changes in resident bacterial populations, not just shifts in which species are present. This would suggest that assessing diet's effect on the microbiome requires strain-level genomic analysis, not species-level profiling alone. Such a finding could inform how nutrition-based interventions are designed and monitored for microbiome-targeted therapies. Because only the title was available, these implications are inferred from the title's framing and should be confirmed against the full study before being treated as established.
The gut microbiome influences physiological responses to exercise by modulating inflammatory markers and metabolite production. Athletes typically exhibit greater microbial diversity, which may be associated with improved performance, but the mechanisms linking different exercise modalities to the gut microbiome are not fully understood. In this study, blood and stool samples were collected from endurance athletes, strength athletes, and non-athletic controls performing two maximal exercise tests (the anaerobic Wingate test and the aerobic Bruce Treadmill Test) to integrate serum biomarker data with gut bacterial metagenomic profiles. While most biochemical markers showed similar post-exercise trends across groups, SPARC (secreted protein acidic and rich in cysteine) and adiponectin levels showed modality-specific responses. Strength-trained participants showed unique microbiome-biomarker associations after the Wingate test. In addition, baseline enrichment of certain bacterial taxa, including Clostridium phoceensis and Catenibacterium spp., correlated with reduced Bruce Treadmill test response in strength-trained individuals. These findings, while requiring further validation, indicate the complex interplay between exercise type, training background, and the gut microbiome, and suggest that specific microbial species may help shape recovery and adaptation.
COVID-19 has had a profound impact on public health globally. However, most studies have focused on patients with long COVID or those in the acute phase of infection, with limited research on the health of individuals who have recovered from mild COVID-19. This study investigates the long-term changes in bacterial and fungal communities in individuals recovering from mild COVID-19 and their clinical relevance.
Healthy individuals from Hainan Province were enrolled before the COVID-19 outbreak, along with individuals recovering from COVID-19 at 3 months and 6 months post-recovery. Stool, blood samples, and metadata were collected. Metagenomic sequencing and Internal Transcribed Spacer (ITS) analysis characterized bacterial and fungal communities, while bacterial-fungal co-occurrence networks were constructed. A random forest model evaluated the predictive capacity of key taxa.
The gut microbiota of COVID-19 recoverees differed significantly from that of healthy individuals. At 3 months post-recovery, probiotics (e.g., Blautia massiliensis and Kluyveromyces spp.) were enriched, linked to improved metabolism, while at 6 months, partial recovery of probiotics (e.g., Acidaminococcus massiliensis and Asterotremella spp.) was observed alongside persistent pathogens (e.g., Streptococcus equinus and Gibberella spp.). Dynamic changes were observed, with Acidaminococcus massiliensis enriched at both baseline and 6 months but absent at 3 months. Co-occurrence network analysis revealed synergies between bacterial (Rothia spp.) and fungal (Coprinopsis spp.) taxa, suggesting their potential roles in gut restoration. The bacterial random forest model (10 taxa) outperformed the fungal model (8 taxa) in predicting recovery status (AUC = 0.99 vs. 0.80).
These findings highlight the significant long-term impacts of mild COVID-19 recovery on gut microbiota, with key taxa influencing metabolism and immune regulation, supporting microbiome-based strategies for recovery management.
Metabolic syndrome (MS) and type 2 diabetes (T2D) are metabolically related diseases with rising global prevalence and increasingly evident links to the intestinal microbiota. Research suggests that imbalances in microbiota composition may play a crucial role in their pathogenesis. Specific population cohorts, such as the one in Galicia, Spain, offer the opportunity to analyze microbiota patterns within a distinct geographical and genetic context. This study was performed to investigate the relationship between the intestinal microbiota and MS and T2D.
A cohort of 79 volunteers was analyzed over a 2-year study period. Recruitment posed significant challenges because of strict inclusion criteria (918PTE0540; PCI2018-093284), which required participants to be free from chronic medications and have a moderate to high risk of developing T2D. Volunteers were classified based on their serum glucose levels, body mass index, and the presence or absence of MS. To analyze the microbiota composition, amplicon sequencing of 16S rRNA genes was performed on stool samples. Alpha diversity was assessed using the Chao and Shannon indices, while beta diversity was evaluated using permutational analysis of variance with Bray-Curtis and Chao distances. Differential abundance analysis was conducted using the LinDA method.
In patients with MS, we observed a higher Firmicutes/Bacteroidetes ratio and an increased prevalence of Blautia compared to healthy patients. than in healthy individuals. Other enriched taxa in patients with MS included Tyzerella, Streptococcus, and Ruminococcus callidus. In patients with T2D, we observed a higher Bacteroidetes/Firmicutes ratio and a decrease in the phylum Actinobacteria compared with healthy individuals. Taxa such as Dorea, Prevotella, Dialister invisus, Fusicatenibacter, and Coprococcus were associated with T2D, while beneficial taxa such as Eubacterium, Ligilactobacillus, and Acidaminococcus were more prevalent in healthy or prediabetic individuals.
This study reveals notable differences in the intestinal microbiota composition among patients with MS and T2D. Changes in microbial composition, particularly the Firmicutes/Bacteroidetes ratio, may serve as indicators of underlying pathology. At more specific taxonomic levels, several enriched taxa were identified in patients with MS, including Blautia, Tyzzerella, Dorea, Streptococcus, and Ruminococcus callidus. Additionally, species such as Dorea longicatena and Dialister invisus were enriched in prediabetic and diabetic patients, whereas beneficial genera (Eubacterium, Acidaminococcus, Bifidobacterium, and Ligilactobacillus) were more prevalent in healthy and prediabetic individuals than in those with T2D.
This study investigated whether gut microbiota composition and plasma metabolic profiles are altered in lymph node tuberculosis (LNTB), a form of tuberculosis whose relationship with gut microbiota had not previously been explored. Researchers used metagenomic sequencing to characterize gut microbial diversity and composition, paired with plasma metabolomics to assess circulating metabolite changes. KEGG pathway analysis was applied to link microbial gene content to metabolic function, focusing especially on short-chain fatty acid (SCFA) biosynthesis. An integrated analysis then examined correlations between specific gut bacteria and plasma metabolites in LNTB.
The abstract does not report specific participant numbers, ages, or geographic setting. It indicates a comparison between individuals diagnosed with lymph node tuberculosis (the LNTB group) and healthy individuals serving as controls. Samples analyzed included gut microbiota (via metagenomic sequencing) and plasma (via metabolomics) from these two groups.
LNTB patients showed significantly altered gut microbial diversity, with notable reductions in SCFA-producing taxa including Ruminococcus, Faecalibacterium, Roseburia, and Blautia compared to healthy individuals. KEGG pathway analysis indicated that this gut dysbiosis negatively affected SCFA biosynthesis and metabolism. Plasma metabolomics revealed disruptions in metabolites tied to SCFA synthesis and inflammation pathways, and integrated analysis found significant correlations between taxa such as Blautia, Butyricicoccus, Coprococcus, Ruminococcus, Bacteroides, and Clostridium and plasma metabolites including alpha-benzylbutyric acid, acetic acid, and succinic acid.
The findings suggest that gut microbiota dysbiosis and consequent metabolic dysfunction, particularly reduced SCFA production, may play a role in LNTB pathophysiology. Because SCFAs and related anti-inflammatory commensal bacteria appear diminished in LNTB, restoring these microbial functions could represent a novel therapeutic target for disease management. This work opens a new avenue for considering the gut-immune axis in tuberculosis affecting lymph nodes, beyond the traditional focus on pulmonary disease.
This cross-sectional study examined how westernization affects the gut microbiome by comparing Indians living in India, Indo-Immigrants, and Indo-Canadians against Euro-Canadian and Euro-Immigrant controls. Stool samples underwent 16S rRNA and shotgun sequencing to characterize microbial taxa and functional gene profiles. Dietary and demographic data were also collected to evaluate lifestyle patterns alongside the microbiome data.
The study population consisted of Indians residing in India, Indo-Immigrants, and Indo-Canadians, compared against Euro-Canadian and Euro-Immigrant control groups. The abstract does not report specific sample sizes or detailed demographic breakdowns for these groups. The comparison design was built around migration status and country of residence rather than clinical diagnosis.
Indians and Indo-Immigrants harbored gut microbiotas distinct from Euro-Canadian and Euro-Immigrant controls, marked by high abundances of Prevotella species and carbohydrate-active enzymes (CAZymes) reflecting a diet rich in complex carbohydrates. Indo-Canadians showed a transitional microbiome profile that moved toward the westernized pattern seen in controls. This shift paralleled increasing dietary acculturation among Indo-Canadians rather than a fixed, heritable microbial signature.
Because 44% of Canadians are first- or second-generation immigrants, and westernized dietary practices are spreading globally, microbiome transitions like this one may be widespread and consequential. Since Indian immigration to westernized countries has surged and post-migration IBD risk rises accordingly, this dietary-driven microbiome shift may help explain that increased disease susceptibility. The authors call for future research into the health implications of such microbiome transitions in immigrant populations and in newly industrialized nations.
This study examined whether rifaximin, a gut-specific non-absorbable antibiotic, could reduce gut-derived systemic inflammation in severe acute pancreatitis (SAP). The researchers combined murine experimental models with a single-center, open-label randomized controlled trial (ChiCTR2100049794). They assessed pancreatic injury, systemic inflammatory markers, and gut microbiota composition, and tested whether rifaximin's effects depended on modulating the microbiota by using antibiotic-treated and germ-free mice.
The animal component used murine models of severe acute pancreatitis, including antibiotic-treated and germ-free mice used to probe the mechanism. The clinical component enrolled 60 patients with predicted severe acute pancreatitis, randomized to receive rifaximin or standard control treatment. No further demographic details are given in the abstract.
In mice, rifaximin reduced pancreatic injury and systemic inflammation and decreased mucin-degrading gut genera such as Akkermansia, but its protective effects persisted even in antibiotic-treated and germ-free mice, indicating mechanisms beyond microbiota modulation. In patients, rifaximin significantly lowered systemic inflammation, with white blood cell count falling from a median of 11.50 x10^9/L to 8.49 x10^9/L and TNF-alpha falling from 15.05 pg/mL to 11.00 pg/mL. However, the rate of culture-confirmed infection was identical between rifaximin and control groups (13.3% vs 13.3%), and adverse events were comparable between groups.
The findings suggest rifaximin can dampen systemic inflammation in severe acute pancreatitis through mechanisms that are not solely dependent on reshaping the gut microbiota, pointing to a possible direct anti-inflammatory or barrier-protective effect. Because inflammation markers improved without any change in infection risk, rifaximin may offer a safe adjunct for controlling inflammatory injury in SAP without added infectious risk. This supports further investigation of rifaximin as a therapeutic strategy for gut-derived inflammation in acute pancreatitis, alongside continued study of its non-microbiota-dependent mechanisms.
This study examined the tracheal and cecal microbiome composition across three broiler chicken genotypes including a heritage New Hampshire × Columbian cross (NHC) and modern Ross × Ross 308 (R308) and Ross YP × Ross 708 (R708) broilers, using full-length 16S rRNA sequencing. Birds were reared in floor pens, and at 56 d of age, cecal and tracheal samples were collected from 8 birds per genotype and subjected to DNA extraction followed by PCR amplification of full-length 16S rRNA. Obtained amplified PCR product was sequenced using MinION. A total of 1.8 million reads for tracheal samples and 1.2 million reads for ceca samples were obtained from 24 birds. Despite similar alpha diversity matrixes (Shannon, Simpson, Pielou's evenness, and Chao1) across genotypes in both tracheal and cecal samples, beta diversity analysis revealed significant differences in community composition. Tracheal and cecal microbiota varied significantly among genotypes, particularly NHC with the R308 and R708 groups. At the phylum level, Bacillota (Firmicutes) dominated both tracheal and cecal samples across genotypes. In the trachea, NHC and R708 birds exhibited high relative abundance of Enterococcus cecorum, while Jeotgalicoccus meleagridis dominated R308. Differential abundance analysis showed higher abundance of potentially beneficial bacteria such as Limosilactobacillus pontis and Aerococcus viridans in R308 and R708, while NHC birds had higher levels of species like Merdibacter massiliensis and Agathobaculum butyriciproducens. Cecal microbiome analysis revealed genotype-specific enrichment of species, with NHC birds showing higher abundance of potential pathogens like Shigella boydii and Escherichia fergusonii compared to R708. In contrast, R308 birds harboured more potentially beneficial taxa, including Lactobacillus acidophilus and Limosilactobacillus vaginalis, compared to R708. Pairwise comparisons further highlighted Intestinibacter bartlettii and other potentially beneficial microbes being significantly enriched in R308 over R708. Overall, while microbial richness remained consistent, significant genotype-associated differences in bacterial community structure and genotype-specific microbial abundance were observed, emphasizing the influence of host genetics on microbiota composition and potential implications for poultry health and performance.
This study aimed to investigate the differences in gut microbiota composition and diversity among healthy controls (HC) and patients with colorectal lesions-including common colorectal polyps, small colorectal adenomas (SCRA), large colorectal adenomas (LCRA), and intramucosal carcinoma (IMC)-to identify bacterial species associated with disease progression and provide novel insights into the diagnosis and treatment of CRC based on the "polyp-adenoma-carcinoma" sequence.
A total of 250 participants were recruited from the First Affiliated Hospital of Anhui Medical University between July 2023 and June 2024. The cohort included 30 HC, 52 with common colorectal polyps, 58 with SCRA, 56 with LCRA, and 54 with IMC. Fecal samples were collected for bacterial DNA extraction, followed by metagenomic sequencing to analyze microbial diversity. Differential microbiota analysis was performed using the R package microbiomeMarker and LEfSe. Group classification and feature identification were conducted using a random forest model. Functional profiling was performed using DIAMOND against the KEGG and MetaCyc databases.
No significant differences in α-diversity were observed across the groups. β-diversity analysis revealed significant differences in Bray-Curtis and Jaccard distances among the groups. The composition and abundance of gut microbiota at the phylum, class, order, family, genus, and species levels were significantly altered. LEfSe analysis identified specific bacterial species with significant differences in IMC compared to other groups. Furthermore, the random forest model effectively distinguished patients with IMC from other groups based on distinct microbial signatures. Functional profiling revealed that the gut microbiota undergoes metabolic reprogramming from a homeostatic to a pro-tumorigenic phenotype during CRC progression as well as reduced protective pathway abundance and impaired energy/biosynthetic metabolism in CRC-associated microbiota.
Gut microbiota profiles varied significantly among HC, polyp, SCRA, LCRA, and IMC groups. Specific microbial signatures were able to effectively differentiate IMC from both HC and non-malignant colorectal lesions, highlighting their potential as diagnostic biomarkers.
This study investigated how the gut microbiota influences differential host resistance to porcine epidemic diarrhea virus (PEDV) infection in piglets. Researchers combined single-cell transcriptomics, 16S amplicon sequencing, metagenomics, and untargeted metabolomics to characterize the microbial and metabolic changes that follow PEDV infection. The work focused on identifying specific bacterial species and their metabolites that mediate protection against this pathogen.
The study used Landrace and Min pig breeds, two breeds with differing natural resistance to PEDV infection. Landrace pigs, which lose resistance quickly after infection, received fecal microbiota transplants from Min pigs, which are comparatively resistant. Animal protection models were then used to test the effects of specific bacteria and metabolites identified through the multi-omics analysis.
PEDV infection caused significant changes in the gut microbiota of piglets, and transplanting fecal microbiota from resistant Min pigs into susceptible Landrace pigs alleviated the infection. Metagenomic and animal protection models identified Lactobacillus reuteri and Lactobacillus amylovorus as playing an anti-infective role. Metabolomic screening linked these bacteria to the secondary bile acids deoxycholic acid (DCA) and lithocithocholic acid (LCA), but only LCA showed a protective effect in the animal model, and LCA supplementation altered the distribution of intestinal T-cell populations, notably enriching CD8+ populations.
These findings identify lithocholic acid as a key gut microbiota-derived metabolite mediating protection against PEDV infection in piglets. The results point to Lactobacillus reuteri and Lactobacillus amylovorus as candidate probiotic strains that could be harnessed to boost disease resistance through bile acid metabolism. This work suggests that modulating the gut microbiota and its bile acid metabolites, particularly LCA, and their effects on intestinal T-cell populations, could be a strategy for improving resistance to enteric viral pathogens in livestock.
This study used species-level shotgun metagenomic sequencing to characterize the gut microbiota of men who have sex with men (MSM). It investigated why the MSM gut microbiome, previously shown to differ from that of non-MSM, so often resembles the microbial communities seen in non-Westernized populations. The researchers also used questionnaire data and machine learning to link specific sexual practices to variation in microbiota composition among MSM.
The study population was men who have sex with men of Western origin, compared against patterns typical of non-Westernized populations. The abstract does not give an exact sample size, but participants contributed both stool samples for shotgun metagenomics and questionnaire responses on sexual practices. This design allowed the authors to relate individual behavioral data to individual gut microbiome profiles within the MSM cohort.
Many MSM with Western origin had gut microbiomes resembling those of non-Westernized populations rather than typical Western gut profiles. These microbiomes were frequently dominated by Prevotellaceae family members, including co-colonization by species from the Segatella copri complex alongside unknown Prevotellaceae members. Questionnaire analysis and machine learning further identified specific sexual practices as microbial features associated with this altered, Prevotellaceae-rich composition.
The findings show that sexual activity itself can be a driver of major gut microbiome alterations, independent of the diet and lifestyle factors usually invoked to explain Westernized versus non-Westernized microbiota differences. Because MSM gut microbiomes can resemble non-Westernized profiles, sexual practice becomes an important variable that population-based microbiota studies may need to account for. This has implications for how researchers select and interpret control or reference populations in microbiome research and for disentangling behavioral from dietary or geographic influences on gut microbial composition.
We used deep sequencing of fecal samples from 23 treatment-naive TB patients and 48 healthy donors to reconstruct the gut microbiome's metabolic capacity and strain/species-level content.
We show that the systematic depletion of the commensal flora of the large intestine, Bacteroidetes, and an increase in Actinobacteria, Firmicutes, and Proteobacteria such as Streptococcaceae, Erysipelotrichaceae, Lachnospiraceae, and Enterobacteriaceae explains the strong taxonomic divergence of the gut community in TB patients. The cumulative expansion of diverse disease-associated pathobionts in patients reached 1/4 of the total gut microbiota, suggesting a heavy toll on host immunity along with MTB infection. Reconstruction of metabolic pathways showed that the microbial community in patients shifted toward rapid growth using glycolysis and excess fermentation to produce acetate and lactate. Higher glucose availability in the intestine likely drives fermentation to lactate and growth, causing acidosis and endotoxemia.
This study examined gut microbial features associated with Parkinson's disease (PD) by meta-analyzing shotgun metagenomic sequencing data across six independent datasets from different countries. The researchers also established GC-MS and LC-MS/MS assays to directly quantify fecal short-chain fatty acids (SCFAs) and fecal polyamines. They analyzed taxonomic composition, functional gene pathways, and carbohydrate-active enzymes (CAZymes) in relation to PD status, adjusting for confounding factors.
The core dataset consisted of 94 PD patients and 73 controls whose fecal samples were shotgun sequenced in Japan. This Japanese cohort was combined with five previously reported datasets from the USA, Germany, China (two separate cohorts), and Taiwan. In total, the meta-analysis spanned six countries, giving the study an international, multi-cohort scope rather than a single-population sample.
Across all six datasets, alpha-diversity was consistently increased in PD. Taxonomic analysis showed Akkermansia muciniphila was increased in PD, while Roseburia intestinalis and Faecalibacterium prausnitzii, both associated with anti-inflammatory, butyrate-related commensal activity, were decreased. Genes for riboflavin and biotin biosynthesis and five of six CAZyme categories were markedly decreased in PD, and fecal SCFAs and polyamines were significantly reduced, with riboflavin/biotin gene abundance positively correlated with these metabolite levels.
The convergent, cross-country decrease in Faecalibacterium prausnitzii, Roseburia intestinalis, SCFAs, and polyamines suggests a reproducible loss of beneficial, anti-inflammatory commensal function in PD gut microbiota. Because the specific bacteria driving reduced riboflavin biosynthesis differed between Japan/USA/Germany and China1/China2/Taiwan, the findings imply that shared functional deficits in PD can arise from different taxonomic routes depending on population. This points toward B-vitamin biosynthesis and short-chain fatty acid/polyamine metabolism as potential functional biomarkers or intervention targets for PD that generalize better across populations than single-taxon signatures.
This study examined how environmental, socioeconomic, and health factors relate to gut microbiome composition at both the species and strain level. Researchers used deeply sequenced metagenomic data to identify associations between bacterial species and a range of host phenotypes and situational factors. They also performed a meta-analysis of species-level profiles across multiple datasets to look for consistent patterns, such as links to body mass index.
The study drew on a community-based cohort of 1,871 people living in 19 isolated villages in the Mesoamerican highlands of western Honduras. This is a non-industrialized, geographically isolated population, a setting the authors note remains uncommon in deep gut microbiome sequencing studies. Additional comparisons were made using species-level profiles from other, unspecified datasets as part of a meta-analysis.
Socioeconomic factors accounted for 51.44% of all associations found between the gut microbiome and human phenotypes, making them the dominant category of influence. Meta-analysis across datasets identified several bacterial species associated with body mass index, consistent with prior research. Incorporating strain-level phylogenetic information changed the overall picture of host-microbiome relationships, especially for factors like household wealth, where wealthier individuals were found to harbor different strains of Eubacterium rectale than less wealthy individuals.
The findings suggest that socioeconomic circumstances are a major driver of gut microbiome variation, potentially more so than many other individual health factors. The demonstration that strain-level differences (not just species presence) track with wealth indicates that species-level analysis alone can miss biologically meaningful variation. The authors conclude that gut microbiome surveillance in such populations could help illuminate broader patterns relevant to both individual and public health.
This study used whole-genome shotgun sequencing and gas chromatography/mass spectrometry to profile gut microbial and metabolic signatures across seven different malignancies. The researchers compared taxonomic and metabolomic configurations in cancer patients against sex- and age-matched healthy controls. The goal was to identify both common and cancer-type-specific gut microbiome and metabolite alterations.
The study included patients with colorectal cancer (40), stomach cancer (45), breast cancer (71), lung cancer (34), melanoma (50), lymphoid neoplasms (60), and acute myeloid leukemia (40). Each cancer group was compared against its own sex- and age-matched healthy control group. In total the analysis spanned 300 cancer patients across seven malignancy types plus their matched controls.
Beta-diversity differed between every cancer group and its healthy controls, while alpha-diversity differed only for the lymphoid neoplasm and acute myeloid leukemia groups. Of 203 unique species identified, 179 were under-represented and 24 were over-represented in cancer patients relative to controls. Faecalibacillus intestinalis was under-represented across all seven cancer groups, and Anaerostipes hadrus was under-represented in all groups except stomach cancer, with a marked reduction in the gut microbiome cancer index in every group except acute myeloid leukemia. Among the short-chain fatty acids and amino acids tested, formic acid concentration was significantly altered.
The consistent depletion of Faecalibacillus intestinalis and altered formic acid levels across seven distinct cancer types suggest these may represent shared, cross-cancer markers of gut dysbiosis rather than disease-specific findings. This points toward a common gut microbial and metabolic signature that could inform future pan-cancer diagnostic or monitoring approaches. Because the pattern held despite differences in cancer biology and location, it strengthens the case for a generalizable link between gut dysbiosis and malignancy.
This study used metagenomic sequencing to characterize taxonomic and functional changes in the gut microbiome of people with Parkinson's disease (PD). The researchers examined how these microbial changes relate to bacterial metabolites and to clinical disease progression. Motor and non-motor symptoms were tracked over up to five yearly study visits using the MDS-UPDRS scale and levodopa equivalent dose. Stool samples collected at baseline were used for the metagenomic analysis.
The study population consisted of 176 individuals with Parkinson's disease and 100 control participants who provided baseline stool samples for metagenomic sequencing. Disease progression was followed longitudinally across as many as five yearly visits using standardized clinical rating scales. The abstract does not specify age, sex distribution, or geographic recruitment site for these participants.
PD-derived stool samples showed reduced intermicrobial connectivity and seven species that were differentially abundant compared to controls. A range of bacterial functions also differed between groups, including depletion of carbohydrate degradation pathways and enrichment of ribosomal genes. Notably, Faecalibacterium prausnitzii-specific reads contributed to more than half of all the differentially abundant functional terms identified. A subset of these disease-associated functional terms correlated with faster progression on MDS-UPDRS part IV and could distinguish slow from fast progressors with moderate accuracy.
The findings reinforce that Parkinson's disease involves large-scale, functional disruption of the gut microbiome, not just shifts in a handful of taxa. The outsized contribution of Faecalibacterium prausnitzii, a key butyrate-producing, anti-inflammatory commensal, to the disrupted functional signature suggests its depletion may be mechanistically important rather than incidental. The link between specific functional terms and faster motor progression raises the possibility that gut microbial function could serve as a biomarker of disease trajectory. These results support further investigation into F. prausnitzii and related carbohydrate-degradation pathways as targets for monitoring or intervention in PD.
This study aimed to compare the gut and oral microbiota composition of professional male football players and amateurs. Environmental and behavioral factors are well known to modulate intestinal microbiota composition. Active lifestyle behaviors are involved in the improvement of metabolic and inflammatory parameters. Exercise promotes adaptational changes in human metabolic capacities affecting microbial homeostasis. Twenty professional football players and twelve amateurs were invited to the study groups. Fecal and oral microbiota were analyzed using next-generation sequencing of the 16S rRNA gene. Diversity in the oral microbiota composition was similar in amateurs and professionals, while the increase in training intensity reduced the number of bacterial species. In contrast, the analysis of the intestinal microbiota showed the greatest differentiation between professional football players and amateurs, especially during intensive training. Firmicutes were characterized by the largest population in all the studied groups. Intensive physical activity increases the abundance of butyrate and succinate-producing bacteria affecting host metabolic homeostasis, suggesting a very beneficial role for the host immune system's microbiome homeostasis and providing a proper function of the host immune system.
This study examined how exclusive enteral nutrition (EEN), a first-line therapy for pediatric Crohn's disease, produces its protective effects on the gut. The researchers used integrated multi-omics analysis of fecal microbiota and metabolites to identify functional network clusters associated with treatment response. They further validated these diet-driven microbiome changes using gut chemostat cultures and by transferring microbiota into germ-free Il10-deficient mice.
The abstract describes a prospective pediatric cohort of treatment-naive Crohn's disease patients, registered as German Clinical Trials DRKS00013306, who were followed as they began EEN therapy. Exact patient numbers are not given in the abstract. Findings from this human cohort were then extended experimentally using gnotobiotic (germ-free) Il10-deficient mice colonized with patient-derived microbiota.
Multi-omics analysis identified individually variable microbiome network clusters, with Lachnospiraceae and medium-chain fatty acids emerging as protective features associated with EEN response. Bioorthogonal non-canonical amino acid tagging pinpointed specific bacterial species that responded to medium-chain fatty acids, and metagenomic analysis revealed high strain-level dynamics during EEN therapy. When patient-derived microbiota were transferred into gnotobiotic Il10-deficient mice, individual patient-specific strain signatures could either prevent or cause inflammatory bowel disease-like inflammation.
The findings show that EEN operates through explicit, functional, and highly individualized changes in the fecal microbiome rather than a single uniform mechanism. Because protective effects were tied to specific strains and metabolites such as medium-chain fatty acids, this suggests that microbiome and metabolite profiling could help predict or enhance EEN response in pediatric Crohn's disease. The demonstration that individual strain signatures can causally prevent or induce inflammation in a gnotobiotic model also supports strain-level and metabolite-targeted approaches as a path toward more precise dietary or microbial therapies for Crohn's disease.
This randomised, parallel, double-blind, placebo-controlled pilot study examined the effect of a heat-treated postbiotic, Bifidobacterium longum CECT 7347 (HT-ES1), in healthy adults with mild to moderate digestive symptoms. Participants received either HT-ES1 or a matching placebo daily for 8 weeks, with an additional follow-up assessment at week 10. The study tracked gastrointestinal symptom scores, gut microbiota composition via 16S rRNA sequencing, biochemical markers, anthropometric parameters, and adverse events.
A total of 60 healthy adults with mild to moderate digestive symptoms were recruited and randomised to receive either the HT-ES1 postbiotic or an identical placebo. The abstract does not specify further demographic details such as age range or sex distribution. The population was drawn from generally healthy individuals rather than a diagnosed patient cohort.
Gastrointestinal symptoms changed minimally between the two groups, but the HT-ES1 group showed a significant decrease in total and non-HDL cholesterol compared to placebo. The intervention group also had a significant increase in the abundance of Faecalibacterium and Anaerobutyricum, both of which correlated positively with butyrate concentrations. Faecal calprotectin rose significantly over time in the placebo group but stayed stable in the HT-ES1 group.
The findings suggest that this heat-treated Bifidobacterium longum postbiotic may support cardiometabolic and intestinal health in healthy adults, even without producing marked changes in digestive symptoms. The rise in butyrate-associated, anti-inflammatory commensals such as Faecalibacterium alongside stable calprotectin levels points to a possible gut-barrier or anti-inflammatory benefit. These results support further, larger trials to confirm postbiotic effects on cholesterol and microbiota composition.
This study investigated the microbiome associated with ovarian cancer (OC) and its potential role in detection, disease progression, and prognosis. Researchers examined microbial taxa across multiple body sites in OC patients compared with a benign cohort. The aim was to identify microbial indicators that could aid early detection, track disease stage and grade, and predict treatment response.
The abstract does not give a specific cohort size or demographic description. It describes an OC patient cohort compared against a benign cohort, with sampling across several body sites; stool and omentum were sampled in the OC cohort but not in the benign cohort. Beyond this, the population can only be described in general terms as ovarian cancer patients versus patients with benign gynecological conditions.
The researchers identified a distinct OC microbiome with general enrichment of several microbial taxa, including Dialister, Corynebacterium, Prevotella, and Peptoniphilus, across body sites in the OC cohort. These same taxa were depleted in advanced-stage and high-grade OC patients compared with early-stage and low-grade patients, suggesting decreased accumulation as disease advances. The mainly pathogenic taxa were also more abundant in OC patients with adverse treatment outcomes compared to those without treatment-related events.
The enrichment and depletion patterns of these taxa suggest they could serve as potential indicators for early detection of ovarian cancer. Their accumulation in patients with adverse treatment outcomes suggests they could also help predict how patients will respond to treatment. Together these findings point to a possible diagnostic and prognostic role for the OC-associated microbiome, though the abstract does not describe validation in an independent cohort.
This study examined fecal bacterial composition, bacterial co-abundance networks, and metagenome function in US adults with type 2 diabetes (T2DM) compared to healthy adults. Samples were grouped into three enterotypes based on dominant bacterial families: Bacteroidaceae (ET-B), Lachnospiraceae (ET-L), and Prevotellaceae (ET-P). Machine learning and network analysis were used to identify the primary bacteria and bacterial interactions associated with T2DM incidence within each enterotype.
The analysis drew on 1,911 fecal bacterial files representing 1,039 adults with T2DM and 872 healthy adults from the Human Microbiome Projects, all based in the United States. Operational taxonomic units were generated from these samples after filtering and cleaning with Qiime2 tools. This represents a large public metagenomic dataset rather than a newly recruited clinical cohort.
The Bacteroidaceae enterotype (ET-B) showed the highest incidence of T2DM among the three enterotypes. Alpha-diversity was significantly lower in T2DM subjects within the Lachnospiraceae (ET-L) and Prevotellaceae (ET-P) enterotypes, but not within ET-B, while beta-diversity showed a clear separation between T2DM and healthy groups across all three enterotypes. An XGBoost machine learning model achieved high accuracy and sensitivity in distinguishing T2DM from healthy samples, and specific taxa, including Enterocloster bolteae, Faecalicatena fissicatena, Clostridium symbiosum, and Faecalibacterium prausnitzii, were found to be more abundant in the T2DM group.
The findings suggest that enterotype context matters for understanding how gut microbiota relate to T2DM, since diversity changes and bacterial signatures differed depending on which enterotype a person fell into. The elevated abundance of Faecalibacterium prausnitzii, an organism generally regarded as a butyrate-producing, anti-inflammatory commensal, alongside T2DM in this dataset highlights the complexity of interpreting single-taxon abundance without accounting for enterotype and network context. Machine learning models built on enterotype-stratified microbiome data may offer a useful approach for identifying T2DM-associated microbial signatures in US populations.
This study examined whether gut microbial communities are linked to the severity of COVID-19 in hospitalized patients. Researchers profiled stool samples using metagenomic sequencing to identify gut microbial taxa, their biochemical pathways, and stool metabolites associated with disease severity. They also built a random forest classifier to test whether microbiome data could distinguish severe from moderate COVID-19, and used network analyses to examine microbial community structure.
The study included 127 hospitalized patients with COVID-19, of whom 79 had severe disease and 48 had moderate disease. These patients collectively provided 241 stool samples collected from April 2020 to May 2021. The classifier's performance was also externally validated in an independent cohort, though details of that cohort are not given in the abstract.
Forty-eight microbial species were associated with severe COVID-19 after accounting for antibiotic use, age, sex, and comorbidities. Severe disease was marked by significant in-hospital depletion of Fusicatenibacter saccharivorans and Roseburia hominis, two commensals previously linked to post-acute COVID syndrome, or long COVID, suggesting they may serve as early biomarkers for its later development. The random forest classifier achieved excellent performance distinguishing severe from moderate COVID-19 stool samples, a result that held up in external validation, and network analysis pointed to fragility in the gut microbial community structure of severe cases.
The findings suggest that gut microbial depletion during acute COVID-19, particularly of Fusicatenibacter saccharivorans and Roseburia hominis, could help identify patients at risk of developing long COVID before it manifests. The strong, externally validated classifier performance indicates that stool-based microbiome signatures could become a practical tool for stratifying COVID-19 severity risk. These results also reinforce the broader role of specific gut commensals in shaping immune resilience during respiratory viral infection.
Allergic diseases affect millions of people worldwide. An increase in their prevalence has been associated with alterations in the gut microbiome, i.e., the microorganisms and their genes within the gastrointestinal tract. Maturation of the infant immune system and gut microbiota occur in parallel; thus, the conformation of the microbiome may determine if tolerant immune programming arises within the infant. Here we show, using deeply phenotyped participants in the CHILD birth cohort (n = 1115), that there are early-life influences and microbiome features which are uniformly associated with four distinct allergic diagnoses at 5 years: atopic dermatitis (AD, n = 367), asthma (As, n = 165), food allergy (FA, n = 136), and allergic rhinitis (AR, n = 187). In a subset with shotgun metagenomic and metabolomic profiling (n = 589), we discover that impaired 1-year microbiota maturation may be universal to pediatric allergies (AD p = 0.000014; As p = 0.0073; FA p = 0.00083; and AR p = 0.0021). Extending this, we find a core set of functional and metabolic imbalances characterized by compromised mucous integrity, elevated oxidative activity, decreased secondary fermentation, and elevated trace amines, to be a significant mediator between microbiota maturation at age 1 year and allergic diagnoses at age 5 years (βindirect = -2.28; p = 0.0020). Microbiota maturation thus provides a focal point to identify deviations from normative development to predict and prevent allergic disease.
This study used metagenomic sequencing to characterize the gut microbiota of patients with non-segmental vitiligo. Researchers examined microbial community composition, diversity, and gene functions using bioinformatic analysis. They also predicted gut metabolic modules with the KEGG and MetaCyc databases to identify functional differences linked to the disease.
The study enrolled 25 patients with non-segmental vitiligo and 25 matched healthy controls. All 50 participants underwent metagenomic sequencing of their gut microbiota for comparison between the two groups.
Alpha diversity of the gut microbiome was significantly reduced in vitiligo patients compared with healthy controls. At the species level, Staphylococcus thermophiles was decreased while Bacteroides fragilis was increased in patients with vitiligo. LEfSe analysis identified additional microbial markers distinguishing vitiligo patients, including Lachnospiraceae_bacterium_BX3, Massilioclostridium_coli, and TM7_phylum_sp_oral_taxon_348, alongside Bacteroides_fragilis.
These findings support a link between altered gut microbial composition and non-segmental vitiligo, reinforcing gut dysbiosis as a feature of the disease. The reduced diversity and specific species shifts, particularly the increase in Bacteroides fragilis, may serve as microbial markers for further investigation. Characterizing associated gene functions and metabolic modules could help clarify mechanisms connecting gut microbiota to vitiligo pathogenesis.
This study investigated whether gut bacteria that produce endogenous ethanol contribute to nonalcoholic steatohepatitis (NASH). Researchers measured fecal ethanol, glucose, total proteins, triglyceride and total cholesterol using high-performance liquid chromatography. They also characterized the gut microbiota using microbial culturomics and 16S rRNA metagenomics targeting the V3V4 hypervariable region to identify which viable bacteria and genetic signatures were enriched in NASH.
The study compared fecal samples from 41 patients with NASH to 24 controls without the disease. This case-control design allowed direct comparison of biochemical parameters and microbial composition between diseased and healthy states. No further demographic details are given in the abstract.
Fecal ethanol and glucose were significantly elevated in NASH patients compared to controls, while triglyceride, total cholesterol and total protein levels did not differ. Culturomics identified enrichment of the ethanol-producing bacteria Enterocloster bolteae and Limosilactobacillus fermentum in NASH samples. 16S rRNA sequencing confirmed enrichment of ethanol-producing bacteria including L. fermentum, corroborating the culture-based findings with independent genetic evidence.
The findings support endogenous ethanol production by specific gut bacteria as a plausible mechanistic contributor to NASH, independent of dietary alcohol intake. By combining culturomics with 16S metagenomics, the study strengthens the case that microbially derived ethanol, rather than only enterobacteria or yeasts previously implicated, may drive liver injury in NASH. This suggests ethanol-producing bacteria such as L. fermentum and E. bolteae could become targets for diagnostic or therapeutic strategies aimed at reducing hepatic damage in NASH patients.
Intestinal flora provides an important contribution to the development of pulmonary tuberculosis (PTB). We performed a cross-sectional study in 52 healthy controls (HCs) and 83 patients with untreated active PTB to assess the differences in their microbiomic and metabolic profiles in faeces via V3-V4 16S rRNA gene sequencing and gas chromatography-mass spectrometry. Patients with PTB had considerable reductions in phylogenetic alpha diversity and the production of short-chain fatty acids, dysbiosis of the intestinal flora and alterations in the faecal metabolomics composition compared with HCs. Significant alterations in faecal metabolites were associated with changes in the relative abundance of specific genera. Our study describes the imbalance of the gut microbiota and altered faecal metabolomics profiles in patients with PTB; the results indicate that the gut microbiota and faecal metabolomic profiles can be used as potential preventive and therapeutic targets for PTB.
This prospective, observational study examined whether gut microbiota composition is associated with immune responses and adverse events following COVID-19 vaccination. Researchers compared two vaccine types: the inactivated CoronaVac vaccine and the mRNA BNT162b2 vaccine. They performed shotgun metagenomic sequencing on stool samples collected at baseline and again one month after the second vaccine dose. Immune responses were assessed using a SARS-CoV-2 surrogate virus neutralisation test and a spike receptor-binding domain IgG ELISA.
The study included 138 adult COVID-19 vaccine recipients, of whom 37 received CoronaVac and 101 received BNT162b2. Stool samples from these vaccinees were collected at two time points, baseline and one month post second dose, for shotgun metagenomic analysis. The abstract does not specify additional demographic details such as age range, sex distribution, or geographic location.
Immune responses were significantly lower in CoronaVac recipients than in BNT162b2 recipients. Among CoronaVac vaccinees, higher persistent levels of Bifidobacterium adolescentis were associated with higher neutralising antibody responses, and their baseline gut microbiome was enriched in carbohydrate metabolism pathways. In BNT162b2 vaccinees, neutralising antibody levels correlated positively with the total abundance of flagellated and fimbriated bacteria, including Roseburia faecis. Prevotella copri and two Megamonas species were enriched in individuals who experienced fewer adverse events after vaccination.
These findings suggest that baseline gut microbiota composition and function may help explain individual variation in vaccine immunogenicity and tolerability. Specific taxa, such as Bifidobacterium adolescentis, Roseburia faecis, Prevotella copri, and Megamonas species, and microbial functional features like carbohydrate metabolism pathways and flagellar or fimbrial machinery, appear linked to stronger antibody responses or fewer adverse events. This raises the possibility that gut microbiome profiling or modulation could eventually inform strategies to improve vaccine efficacy or reduce adverse events. Further research is needed to determine whether these associations are causal and generalizable across vaccine platforms and populations.
This scoping review examined the human gut microbiota and its relation to glucose metabolism, insulin resistance, and type 2 diabetes risk. The authors searched PubMed and screened 5983 records down to 45 original observational studies. They focused on identifying key bacterial taxa associated with markers and stages of glucose dysregulation, independent of overweight, obesity, and metabolic drugs. The review also considered the potential mediating role of short-chain fatty acids (SCFAs) and the influence of diet and diet-microbiota derived metabolites.
The review drew on human observational studies conducted in healthy adults as well as adults with metabolic disease and associated risk factors. Rather than a single cohort, the evidence base was pooled across 45 separate original studies identified from the PubMed literature. Specific sample sizes or demographic details for individual cohorts are not given in the abstract.
Across the reviewed studies, alpha diversity and 45 distinct bacterial taxa were associated with glucose metabolism outcomes. Six taxa emerged as most frequently linked to glucose metabolism, including Akkermansia muciniphila, Bifidobacterium longum, the Clostridium leptum group, and Faecalibacterium prausnitzii. The authors present evidence supporting SCFAs as a mechanism that may mediate the relationship between these gut bacteria and glucose regulation. Diet and microbiota-derived metabolites are also highlighted as relevant contributors to these associations.
Identifying specific gut bacteria, including SCFA-associated and anti-inflammatory commensals such as Faecalibacterium prausnitzii, consistently linked to glucose metabolism could open new avenues for type 2 diabetes prevention. Because these associations were found independent of obesity and metabolic drug use, the gut microbiota may represent an independent target for intervention. The proposed role of SCFAs and diet-derived metabolites suggests that dietary strategies aimed at shaping the microbiota could be a practical entry point for future prevention efforts. Overall, the findings support further mechanistic and interventional research into these key taxa and their metabolic products.
This study examined the gut microbiome in Parkinson's disease (PD) using large-scale, high-resolution shotgun metagenomic sequencing of fecal DNA. The researchers applied uniform, standardized methods throughout, followed by metagenome-wide association studies requiring agreement between two independent statistical methods (ANCOM-BC and MaAsLin2) before declaring a disease association. They also conducted network analysis to identify clusters of co-occurring microbial species and functional profiling to characterize microbial genes and pathways.
The study enrolled 490 individuals with Parkinson's disease and 234 control individuals. Fecal samples from this cohort underwent deep shotgun sequencing to generate the metagenomic data analyzed in the study. The abstract does not provide further demographic detail on the participants.
Over 30 percent of the species, genes, and pathways tested showed altered abundances in Parkinson's disease, indicating widespread dysbiosis. PD-associated species organized into polymicrobial clusters that grew, shrank, or competed together rather than acting independently. The PD microbiome was disease permissive: it showed overabundance of pathogens and immunogenic components, dysregulated neuroactive signaling, an excess of molecules that induce alpha-synuclein pathology, and overproduction of toxicants, alongside a reduction in anti-inflammatory and neuroprotective factors that would otherwise support recovery.
By validating in human PD patients findings previously seen only in experimental models, this study strengthens the case that the gut microbiome contributes to multiple disease mechanisms in Parkinson's disease. The reconciliation of prior human PD microbiome literature helps resolve inconsistencies across earlier studies and establishes a more standardized foundation for future research. The reduction in anti-inflammatory and neuroprotective microbial factors points to a loss of protective capacity that may limit the body's ability to counteract disease processes, suggesting the microbiome as a potential target for future mechanistic and therapeutic investigation.
This study examined the effect of antiparkinsonian medication, specifically levodopa (LD) and levodopa-carbidopa intestinal gel (LCIG), on the gut microbiota and fecal metabolome in Parkinson disease (PD). Fecal DNA was analyzed using next-generation sequencing of the V3 and V4 regions of the 16S rRNA gene. Fecal metabolic extracts were also evaluated using gas chromatography mass spectrometry to characterize metabolome differences across treatment groups.
The study included 107 patients with a clinical diagnosis of Parkinson disease. Patients were divided into three groups: an LCIG group (n = 38) receiving levodopa-carbidopa intrajejunal gel, an LD group (n = 46) receiving oral levodopa, and a Naive group (n = 23) not taking any antiparkinsonian medications. This design allowed comparison of gut microbiota composition across different treatment exposures within a PD population.
Multivariate analysis showed that the LCIG group had a significantly higher abundance of Enterobacteriaceae, Escherichia, and Serratia compared to the LD group. Compared to the Naive group, the LD group showed a reduction of Blautia and Lachnospirae. The LCIG group additionally showed an increase in Proteobacteria and Enterobacteriaceae alongside a reduction in Firmicutes, Lachnospiraceae, and Blautia relative to the Naive group.
The findings suggest that the route and form of levodopa therapy, oral versus intrajejunal gel, are associated with distinct gut microbiota profiles in Parkinson disease. The reduction of Blautia and Lachnospiraceae, taxa associated with short-chain fatty acid production, alongside enrichment of Enterobacteriaceae in LCIG-treated patients points to a treatment-related shift toward a less favorable microbial composition. These distinctive features may warrant further investigation into how PD medication choice shapes gut microbial and metabolic health over the course of treatment.
This study examined whether the gut microbiome carries a detectable signature of prediabetes, a stage preceding type 2 diabetes mellitus (T2D). Researchers sequenced the V1-V5 variable regions of the 16S rRNA gene to profile gut microbiota composition. They also measured fasting serum inflammatory biomarkers in the same participants. The goal was to identify robust microbial signatures that could aid early diagnosis and prevention of T2D.
The study analyzed two cohorts, one from India and one from Denmark, combining prediabetic and normoglycemic individuals. In total, 262 prediabetic subjects were compared against 275 normoglycemic subjects. This trans-ethnic design allowed the researchers to correct for a strong country-specific cohort effect and look for microbial patterns shared across both populations.
After correcting for cohort effects, 16 operational taxonomic units (OTUs) were enriched in normoglycemic subjects relative to those with prediabetes, including members of Prevotella9, Phascolarctobacterium, Barnesiella, Flavonifractor, Tyzzerella_4, Bacteroides, Faecalibacterium, and Agathobacter. Faecalibacterium, a genus that includes the anti-inflammatory, butyrate-producing species Faecalibacterium prausnitzii, was among the taxa depleted in prediabetic subjects. Conversely, 144 OTUs were found enriched in the prediabetic subjects, indicating a broader shift in community composition alongside the loss of these beneficial commensals.
The depletion of Faecalibacterium and other short-chain-fatty-acid-associated genera in prediabetes, observed consistently across two ethnically distinct cohorts, supports gut microbiota as a candidate early marker of metabolic disease risk. Because these signatures held after correcting for country-specific effects, they suggest a trans-ethnic microbial pattern rather than a population-specific artifact. This strengthens the rationale for using microbiome profiling in early prediabetes screening and for exploring interventions that restore anti-inflammatory, butyrate-producing commensals before progression to overt T2D.
This study examined whether the intestinal microbiome influences clinical outcome and treatment side effects in early breast cancer. Researchers used shotgun metagenomics to characterize fecal microbiota composition and paired this with plasma metabolomics. They looked at associations between the gut microbiota, measured at baseline and after chemotherapy, and both breast cancer prognosis and therapy-induced side effects. Findings were then tested for clinical relevance in an immunocompetent mouse model colonized with patient microbiota and challenged with mouse breast cancer and chemotherapy.
The human cohort consisted of 76 early breast cancer patients contributing 121 fecal specimens, with 45 patients providing paired samples collected before and after chemotherapy. These patients were enrolled in the CANTO prospective study, which was designed to record side effects associated with clinical management of breast cancer. The findings were further validated in immunocompetent mice colonized with breast cancer patient microbiota.
Specific gut commensals were found to be overabundant in breast cancer patients compared with healthy individuals. These overabundant commensals were associated with worse breast cancer prognosis. Chemotherapy modulated the abundance of these gut microbes, and the same microbes appeared to influence weight gain and neurological side effects linked to breast cancer therapies.
The results suggest that gut microbiota composition could serve as a modifiable factor affecting both cancer prognosis and treatment tolerability in early breast cancer. Because chemotherapy itself reshapes these microbial communities, monitoring or targeting the microbiome during treatment may offer a way to improve outcomes and reduce side effects. The authors note that these findings, obtained in adjuvant and neoadjuvant settings, warrant prospective validation before any clinical application.
Olfactory dysfunction is a pre-motor symptom of Parkinson's disease (PD) that appears years prior to diagnosis and can affect quality of life in PD. Changes in microbiota community in deep nasal cavity near the olfactory bulb may trigger the olfactory bulb-mediated neuroinflammatory cascade and eventual dopamine loss in PD. To determine if the deep nasal cavity microbiota of PD is significantly altered in comparison to healthy controls, we characterized the microbiota of the deep nasal cavity using 16S rRNA gene amplicon sequencing in PD subjects and compared it to that of spousal and non-spousal healthy controls. Correlations between microbial taxa and PD symptom severity were also explored. Olfactory microbial communities of PD individuals were more similar to those of their spousal controls than to non-household controls. In direct comparison of PD and spousal controls and of PD and non-spousal controls, significantly differently abundant taxa were identified, and this included increased relative abundance of putative opportunistic-pathobiont species such as Moraxella catarrhalis. M. catarrhalis was also significantly correlated with more severe motor scores in PD subjects. This proof-of-concept study provides evidence that potential pathobionts are detected in the olfactory bulb and that a subset of changes in the PD microbiota community could be a consequence of unique environmental factors associated with PD living. We hypothesize that an altered deep nasal microbiota, characterized by a putative pro-inflammatory microbial community, could trigger neuroinflammation in PD.
This study examined how gut microbiota composition changes after stroke and whether those changes relate to functional recovery. Researchers compared fecal microbial diversity, composition, and species cooccurrence between stroke patients and healthy controls. They used 16S rRNA gene sequencing (V3-V4 regions) on the Illumina MiSeq platform to characterize the bacterial communities. Random forest and receiver operating characteristic analyses were then applied to identify bacterial genera that might serve as diagnostic biomarkers linked to poststroke outcomes.
The cohort consisted of thirty-eight patients who had experienced a stroke and thirty-five healthy controls matched to the patients by demographics. Fecal DNA was extracted from all participants for microbial sequencing. This was a prospective cohort study comparing a clinical stroke population against a demographically similar healthy comparison group.
Poststroke patients showed significantly higher alpha diversity of gut microbiota than healthy controls. Beta diversity analysis confirmed that overall microbiota composition differed significantly between the two groups. At the genus level, nine genera increased significantly in abundance in poststroke patients, while eighty-two genera decreased significantly, indicating a broad and pronounced shift in the gut microbial community following stroke.
The findings support the existence of a distinct poststroke gut microbiota signature linked to the gut-microbiota-brain axis. Because specific bacterial genera were identified as potential discriminant markers with ties to functional outcomes, gut microbiota profiling may eventually help predict or monitor functional recovery after stroke. This adds to evidence that stroke does not just affect the brain but is accompanied by substantial, measurable disruption of the gut microbial ecosystem.
This study investigated the composition of the gut microbiome in renal transplant recipients (RTRs) and compared it with that of healthy controls. The researchers used 16S rRNA sequencing of fecal samples to characterize microbiome composition and diversity. They then applied multivariate association with linear models (MaAsLin) to identify clinical and pharmacological determinants of the gut microbiome in RTRs, including immunosuppressive drugs and antibiotic exposure.
The study included 139 renal transplant recipients (50% male, mean age 58.3 plus or minus 12.8 years) and 105 healthy controls (57% male, mean age 59.2 plus or minus 10.6 years), all participants in the TransplantLines Biobank and Cohort Study (NCT03272841). The median time since transplantation among RTRs was 6.0 years, with a range of 1.5 to 12.5 years. Fecal samples were collected from both groups for microbiome analysis.
The gut microbiome composition of RTRs was significantly different from that of healthy controls, and RTRs had significantly lower gut microbiome diversity (p less than 0.01). Proton-pump inhibitors, mycophenolate mofetil, and estimated glomerular filtration rate (eGFR) were identified as significant determinants of the gut microbiome in RTRs (p less than 0.05). These findings point to specific medications and kidney function as key factors shaping post-transplant dysbiosis, rather than transplantation alone.
The findings indicate that renal transplant recipients experience measurable intestinal dysbiosis linked to specific modifiable factors, particularly proton-pump inhibitor use and mycophenolate mofetil therapy. This suggests that clinicians managing RTRs might consider the gut microbiome impact of routine medication choices as part of post-transplant care. Further research could explore whether adjusting these determinants influences microbiome recovery or long-term transplant outcomes.
Recently, gut microbiota have been studied extensively for health promotion, disease prevention, disease treatment, and exercise performance. It is recommended that athletes avoid dietary fiber and resistant starch to promote gastric emptying and reduce gastrointestinal distress during exercise, but this diet may reduce microbial diversity and compromise the health of the athlete's gut microbiota. This study compared fecal microbiota characteristics using high-throughput sequencing among healthy sedentary men (as controls), bodybuilders, and distance runners, as well as the relationships between microbiota characteristics, body composition, and nutritional status.
Body composition was measured using DXA, and physical activity level was assessed using IPAQ. Dietary intake was analyzed with the computerized nutritional evaluation program. The DNA of fecal samples was extracted and it was sequenced for the analysis of gut microbial diversity through bioinformatics cloud platform.
We showed that exercise type was associated with athlete diet patterns (bodybuilders: high protein, high fat, low carbohydrate, and low dietary fiber diet; distance runners: low carbohydrate and low dietary fiber diet). However, athlete type did not differ in regard to gut microbiota alpha and beta diversity. Athlete type was significantly associated with the relative abundance of gut microbiota at the genus and species level: Faecalibacterium, Sutterella, Clostridium, Haemophilus, and Eisenbergiella were the highest (p < 0.05) in bodybuilders, while Bifidobacterium and Parasutterella were the lowest (p < 0.05). At the species level, intestinal beneficial bacteria widely used as probiotics (Bifidobacterium adolescentis group, Bifidobacterium longum group, Lactobacillus sakei group) and those producing short chain fatty acids (Blautia wexlerae, Eubacterium hallii) were the lowest in bodybuilders and the highest in controls. In addition, aerobic or resistance exercise training with an unbalanced intake of macronutrients and low intake of dietary fiber led to similar diversity of gut microbiota. Specifically, daily protein intake was negatively correlated with operation taxonomic unit (r = - 0.53, p < 0.05), ACE (r = - 0.51, p < 0.05), and Shannon index (r = - 0.64, p < 0.01) in distance runners..
Results suggest that high-protein diets may have a negative impact on gut microbiota diversity for athletes, while athletes in resistance sports that carry out the high protein low carbohydrates diet demonstrate a decrease in short chain fatty acid-producing commensal bacteria.
This study examined how mode of delivery affects the earliest colonization of the infant gut microbiota during the neonatal period (up to one month of age) and into infancy. The researchers used longitudinal sampling combined with whole-genome shotgun metagenomic analysis to track which microbial strains and species established themselves in newborns over time. They specifically compared babies born by caesarean section to those born vaginally, and also looked at the effects of maternal antibiotic prophylaxis and breastfeeding status during the neonatal window.
The cohort comprised 596 full-term babies born in UK hospitals, from whom 1,679 gut microbiota samples were collected at multiple time points during the neonatal period and later in infancy. For a subset of these infant-mother pairs, matched maternal samples were also collected, totaling 175 mothers paired with 178 babies. This gave the study both a large infant sample size and a smaller nested set of mother-infant pairs for tracking strain transmission.
Babies delivered by caesarean section showed disrupted transmission of maternal Bacteroides strains, meaning these commensal organisms were less successfully passed from mother to infant compared to vaginal delivery. Caesarean-born infants also showed high-level colonization by opportunistic pathogens associated with the hospital environment, including Enterococcus, Enterobacter, and Klebsiella species. These same disruptions, though to a lesser extent, were also observed in vaginally delivered babies whose mothers received antibiotic prophylaxis and in infants who were not breastfed during the neonatal period.
The findings suggest that both caesarean delivery and antibiotic exposure around birth can independently disrupt the normal, low-risk colonization of the infant gut by maternal commensal strains. This disruption opens the door for opportunistic, hospital-associated pathogens to establish themselves early in life instead. Because early gut microbiota composition has been linked to later childhood and lifelong disease risk, these results point to birth mode, antibiotic use, and breastfeeding as modifiable factors that could be targeted to support healthier early microbiome establishment.
The study investigated how fecal microbiota metabolize non-digestible oligo- and polysaccharides, using isothermal microcalorimetry to track fermentation in real time. Five substrates were tested: raffinose, melibiose, an oligo- and polysaccharide mixture produced from raffinose by levansucrase, levan synthesized from raffinose, and levan from timothy grass. Growth was assessed from heat evolution curves along with organic acid and gas production, and taxonomic shifts were profiled by 16S rDNA sequencing.
The work used pooled fecal samples as inocula rather than individual human subjects tested directly. Three fecal pools were compared: one from overweight children, one from normal-weight children, and one from healthy adult volunteers. A pure culture of Bacteroides thetaiotaomicron was included as a reference colon bacterium alongside these pooled samples.
Raffinose and melibiose promoted bifidobacteria growth across all three fecal pools, but each pool showed distinct additional responses. In the overweight children's pool, lactate-producing bacteria such as Streptococcus and Enterococcus became enriched, making lactic acid the dominant fermentation product from the short saccharides. In the normal-weight children's pool, acetic and butyric acids predominated instead, coinciding with enrichment of Catenibacterium, while in the adult pool the levans specifically promoted Bacteroides and Lachnospiraceae.
The findings indicate that fecal microbiota from overweight versus normal-weight children ferment the same prebiotic-type substrates into different metabolic end products, not just different taxa. Because overweight children's microbiota favored lactic acid production over the acetate and butyrate seen in normal-weight children, substrate choice and host metabolic status together shape fermentation outcomes. This suggests that prebiotic selection may need to be tailored by weight status or metabolic phenotype rather than applied uniformly across pediatric populations.
This study examined differences in intestinal flora structure between obese and normal-weight school-age children. Researchers used Illumina Miseq next-generation sequencing with 16S rDNA high-throughput sequencing technology to characterize gut bacterial communities. Gut bacteria were classified into Operational Taxonomic Units (OTUs) using the RDP 16S rRNA database and RDP classifier. Both alpha diversity (within-sample diversity) and beta diversity (between-sample dissimilarity) were calculated to compare the two groups.
The study included 39 obese school-age children and 38 normal-weight control children of the same age range. The abstract does not specify the children's exact ages, sex distribution, or geographic location beyond this case-control design. Comparisons were made strictly between these two defined groups based on obesity status.
Intestinal flora in obese children showed lower alpha diversity than in normal-weight controls. Significant differences in the relative abundance of intestinal flora were detected at multiple levels of taxonomic classification. Beta diversity comparisons further confirmed that the microbial community structure differed meaningfully between the obese and normal groups. The abstract does not name specific bacterial taxa or note Faecalibacterium prausnitzii, butyrate, or other anti-inflammatory commensals.
Identifying which specific intestinal bacteria differ between obese and normal-weight children may help clarify the role these organisms play in the development of childhood obesity. This case-control comparison suggests reduced gut microbial diversity could be a feature of pediatric obesity. The findings may support future work aimed at finding new approaches, such as microbiome-targeted strategies, for addressing childhood obesity. Because the abstract's findings section was truncated, further specific implications beyond this general direction cannot be confirmed.
Obesity has become one of the most serious social problems in developed countries, including Japan. The relationship between the gut microbiota and obesity has recently attracted the attention of many researchers. Although the gut microbiota was long thought to contribute to obesity, the exact association remains largely unknown. We examined the human gut microbiota composition in a Japanese population in order to determine its relationship to obesity.
Stool samples from 23 non-obese subjects (body mass index [BMI] <20 kg/m(2)) and 33 obese subjects (BMI ≥25 kg/m(2)) were collected and DNA was extracted prior to colonoscopy. After terminal restriction fragment length polymorphism (T-RFLP) analysis, samples from 10 subjects (4 non-obese and 6 obese) were selected and subjected to next-generation sequencing for species-level analysis.
T-RFLP analysis showed significantly reduced numbers of Bacteroidetes and a higher Firmicutes to Bacteroidetes ratio in obese subjects compared with non-obese subjects. Bacterial diversity was significantly greater in obese subjects compared with non-obese subjects. Next-generation sequencing revealed that obese and non-obese subjects had different gut microbiota compositions and that certain bacterial species were significantly associated with each group (obese: Blautia hydrogenotorophica, Coprococcus catus, Eubacterium ventriosum, Ruminococcus bromii, Ruminococcus obeum; non-obese: Bacteroides faecichinchillae, Bacteroides thetaiotaomicron, Blautia wexlerae, Clostridium bolteae, Flavonifractor plautii).
Gut microbial properties differ between obese and non-obese subjects in Japan, suggesting that gut microbiota composition is related to obesity.
The involvement of the gut microbiota in metabolic disorders, and the ability of whole grains to affect both host metabolism and gut microbial ecology, suggest that some benefits of whole grains are mediated through their effects on the gut microbiome. Nutritional studies that assess the effect of whole grains on both the gut microbiome and human physiology are needed. We conducted a randomized cross-over trial with four-week treatments in which 28 healthy humans consumed a daily dose of 60 g of whole-grain barley (WGB), brown rice (BR), or an equal mixture of the two (BR+WGB), and characterized their impact on fecal microbial ecology and blood markers of inflammation, glucose and lipid metabolism. All treatments increased microbial diversity, the Firmicutes/Bacteroidetes ratio, and the abundance of the genus Blautia in fecal samples. The inclusion of WGB enriched the genera Roseburia, Bifidobacterium and Dialister, and the species Eubacterium rectale, Roseburia faecis and Roseburia intestinalis. Whole grains, and especially the BR+WGB treatment, reduced plasma interleukin-6 (IL-6) and peak postprandial glucose. Shifts in the abundance of Eubacterium rectale were associated with changes in the glucose and insulin postprandial response. Interestingly, subjects with greater improvements in IL-6 levels harbored significantly higher proportions of Dialister and lower abundance of Coriobacteriaceae. In conclusion, this study revealed that a short-term intake of whole grains induced compositional alterations of the gut microbiota that coincided with improvements in host physiological measures related to metabolic dysfunctions in humans.
2026-07-04
Blautia wexlerae majorTaxon page created: biology (morphology, health role, beneficial factors), its metabolic role, what depletes it, supportive interventions, the data-derived Conditions table across 39 conditions, and the full research feed.
Hosomi K, Saito M, Park J, Murakami H, Shibata N, Ando M, Nagatake T, et al.
Oral administration of Blautia wexlerae ameliorates obesity and type 2 diabetes via metabolic remodeling of the gut microbiota.Nat Commun. 2022
Hiippala K, Jouhten H, Ronkainen A, Hartikainen A, Kainulainen V, Jalanka J, Satokari R.
The potential of gut commensals in reinforcing intestinal barrier function and alleviating inflammation.Nutrients. 2018
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