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A specific stool Lachnoclostridium marker, called m3, rises steadily from a healthy colon to a polyp to cancer, and it detects pre-cancerous adenomas better than the standard stool blood test.
Lachnoclostridium is a heterogeneous genus of gut Lachnospiraceae, reclassified from several former Clostridium species. Its defining role on this database is as a colorectal cancer biomarker: a specific fecal Lachnoclostridium marker (m3) increases from healthy colon to adenoma to cancer and outperforms the standard fecal immunochemical test at detecting pre-cancerous adenomas.
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 MoreLachnoclostridium is a genus of Gram-positive, anaerobic gut bacteria in the Lachnospiraceae family, created by reclassifying several species formerly placed in Clostridium. It is a heterogeneous, ordinary component of the gut community, and its naming still varies between databases.[1] On this database it appears as a differentially abundant taxon across many human microbiome studies.
Lachnoclostridium's standout role is as a colorectal cancer biomarker. A specific fecal Lachnoclostridium species marker, called m3, is progressively enriched from a healthy colon to a pre-cancerous adenoma to established cancer, and it detects adenomas non-invasively better than the standard fecal immunochemical test (FIT).[1] As a Firmicutes commensal genus it sits outside the bacterial metallome framework this database applies to nickel- and manganese-driven pathogens; its relevance here is diagnostic, as a stool signal that tracks colorectal neoplasia.
Lachnoclostridium species are Gram-positive (structurally), strictly anaerobic, rod-shaped members of the Lachnospiraceae, a core family of gut fermenters.[1] The genus was carved out of the old, catch-all Clostridium and remains taxonomically mixed, which matters for interpreting any genus-level signal.
As Lachnospiraceae, Lachnoclostridium members ferment dietary substrates in the anaerobic colon, and the genus spans a range of behaviors rather than a single role.[1] Its value on this database is not a fixed beneficial or harmful function but a diagnostic one: a specific member's fecal abundance tracks the healthy-to-adenoma-to-cancer sequence in the colon.[1]
The genus's best-characterized feature is the performance of its fecal marker in colorectal screening.
| Feature | Description and role |
|---|---|
| Adenoma-to-cancer gradient | The fecal Lachnoclostridium marker m3 rises progressively from normal colon to adenoma to colorectal cancer across independent cohorts.[1] |
| Adenoma detection better than FIT | m3 detected pre-cancerous adenomas that the fecal immunochemical test largely missed, and combining the two improved sensitivity for advanced adenoma.[1] |
| Screening in asymptomatic people | A four-marker panel including the Lachnoclostridium marker was more sensitive than FIT for detecting neoplasia in asymptomatic subjects.[2] |
| Recurrence surveillance | The m3 marker increased in patients whose adenomas recurred after polypectomy, supporting its use in follow-up.[3] |
Lachnoclostridium's clinical associations center on colorectal neoplasia, where its fecal marker is a validated screening signal.
| Association | Direction and interpretation |
|---|---|
| Colorectal adenoma | The fecal marker is enriched in adenoma and detects it non-invasively, a key window for early, curable intervention.[1] |
| Colorectal cancer | Marker abundance is highest in established cancer; combined with other markers and FIT it reaches high diagnostic accuracy.[1][2] |
| Post-polypectomy recurrence | A rising marker after polyp removal flags adenoma recurrence during surveillance.[3] |
Lachnoclostridium is a normal gut genus and a diagnostic marker, not an infection to clear or a treatment target; the entries below are classified by our validation method and are not medical advice.
| Use | Class | MBTI Status |
|---|---|---|
| Fecal Lachnoclostridium marker for colorectal screening | Diagnostic | Validation In Progress |
| Marker-based post-polypectomy surveillance | Diagnostic | Validation In Progress |
Where Lachnoclostridium (NCBI:txid1506553) appears as a differentially abundant taxon across the Microbiome Medicine corpus. Each row aggregates every experiment in which the genus 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 136 conditions and 167 studies, the signal is genuinely mixed: enriched in 68, depleted in 37, and direction-conflicting in 31 (directional agreement 0.63). Because Lachnoclostridium is a heterogeneous, reclassified genus whose members behave differently, the genus-level signal varies by condition, so the aggregate evidence tier is Low.
How to read these. Lachnoclostridium is a taxonomically mixed genus assembled from former Clostridium species, so a genus-level differential signal blends members with different behaviors and cannot be read as one effect. Its best-validated signal is a specific species marker (m3) for colorectal neoplasia, not a uniform genus-wide change, which is why direction conflicts between cohorts and the aggregate tier stays Low.
Internal summaries of the 167 studies we reviewed in which Lachnoclostridium 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 randomized, double-blind, placebo-controlled trial tested whether daily supplementation with two specific probiotic strains, Bifidobacterium animalis subsp. lactis XLTG11 and Lactiplantibacillus plantarum CCFM8661, could reduce recurrent respiratory tract infections (RRTIs) in children. Over 180 days, the study tracked infection frequency and duration alongside changes in gut microbiota composition, functional metabolic pathways, and immune biomarkers. The design allowed the researchers to link clinical respiratory outcomes to underlying shifts in the gut microbial community and immune regulation.
The study enrolled 120 children who had been diagnosed with recurrent respiratory tract infections. Participants were randomly assigned to receive either the probiotic combination or a matched placebo daily for 180 days. The abstract does not provide further demographic details such as age range or sex distribution.
Children receiving the probiotics had significantly reduced duration and frequency of fever, cough, upper respiratory tract infections, trachea or bronchitis, pneumonia, and overall RRTI recurrence compared with placebo (all p < 0.05). Gut microbiota profiling at day 180 showed clear community differences between groups, with the probiotic group showing greater abundance of beneficial commensal taxa and the placebo group showing more opportunistic genera. Functional pathway analysis pointed to enhanced metabolic stability in the probiotic recipients, and immune biomarker patterns showed comparatively stable IgG, IgM, and complement C3 levels, suggesting a more regulated humoral immune response. Growth trajectories remained normal in both groups.
These findings support strain-defined probiotic supplementation as a viable adjunct strategy for reducing the burden of recurrent respiratory infections in children. The parallel shifts in gut microbial composition, metabolic function, and humoral immune stability suggest the respiratory benefit may be mediated through gut-immune axis modulation rather than a direct respiratory-tract effect. Because growth remained normal, the intervention appears well tolerated over a six-month period, supporting its potential for longer-term pediatric preventive use pending further confirmatory trials.
Insomnia is a prevalent sleep disorder associated with broad metabolic, immune, and neuropsychiatric consequences, yet its association with the gut microbiome remains difficult to define across individuals. Here, we performed a cross-cohort meta-analysis of five publicly available human fecal 16S rRNA case-control datasets to identify conserved microbiome features associated with insomnia. All raw sequencing data were reprocessed using a unified analytical workflow, generating a harmonized cohort of 468 individuals while controlling for cohort-specific effects. Across cohorts, insomnia was associated with directionally consistent differences in gut microbiome structure, including a statistically significant increase in Shannon diversity (p = 0.003) and a significant group effect after covariate adjustment. Integrating four complementary statistical approaches, we identified a core set of eight gut taxa that were consistently associated with insomnia across analyses. Functional prediction and integrative filtering indicated that insomnia-related microbial changes extended beyond taxonomy, with coordinated shifts in metabolic potential encompassing pathways previously linked to host immune and neurobiological processes, thereby suggesting relevance to biological systems implicated in sleep regulation. Notably, these functional alterations were concentrated within a limited subset of taxa rather than broadly distributed across the community. Among them, the Burkholderia-Caballeronia-Paraburkholderia complex emerged as a dominant functional contributor. Independent correlation analyses validated key taxon-function relationships and reinforced a model of focused, pathway-specific microbiome remodeling. Together, these findings demonstrate that insomnia is associated with a reproducible gut microbiome signature characterized by targeted functional remodeling driven by specific microbial taxa. This study provides a cross-cohort framework for investigating microbiome-mediated metabolic and immune contexts relevant to sleep regulation.
This study tested whether gut microbiota and short-chain fatty acids (SCFAs) can support early Parkinson's disease (PD) diagnosis. A key goal was separating PD from essential tremor (ET), a common early mimic. Fecal samples were analyzed by 16S rRNA gene sequencing using both DADA2 denoising and OTU clustering. SCFAs were measured by gas chromatography-mass spectrometry. Differential taxa were found with five statistical methods, then ranked by random forest and tested with ROC curves.
Participants were 104 drug-naive early PD patients, 69 ET patients, and 61 healthy controls, recruited at Ruijin Hospital in Shanghai, China. All were aged 35 to 80 years. PD patients were at Hoehn and Yahr stage 2.5 or below and took no anti-Parkinsonian drugs. PD was split into tremor-dominant and non-tremor-dominant subtypes. Samples were divided into a test set (73 PD, 48 ET, 43 controls) and a validation set (31 PD, 21 ET, 18 controls).
Compared with healthy controls, PD showed reduced Citrobacter and Haemophilus, increased Eggerthella, and elevated isovaleric and isobutyric acids. The combined microbiota and SCFA model reached a validation AUC of 0.864. PD versus ET showed decreased Bilophila, Bacteroides, and Haemophilus, plus higher isovaleric, isobutyric, and valeric acids (validation AUC 0.825). Tremor-dominant PD was distinguished from ET (validation AUC 0.780). Tremor-dominant and non-tremor-dominant PD differed only in lower Dialister.
Gut microbiota and SCFAs may act as non-invasive candidate biomarkers for early, drug-naive PD. They could help separate PD from essential tremor, a long-standing clinical challenge. The branched-chain fatty acid rise suggests increased protein fermentation from dysbiosis. Findings are exploratory, from a single center, with modest subtype separation, so larger multi-center cohorts are needed before clinical use.
Researchers compared gut microbiota composition and short-chain fatty acid (SCFA) levels among children aged 6 to 12 with ADHD, both unmedicated and on psychostimulant medication, versus healthy controls.
Fecal samples from 30 children (10 unmedicated ADHD, 10 medicated ADHD, 10 healthy controls) underwent 16S rRNA sequencing and targeted metabolomics to profile bacterial taxa and SCFA concentrations.
Unmedicated ADHD children had lower levels of Tyzzerella, Prevotellaceae, and Coriobacteriaceae than controls, and propionic acid was negatively associated with ADHD symptom severity. Medicated ADHD children showed lower microbial diversity, distinct taxa, and lower SCFA levels than unmedicated children.
The findings point to gut microbiota and SCFAs, particularly propionic acid, as possible biomarkers linked to ADHD symptoms and suggest gut health monitoring could inform future ADHD management.
This randomized, double-blind, placebo-controlled trial tested whether the probiotic Weizmannia coagulans BC99 protects the liver of long-term alcohol drinkers. It examined liver function, kidney function, inflammation, and gut microbiota. Participants took BC99 or a maltodextrin placebo daily for 60 days. Blood and stool were sampled at day 1 and day 60. Gut bacteria were profiled by 16S rRNA gene sequencing, with LEfSe and random forest analyses used to identify key strains.
The trial enrolled 70 long-term drinkers aged 18 to 65 in Luoyang, China, all consuming at least 20 g of alcohol per day for over a year. They were split evenly into a BC99 group and a placebo group. Sixty participants completed the study. Mean age was about 43 years, and baseline characteristics did not differ between groups. People with hepatitis, cirrhosis, hypertension, or diabetes were excluded. The probiotic dose was 3 g per day at 1 times 10 to the tenth CFU.
After 60 days, the BC99 group showed significant drops in AST, total bilirubin, and gamma-GT (p less than 0.01). The abnormal rates of AST and gamma-GT fell from about 35 percent and 30 percent to zero. Kidney markers BUN and uric acid dropped, and the BUN to creatinine abnormality count fell from 14 to 5 subjects. BC99 lowered pro-inflammatory TNF-alpha and IL-6 (IL-6 fell over 30 percent) and raised anti-inflammatory IL-10. In the gut, BC99 raised Firmicutes and beneficial genera including Prevotella and Faecalibacterium, while reducing Proteobacteria and conditionally pathogenic bacteria.
The results indicate that BC99 supplementation can ease alcohol-related liver injury in long-term drinkers, offering a possible protective strategy alongside efforts to reduce drinking. The benefit appears tied to rebalancing the gut microbiota, boosting short-chain fatty acid producers and curbing pro-inflammatory, endotoxin-linked bacteria. As a single-center 60-day trial with dropouts, the findings need larger and longer studies. The exact microbial metabolites driving the effect remain to be identified. The probiotic was supplied by a commercial manufacturer, Wecare Probiotics.
This study examined whether the probiotic Bifidobacterium longum subsp. longum BL21 could mitigate symptoms of polycystic ovary syndrome (PCOS) in a DHT-induced (prenatal androgen-induced) mouse model. The researchers focused on BL21's effects on metabolic dysregulation, inflammation, and neuroprotection, framed through the gut-brain-ovary axis. Mice received a daily oral dose of 1 x 10^9 CFU of BL21 for a continuous 8-week treatment period. Outcomes assessed included body weight, glucose tolerance, serum BDNF, inflammatory markers, sex hormone levels, and gut microbiota composition via 16S rRNA gene sequencing.
The subjects were twenty-four ICR mice with prenatal androgen (DHT)-induced PCOS, an established animal model rather than human patients. The abstract does not specify how the 24 mice were divided among treatment and control groups. All findings therefore come from a controlled mouse model of PCOS, not from a human cohort.
BL21 significantly increased sex hormone levels, particularly follicle-stimulating hormone (FSH) and estradiol (E2), suggesting improved ovarian function (P < 0.05). The probiotic also curbed weight gain and improved glucose tolerance in the PCOS mice (P < 0.05). Additionally, BL21 reduced inflammatory markers, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and lipopolysaccharides (LPS), while increasing the anti-inflammatory marker IL-10. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so this study is summarized on its own terms.
These results position Bifidobacterium longum subsp. longum BL21 as a novel candidate approach for addressing hormonal, metabolic, and inflammatory disturbances in PCOS. The findings support the concept of a gut-brain-ovary axis, in which a targeted probiotic can influence ovarian hormone output and systemic inflammation together. Because this work was conducted in a mouse model, further research would be needed to establish whether similar effects occur in humans with PCOS.
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.
Researchers compared fecal microbiota between Crohn's disease patients with intestinal fibrous stenosis and those without stenosis, using a single-center cross-sectional cohort in China. The goal was to see whether gut microbes could help predict which patients develop fibrous stenosis, a complication current clinical tools struggle to forecast.
Fecal samples from 53 Crohn's disease patients (confirmed by MRI-based enterography for stenosis status) underwent shotgun metagenomic sequencing. The team compared microbial diversity, taxon abundance (order through species level), LEfSe biomarker analysis with ROC prediction accuracy, and KEGG and eggNOG functional pathway enrichment between the two groups.
Overall community diversity did not differ between groups, but 70 taxa showed significantly different abundance. Genus-level Bacteroides and Enterocloster predicted fibrous stenosis, while Actinobacteria, Bacilli, Lactobacillales, Streptococcaceae and Streptococcus predicted non-stenosis, with single-marker AUCs of 0.675 to 0.746 and a combined non-stenosis marker AUC of 0.730. Functionally, fibrous stenosis samples showed altered sphingolipid metabolism, lipoic acid metabolism, and neomycin/kanamycin/gentamicin biosynthesis pathways, plus differences across four eggNOG functional categories.
Even without overall diversity differences, specific fecal taxa and their metabolic functions tracked with fibrous stenosis, a complication that often forces endoscopic or surgical intervention once medications stop working. The findings point to fecal microbiota, particularly Bacteroides and Enterocloster abundance, as a potential non-invasive marker to flag Crohn's patients at risk for stricturing disease before it fully develops.
This single-arm pilot trial examined how a short, intensive meditation retreat changes the oral and gut microbiome. It focused on Arhatic Yoga practices combined with a vegetarian diet. Researchers collected oral and fecal samples at the start, middle, and end of a nine-day retreat in Bovina, New York. They used 16S rRNA gene amplicon sequencing and predicted metabolic functions with PICRUSt2, testing diversity changes over the three timepoints.
The study enrolled 27 healthy adult Arhatic Yoga practitioners, with 24 fecal samples and 11 saliva samples analyzed. Participants were over 18 years old and followed an identical vegetarian diet. All practitioners had prior training and distinct experience levels, practicing meditation from once weekly to more than three times weekly. Being single-arm, the study used the three retreat timepoints as comparators rather than a separate control group.
Oral microbiome richness and evenness changed significantly by the retreat's end (p below 0.05), while gut composition shifted in beta diversity (PERMANOVA p below 0.05 between early timepoints). Gut alpha diversity did not change significantly. Short-chain fatty acid producing and gut-barrier-supporting genera increased, categorized as persistent responders over time. Predicted functions showed enriched cysteine, methionine, and selenocompound metabolism. Age and gender did not significantly affect microbiome composition.
The results suggest meditation with a vegetarian diet can shift oral and gut microbiomes toward health-promoting bacteria within just days. Such microbes may influence gut-brain and gut-barrier function. The authors propose these microbial consortia could inform future probiotics. Because this was a small single-arm pilot without a control group or metabolite measurements, diet and meditation effects cannot be separated, and causation cannot be inferred.
This study examined whether probiotic supplementation could offset the effects of prenatal opioid exposure (POE) on pain sensitivity and gut microbial composition. It focused specifically on whether these effects differ by sex in offspring exposed to opioids in utero. The researchers also used RNA sequencing of the prefrontal cortex to look for sex-based molecular differences linked to POE.
The study used male and female C57BL/6 mouse offspring that were prenatally exposed to opioids. This is an animal model designed to reflect the growing number of human infants exposed to opioids in utero due to rising opioid use disorder among women of reproductive age. No human cohort was studied directly.
Prenatal opioid exposure produced clearly sex-dependent effects on both nociception and the gut microbiome. Opioid-exposed females showed enrichment of commensal bacteria, including Lactobacillus, compared to opioid-exposed males, and displayed decreased nociceptive sensitivity. Opioid-exposed males, in contrast, showed increased nociceptive sensitivity, and prefrontal cortex RNA sequencing revealed additional sex-based molecular differences. Probiotic supplementation mitigated these sex-dependent changes in both pain sensitivity and gut dysbiosis.
The findings suggest that sex is an important variable in how prenatal opioid exposure alters the gut microbiome and pain processing in offspring, and that these two effects may be mechanistically linked. Because probiotic supplementation mitigated both the microbial dysbiosis and the nociceptive changes, targeting the gut microbiome could be a viable strategy for reducing adverse outcomes in opioid-exposed infants. This work also underscores the need for sex-specific approaches when designing microbiome-based interventions for prenatal opioid exposure.
This study investigated Roseburia hominis as a novel candidate probiotic (next-generation live biotherapeutic) for treating obesity and related metabolic disease. The researchers first examined how R. hominis abundance related to obesity status, then tested whether supplementing R. hominis could prevent metabolic disturbances in a diet-induced obesity model. They also explored a possible mechanism involving nicotinamide riboside production and Sirtuin1/mTOR signaling.
The abstract describes stool samples compared between obese subjects and lean controls, indicating a human cohort used to establish the association between R. hominis abundance and body mass index and serum triglycerides. The interventional portion of the study was conducted in mice fed a high-fat diet to model diet-induced obesity. Specific numbers of human subjects or mice, and demographic details, are not given in the abstract.
Roseburia hominis was depleted in the stool of obese subjects compared with lean controls, and its abundance was negatively correlated with body mass index and serum triglycerides. In high-fat-diet mice, supplementing R. hominis prevented body weight gain, corrected glucose and lipid metabolism disorders, prevented fatty liver, inhibited white adipose tissue expansion, and reduced brown adipose tissue whitening, while boosting lean-associated microbial species. These effects were linked in part to R. hominis production of nicotinamide riboside and upregulation of the Sirtuin1/mTOR signaling pathway.
The findings position Roseburia hominis as a promising next-generation live biotherapeutic candidate for preventing obesity and metabolic disease. Because its depletion tracks with obesity and adverse metabolic markers in humans, restoring this commensal species could represent a targeted microbiome-based strategy rather than a broad-spectrum probiotic approach. The nicotinamide riboside and Sirtuin1/mTOR mechanism offers a specific pathway for further mechanistic and translational research.
This study investigated whether alterations in the gut microbiome are associated with allograft rejection in kidney transplant (KT) recipients. Researchers used 16S rRNA gene amplicon sequencing to characterize gut microbiome composition and function over time. They tracked how the microbiome changed from the pre-transplant, chronic kidney disease (CKD) state through recovery, and examined shifts occurring before and after rejection events. Functional analysis focused on the microbiome's capacity to produce short-chain fatty acids, including propionate and butyrate.
The study analyzed 562 samples collected from 245 individuals as part of a multicenter prospective study. Of these participants, 217 had received a kidney transplant. This design allowed comparison of microbiome trajectories across the CKD-to-post-transplant recovery period and around the time of graft rejection events.
Overall, gut microbiome composition gradually recovered after transplantation, mirroring the CKD-to-health transition, as shown by increasing Shannon diversity. However, prior to graft rejection, microbial diversity decreased along with a reduction in short-chain fatty acid-producing taxa. Functional analysis confirmed a decreased potential for short-chain fatty acid production before rejection, and this was validated using quantitative PCR targeting propionate and butyrate production potential. After rejection, these microbiome features normalized again, and the alterations preceding rejection partially overlapped with microbiome signatures previously reported in CKD patients.
The findings suggest that gut microbiome changes, particularly loss of diversity and short-chain fatty acid-producing taxa, may precede and potentially help predict graft rejection in kidney transplant recipients. This raises the possibility that monitoring microbiome composition and short-chain fatty acid production capacity could serve as an early warning signal for clinicians. Because these pre-rejection alterations partially resemble CKD-associated microbiome signatures, they may reflect a shared pathway of microbial dysfunction linked to immune dysregulation. This work supports further exploration of the gut microbiome as a noninvasive biomarker source and a potential target for interventions to support graft survival.
This cross-sectional study looked for early gut microbiome features linked to steatotic liver disease (SLD) in young adults. It aimed to spot microbial changes before advanced liver disease develops. Liver fat was measured with validated MRI volumetric liver fat fraction, and participants were grouped as no, mild-moderate, or severe SLD. Stool microbiota was profiled by 16S rRNA gene sequencing, comparing diversity and taxon abundance across the SLD groups.
The study drew 588 community-dwelling adults, all aged 27 years, from the Raine Study in Western Australia. About 52 percent were female, with a median body mass index of 24. Of these, 488 (83 percent) had no SLD, 76 (12.9 percent) had mild-moderate SLD, and 24 (4.1 percent) had severe SLD. People with other liver diseases or conditions affecting the gut microbiome were excluded from the analysis.
Severe SLD was linked to significantly lower microbial diversity, including observed features (p=0.015), Pielou evenness (p=0.001), and Shannon diversity (p=0.002). Composition differed for both mild-moderate (p=0.004) and severe SLD (p=0.001). Severe SLD showed depletion of butyrate producers including Coprococcus, Faecalibacterium, and Odoribacter after adjustment (FDR q below 0.1). Proinflammatory taxa such as Lachnoclostridium were higher in SLD, echoing patterns seen in other inflammatory diseases.
The results show gut microbiome changes accompany fatty liver even in young adults, before advanced disease. Depleted butyrate-producing bacteria may be relevant to SLD development. This overlap with obesity, cardiovascular disease, and inflammatory bowel disease suggests a shared inflammatory microbial signature. Because the design was cross-sectional, causation cannot be established, but the pattern offers a potential basis for early risk identification and butyrate-targeted interventions.
The study examined how Zhuyang Tongbian Decoction (ZTD), a treatment for functional constipation (FC), affects the gut microbiome and related inflammatory markers. Researchers used 16S rRNA sequencing, metagenomics, and metabolomics to track changes in intestinal flora composition and microbiota metabolic function. They also measured fecal short-chain fatty acid (SCFA) levels and serum concentrations of TLR4, NF-κB, TNF-α, and IL-6 before and after treatment.
The study included 40 patients with functional constipation, randomly divided into a control group (20 cases, treated with lactulose) and a treatment group (20 cases, treated with ZTD). Twenty healthy volunteers were also recruited during the same period, presumably for comparison. Sample sizes were small, consistent with the pilot nature of the study.
The ZTD treatment group showed a significant increase in beneficial bacteria, including Bifidobacterium, Lactobacillus, and Faecalibacterium prausnitzii (P < 0.05). Desulfobacterota and Ruminococcus were significantly reduced in the treatment group (P < 0.05). Fecal acetic and propionic acid levels, both short-chain fatty acids linked to anti-inflammatory commensal activity, were also affected by treatment, though the abstract text describing the exact direction and magnitude was cut off.
The findings suggest ZTD may relieve functional constipation partly by reshaping the gut microbiota toward beneficial, SCFA-producing organisms such as Faecalibacterium prausnitzii while reducing potentially less favorable taxa. This points to a microbiome-mediated mechanism, possibly involving reduced inflammatory signaling through the TLR4/NF-κB pathway, as part of ZTD's therapeutic effect. As a pilot study with a small sample size, these results support further, larger trials to confirm the mechanism and clinical benefit.
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 asked whether the seasons change the gut microbiome and the circulating endocannabinoidome together in humans. The endocannabinoidome is a network of fat-derived signaling molecules tied to inflammation and metabolism. Researchers sampled the same people at the end of winter and the end of summer. They measured fecal bacteria by 16S rRNA sequencing and plasma lipid mediators by mass spectrometry, while tracking diet, activity, and vitamin D.
The cohort was 48 adults living in Quebec City, Canada, at latitude 46.8 degrees north. This city swings from about minus 18 degrees Celsius in winter to 25 degrees Celsius in summer. Participants gave plasma and fecal samples at both a winter and a summer visit, roughly six months apart. People with recent antibiotic use, enteropathies, pregnancy, or heavy alcohol or cannabis use were excluded. All were relatively healthy adults in an industrialized setting.
Most circulating N-acylethanolamine mediators dropped in summer versus winter, including PEA, LEA, EPEA, and DHEA. The endocannabinoid AEA did not fall, and among the 2-monoacylglycerols only 2-PG rose. Gut bacterial composition also shifted, with some families decreasing and others increasing in summer. The size of the microbiome shift tracked the size of the mediator shift. These changes were not explained by adiposity, dietary intake, physical activity, or vitamin D status.
The findings argue that season is a real confounder in studies of the gut microbiome and lipid signaling. Trials measuring these systems may need to account for the time of year. Because vitamin D and lifestyle did not explain the changes, other seasonal cues such as temperature or time indoors may drive them. This is one cohort sampled over a single year, so recurrence and causation remain unproven. The associations are correlational.
The study explored how the gut microbiome relates to anti-tuberculosis drug-induced liver injury (ADLI). Liver injury is a serious complication of tuberculosis treatment, and its microbial basis was unclear. Using a nested case-control design, researchers compared tuberculosis patients who developed liver injury with matched patients who did not. Stool samples underwent 16S ribosomal DNA sequencing before and during treatment. Mouse models tested individual and combined anti-tuberculosis drugs.
The human study collected 400 faecal samples from newly diagnosed pulmonary tuberculosis patients at an infectious disease hospital in China. It included 100 liver-injury patients and 100 matched controls, each sampled before (T1) and after (T2) treatment. All patients received the same standard isoniazid, rifampicin, pyrazinamide and ethambutol regimen. The animal arm used 64 male C57BL/6 mice in eight groups, dosed by gavage for 14 days with single drugs or combinations.
Anti-tuberculosis treatment lowered gut microbial richness and diversity in both groups, with a decline in the phylum Firmicutes and significant structural changes. Inflammatory cytokines rose markedly in the liver-injury group after treatment. Mean TNF-alpha reached 304.67 versus 164.02 in the non-injury group, IL-6 reached 15.41 versus 4.57, and IL-1beta reached 21.29 versus 12.06. Liver-injury and non-injury patients showed distinct differential genera at both time points. In mice, each drug and combination caused liver injury and its own dysbiosis pattern, including changes in Bifidobacterium.
The work indicates that anti-tuberculosis therapy disrupts the gut microbiome and that liver injury is accompanied by specific microbial and inflammatory signatures. Depletion of beneficial short-chain fatty acid producers and expansion of opportunistic bacteria may intensify inflammation. This suggests the gut microbiome could help identify patients at risk of drug-induced liver injury. The study was single-center with an uncontrolled diet, so it shows associations. Microbiome-targeted strategies to reduce liver injury would need further testing.
This study tracked how the gut microbiome changed when volunteers were deliberately infected with Shigella in a controlled human infection model. Researchers profiled fecal microbiomes by 16S rRNA sequencing before and during infection, after antibiotics, and after recovery. The design compared people who developed shigellosis, meaning severe symptoms like severe diarrhea, fever, or abdominal pain, against those who did not. The goal was to explain why some exposed people get sick while others stay asymptomatic, and to find microbiome features linked to protection or susceptibility.
The study followed 45 adults infected with Shigella strain 53G in a controlled challenge trial registered as NCT02816346. Participants ranged across young and middle-aged adults and included both men and women. All were monitored longitudinally through infection, antibiotic treatment, and clinical recovery. This human challenge design let researchers observe the same individuals before and after a known exposure. Participants were classified by whether they progressed to shigellosis or avoided severe symptoms.
Alpha diversity dropped more sharply in individuals who developed shigellosis. Shifts in microbial composition during infection and antibiotic treatment were significantly larger in the shigellosis group than in those without severe disease. People with shigellosis kept persistent microbiome changes after recovery, including taxa associated with gut inflammation. Those without shigellosis returned to a composition resembling their pre-infection state. Participants who avoided shigellosis started with a greater abundance of taxa tied to short-chain fatty acid production. This baseline difference distinguished those who would develop severe disease from those who would not.
The results suggest the baseline microbiome may shape who develops severe Shigella disease, pointing to short-chain-fatty-acid-producing taxa as potential protective factors. This could inform preventive or microbiome-based strategies against diarrheal illness. Persistent post-recovery changes may help explain chronic sequelae after enteric infection, such as irritable bowel syndrome and altered gut permeability. The cohort was small and studied under controlled conditions, so associations do not prove that these taxa cause protection.
This study searched for gut bacteria that can help trigger multiple sclerosis, an autoimmune disease of the central nervous system. Researchers used a two-step strategy to move past mere association. First they compared gut microbes in identical twins where only one twin had MS, minimizing genetic and early-life confounders. Then they transferred bacteria from the small intestine of selected twins into germfree mice bred to develop MS-like disease.
The human cohort was 81 monozygotic twin pairs discordant for MS, with fecal 16S rRNA sequencing. Four pairs also volunteered for enteroscopy to sample the ileum and colon directly. The animal model used germfree transgenic RR mice carrying a T-cell receptor against myelin, which develop spontaneous experimental autoimmune encephalomyelitis only after bacterial colonization. Human ileal material was gavaged into these mice, and both sexes of mice were tested.
Among the 81 twin pairs, 51 bacterial taxa differed by disease status, including reduced propionate producers in MS twins. Fecal diversity itself did not differ. Ileal microbiota from an MS twin triggered disease in 5 of 6 female mice, while material from her healthy cotwin caused none. In a second male twin pair, MS material caused disease at a significantly higher rate. Sickened mice showed dominant blooming of two Lachnospiraceae species and increased Th17 cells.
The work moves gut-MS research from correlation toward function, identifying specific ileal Lachnospiraceae bacteria that can spark MS-like disease in susceptible mice. This could open selective microbiome-targeted therapies. The female bias in affected mice echoes the female preponderance of human MS. These are proof-of-concept results from very few human donors, and mouse immunity differs from human. The culprit species were minor in human stool, so findings need confirmation by monocolonization and larger studies.
This translational study asked how commensal Bacteroides and their type VI secretion system (T6SS) influence gastrointestinal acute graft-versus-host disease after stem cell transplantation. The T6SS is a bacterial weapon that injects toxins into competing microbes. Researchers profiled gut microbiota, immune markers, metagenomes, and metabolites in transplant patients. They then built a mouse model, compared wild-type bacteria against a T6SS-deleted mutant, and used mediation analysis to link T6SS, bile acids, and disease in patient samples.
The clinical cohort was 71 patients undergoing allogeneic haematopoietic stem cell transplantation, including 24 with gastrointestinal graft-versus-host disease and 47 without. Groups were balanced on age, sex, donor type, and conditioning regimen. The experimental arm used a mouse bone marrow transplantation model in BALB/c recipients. Mice received wild-type Bacteroides, a T6SS-deleted mutant, or control, plus separate experiments giving the primary bile acid chenodeoxycholic acid. Tissues were analysed by flow cytometry, histology, and cytokine assays.
Patients with gastrointestinal graft-versus-host disease had lower microbial richness, more activated CD4 T cells, and elevated cytokines including IL-6, IL-8, and TNF-alpha. Non-disease patients carried higher abundance of T6SS structural genes. In mice, wild-type Bacteroides improved survival, preserved the intestinal barrier and mucus layer, raised tight junction proteins, and reduced T-cell activation, while the T6SS-deleted mutant lost all protection. KEGG analysis showed primary bile acid biosynthesis was the most affected pathway. Primary bile acids accumulated with T6SS loss, and giving chenodeoxycholic acid shortened survival by activating T cells and breaking the barrier.
The findings point to the T6SS-bile acid axis as a possible therapeutic target for graft-versus-host disease after transplantation. Boosting commensal T6SS activity or lowering primary bile acids may protect the intestinal barrier. Mediation analysis in patients suggested T6SS gene families reduce disease risk partly through primary bile acids. Much of the mechanism rests on mouse models, so human causal effects remain unproven. The authors propose engineered T6SS bacteria and novel bile acid interventions as future research directions.
This study examined how fasting changes the gut microbial community and whether combining fasting with microbiota-accessible carbohydrates (MACs) could be used to deliberately reshape gut bacteria. The researchers tested whether fasting creates conditions that make MAC administration more effective at increasing specific commensal bacteria. They also compared fecal IgA levels between fasting plus MAC intervention and MAC administration alone. The effects of different types of MACs on the resulting microbiota composition were also assessed.
The abstract does not specify a human cohort or sample size, and the experiments appear to be conducted in an animal or laboratory model system used to test fasting and MAC interventions on the gut microbiome. No demographic, clinical, or population details are given. The subjects were evaluated for changes in gut bacterial composition and fecal IgA levels following the interventions.
Fasting altered the structure of the gut microbial community on its own, and combining fasting with MAC administration produced more profound effects than MAC administration alone. The fasting plus MAC intervention increased specific gut bacteria and raised fecal IgA levels compared with MACs given without fasting. These compositional changes were specific to the type of MAC used, and the researchers identified a protocol that effectively combined fasting with MACs to increase levels of Bifidobacterium.
The findings suggest that fasting can prepare a favorable gut environment that enhances the ability of microbiota-accessible carbohydrates to selectively modulate specific bacterial populations. This points to a practical strategy for targeted, MAC-specific enrichment of beneficial bacteria such as Bifidobacterium by pairing dietary carbohydrate interventions with fasting periods. Because the effect also raised fecal IgA, fasting plus MAC protocols may influence mucosal immune readouts alongside microbiome composition. Salmonella, Salmonella enterica, typhoid, and Enterobacteriaceae are not mentioned in this abstract.
This study asked whether the gut microbiota mediates exercise's dose-dependent effect on memory and hippocampal neurogenesis. Researchers compared sedentary mice with moderate and intense treadmill running groups. They measured object recognition and object location memory, counted neural precursors and progenitors, and sequenced the caecal microbiota. To test causation, they transplanted feces from exercised donors into sedentary mice and repeated the behavioral and neurogenesis assays.
The subjects were 100 male C57BL/6J mice, aged 11 weeks at the start and euthanized at 17 weeks, in Spain. Ten mice went to each behavioral group. Groups were sedentary, moderate runners at 1200 cm/min for 40 minutes, intense-time runners at 60 minutes, and intense-velocity runners at 1800 cm/min. Microbiota composition used 5 mice per group, and fecal transplant experiments used 6 per group. No humans were studied.
Only moderate exercise improved memory. The moderate group had the highest discrimination indices in object recognition and location tests (p below 0.001), while intense-time and intense-velocity groups did not improve, an inverted-U dose response. Moderate exercise raised the number of neural precursors and immature neurons, which correlated with cognitive gains. Microbiota diversity was higher in moderate runners, with a distinct profile. Fifteen genera differed across groups and four correlated with cognition. Transplanting moderate-runner feces into sedentary mice reproduced both the memory and neurogenesis benefits.
The results provide causal evidence that exercise-induced gut microbiota changes are sufficient to transfer cognitive and neurogenic benefits to sedentary animals. This links exercise dose, the gut, and brain function. The inverted-U pattern implies that more exercise is not always better for cognition, supporting the idea of personalized exercise doses. Because the work is in male mice only, translation to humans and to females remains to be established.
This study examined cocoa (Theobroma cacao L.) bean fermentation, the spontaneous process that shapes the final flavour of chocolate. The researchers investigated how abiotic factors (pH and temperature) and biotic factors (bacterial and fungal microbiota) interact to produce key flavour attributes in premium chocolate. They used genome-resolved metagenomics to identify the metabolic traits within the fermentation microbial community responsible for flavour development. They then tested whether a defined microbial consortium could reproduce those fine flavour attributes under controlled conditions.
The study drew on cocoa bean fermentation samples collected from farms in Colombia. From these samples, the researchers characterized the natural bacterial and fungal community and used genome-resolved metagenomics to build a picture of the metabolic capacities present. They then assembled a separate, defined and metabolically competent microbial consortium, rather than studying a human or animal cohort, to test controlled fermentation. A trained tasting panel was also used to evaluate the resulting chocolate.
The pH, temperature, and combined bacterial and fungal microbiota composition of the fermentation samples all influenced key flavour attributes of the resulting premium chocolate. Genome-resolved metagenomics showed that the metabolic traits needed for flavour development were redundantly encoded across multiple members of the fermentation community, not confined to a single organism. Using a defined microbial consortium built from this information, the researchers replicated fine flavour attributes of chocolate under controlled conditions. This was confirmed through omics analyses, metabolic network modeling, and evaluation by a trained tasting panel.
These findings show that the flavour-relevant functions of spontaneous cocoa fermentation can be captured in a defined, reproducible microbial consortium rather than relying on uncontrolled natural fermentation. This provides a basis for designing standardized fermentation starters that can reliably reproduce fine chocolate flavour characteristics. Such starters could help cocoa producers achieve consistent premium quality across batches and locations. The approach also demonstrates a model for linking metagenomic and metabolic data to sensory outcomes in food fermentation more broadly.
This study examined seasonal changes in gut microbiota composition and function across four bear species: giant pandas, Asian black bears, brown bears, and polar bears. Researchers combined comparative seasonal microbiome analysis with fecal microbiota transplantation (FMT) experiments in mice to test whether bear gut microbiota actively drives host energy metabolism. The core question was whether giant pandas, long considered metabolically unique due to their specialized herbivorous diet and low metabolic rate, actually rely on a distinct microbial regulatory mechanism compared to other bears.
The subjects were four Ursidae species: giant pandas (Ailuropoda melanoleuca), Asian black bears (Ursus thibetanus), brown bears (Ursus arctos), and polar bears (Ursus maritimus), sampled across seasons to capture gut microbiota dynamics. The abstract does not specify exact animal counts or sampling sites. Recipient mice were also used as a secondary population in the fecal microbiota transplantation experiments to test the functional effects of bear gut microbiota on host metabolism and appetite.
The gut microbial composition was similar across all four bear species, with Firmicutes and Proteobacteria as the dominant phyla. Firmicutes became enriched in winter, which enhanced lipid metabolism and helped the bears adapt to seasonal dietary differences, pointing to a convergent microbial functional strategy shared across the Ursidae family rather than a panda-specific mechanism. In FMT experiments, winter bear gut microbiota transferred stronger capacity to regulate host energy metabolism and appetite in mice, increasing energy intake, demonstrating that these microbial shifts causally promote seasonal metabolic adaptation.
By showing convergent, shared microbial functional strategies across giant pandas, black bears, brown bears, and polar bears, the findings challenge the long-standing view that giant panda gut microbiota is metabolically unique among bears. This reframes seasonal energy adaptation in Ursidae as a family-wide, diet-responsive microbiome trait rather than an evolutionary novelty confined to pandas. The FMT results also suggest that bear-derived winter microbiota could serve as a model system for studying microbiome-driven regulation of energy intake and appetite in mammals more broadly.
Researchers asked whether gut and oral microbiome profiles taken at hospital admission reliably predict severity and complications of acute pancreatitis. They tested this across 276 prospectively enrolled patients from 20 Dutch hospitals.
Admission saliva and rectal samples underwent 16S rDNA sequencing. Genus abundance and diversity were compared across severity subgroups, and each association was scored as moderately robust (significant in 2 models) or highly robust (significant in 3 or more models).
Rectal alpha diversity was lower in necrotising (Shannon Index 3.55, n=49) than oedematous pancreatitis (3.63, n=218, p=0.026). Of 270 rectal and 138 saliva genera linked to severity or complications, only 3 (Anaeroglobus and Finegoldia in saliva, Lachnospiraceae_FE2018_group in rectal samples) reached high robustness, and 10 of 14 previously reported associations pointed the opposite direction here.
The scarcity of replicable admission microbiome signals, despite hundreds of tested genera, suggests single-timepoint profiling is an unreliable severity marker. The authors call for longitudinal studies to clarify whether microbiome shifts drive or merely follow disease progression.
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 characterized gut microbiota in Colombian children with autism spectrum disorder (ASD) and tested two microbiota-targeted interventions. The interventions were an anti-inflammatory diet and a probiotic formulation. Researchers ran shotgun metagenomic sequencing on fecal samples in a two-phase design. Phase one compared children with ASD to typically developing (TD) controls. Phase two randomized children with ASD to a 12-week intervention. They measured alpha diversity (Shannon, Pielou, Chao1), differential genus abundance, and correlations between bacterial genera and 11 plasma cytokines.
Subjects were children in Colombia, a Latin American population under-represented in prior microbiome work. Phase one included 23 children with ASD and 7 typically developing controls. Phase two enrolled 17 children with ASD who completed the 12-week intervention. They were split across three arms: control (n=6), anti-inflammatory diet (n=5), and probiotics (n=6). Analyses also stratified children by the presence of functional gastrointestinal disorders (FGIDs), comparing ASD and TD subgroups with and without gut symptoms.
Children with ASD showed a higher Firmicutes/Bacteroidetes ratio (0.71) than TD children (0.48) and enrichment of seven pro-inflammatory genera. Global alpha diversity did not differ significantly (Shannon P = 0.21). Within ASD, having FGIDs was linked to reduced microbial richness versus TD children (Chao1 P = 0.033). Cytokine-microbiota networks in ASD were fragmented, dominated by IFN-gamma and MCP-1 hubs. After the diet, six genera rose significantly (top two at FDR P = 0.014 and 0.024). Probiotics produced significant genus shifts and reoriented immune networks toward regulatory cytokines and SCFA-producing taxa.
The findings support gut microbiota as both a biomarker and a therapeutic target in autism, and add data from an under-studied Latin American population. Both diet and probiotics reorganized microbe-immune networks toward cooperative, regulatory configurations, even though overall diversity barely moved. This suggests targeted network effects rather than broad diversity shifts. The authors stress caution. Small arm sizes, a short 12-week window, and no SCFA metabolomic validation limit inference. Larger randomized trials with multi-omics are needed before clinical claims.
This study examined whether person-to-person transmission of gut microbes, not just diet, helps explain why traditional microbiomes shift toward an industrialized pattern after immigration. Researchers used germ-free mice colonized with human donor stool to test how sharing air and physical contact between mice carrying different donor microbiomes affects microbial composition. They then exposed the resulting microbiomes to dietary ingredients and food additives common in industrialized diets to see how composition changes translated into metabolic outcomes, including weight gain.
The study did not involve human subjects directly. Instead, germ-free mice were colonized with human donor stool collected from the United States and from Thailand, creating humanized mouse models representing an industrialized and a traditional microbiome. Transmission and metabolic effects were then measured in these colonized mice under shared-air or co-housing conditions.
Both shared air and physical contact enabled bidirectional microbial transmission between the U.S. and Thai humanized mice. U.S. mucus-degrading taxa such as Akkermansia transferred into Thai microbiomes, while potentially health-promoting Thai-derived bacteria colonized U.S. microbiomes, with the host's baseline microbiome shaping how much remodeling occurred. When exposed to industrialized dietary ingredients and food additives, the U.S. microbiome responded differently than the Thai microbiome, with food additives reducing Akkermansia and the U.S. microbiome showing a predisposition toward weight gain under these dietary conditions.
The findings suggest that shared living environments, not diet alone, are an underappreciated route by which industrialized-style microbiomes and their metabolic consequences spread between people. Notably, sharing air supply or co-housing with a Thai-derived microbiome mitigated the U.S. microbiome's predisposition toward diet-induced weight gain, pointing to a protective effect of microbial transmission from traditional microbiomes. This implies that interventions aimed at preventing microbiome-related metabolic disease may need to consider household and community-level microbial exposure alongside dietary changes.
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 cross-sectional study examined how dietary patterns relate to gut microbiota, the metabolite TMAO, and inflammation in chronic kidney disease (CKD). It focused on low-protein high-fiber (LP-HF) versus high-protein low-fiber (HP-LF) diets. Diet was assessed by three-day food records with nutrient analysis. Fecal microbiota was profiled by 16S rRNA sequencing. Plasma was analyzed for TMAO and cytokines. Fecal butyryl-CoA transferase and plasma intestinal fatty-acid-binding protein were measured as markers of butyrate production and gut permeability.
The study enrolled 135 patients with non-dialysis CKD and 19 healthy controls in Bangkok, Thailand. CKD patients were in stages 3a, 3b, and 4, and were older than controls with higher BMI, HbA1c, and triglycerides. Mean age of CKD patients was 65 years, and 54% were men. Mean estimated glomerular filtration rate was 43 mL/min/1.73 square metres. By diet, CKD subgroups included 17 on LP-HF and 32 on HP-LF. Subgroups had similar clinical parameters apart from dairy protein and fiber intake.
CKD patients differed from controls in beta diversity (p = 0.003) and had depleted short-chain fatty acid producers, including Bifidobacterium, Faecalibacterium, and Subdoligranulum. Plasma TMAO was far higher in CKD than controls (11.46 vs 2.43 micromolar, p < 0.001). Fecal butyrate marker BCoAT was lower and gut permeability marker I-FABP was higher in CKD. IL-8, IL-18, and MCP-1 were also elevated. The LP-HF subgroup had more SCFA producers like the Lachnospiraceae NK4A136 group and Eubacterium ruminantium group. The HP-LF subgroup was enriched in Klebsiella and had higher TMAO, IL-18, and MCP-1.
The results suggest a low-protein, high-fiber diet is associated with a less dysbiotic gut profile in CKD, favoring short-chain fatty acid producers over proteolytic taxa. This dietary pattern tracked with lower TMAO and lower inflammatory markers. Because TMAO and inflammation are linked to cardiovascular and kidney disease progression, shifting diet toward fiber and away from protein could plausibly benefit gut and metabolic health. The study is cross-sectional and observational, so it cannot prove that diet causes the microbiota or biomarker differences. Controls were younger and fewer, and dietary subgroups were small, so findings need confirmation in trials.
Researchers tested whether Sini-San (SNS), a classical traditional Chinese medicine formula, protects against liver fibrosis by acting on bile acid metabolism and the gut-liver axis.
Liver fibrosis was induced in mice with carbon tetrachloride injections or a high-fat, high-sugar diet, then treated orally with SNS. Investigators measured liver injury markers, fibrosis and apoptosis proteins, serum bile acid profiles by LC-MS/MS, bile acid enzyme and transporter expression, and gut microbiota by 16S rRNA sequencing, then repeated key experiments with choline chelation, antibiotic-induced pseudo-sterile conditions, and fxr knockout mice.
Fibrotic mice showed dysregulated bile acid synthesizing enzymes (CYP7A1, CYP27A1), transporters (Bsep, Ntcp, Asbt, Oatp), the FXR receptor, and disrupted gut microbiota. SNS treatment reduced liver injury and fibrosis, corrected bile acid imbalance, normalized these genes, and restored microbial diversity, but its antifibrotic effect was lost after choline chelation, antibiotic treatment, or fxr knockout.
The findings indicate Sini-San's antifibrotic action depends on an intact gut microbiota and FXR signaling, positioning bile acid and gut-liver axis modulation as a multitargeted therapeutic mechanism for liver fibrosis.
We aim to analyse the microbiota composition in RLS patients and its relationship with the different RLS phenotypes.
We recruited idiopathic RLS (RLS) and insomnia (INS) patients and healthy subjects (CTRL). Validated questionnaires (PSQI, IRLS, ISI, BDI-II) were administered in the RLS and INS. Fecal microbiota was analysed by 16S rRNA gene sequencing according to Illumina metagenomics standard procedure on MiSeq Platform. Dada2 pipeline was used to process sequencing data, while DESeq2 and Aldex2 tools were used to calculate differential abundance taxa, correcting for age, sex, Body Mass Index, sequencing run and presence of mood disorders.
The sample included 37 RLS (28 females, mean age 64.78 years), 31 INS (22 females, mean age 60.64 years) and 33 CTRL (24 females, mean age 62.54 years). Differential abundance analysis revealed a statistically significant decrease in the abundance of Lachnoclostridium and Flavonifractor genera in RLS compared to CTRL and INS, but not in the INS compared to CTRL. Lachnoclostridium abundance tended to decrease with long disease duration and a predominant motor phenotype. In the RLS group, several genera were identified as significantly associated with IRLS and PSQI scores.
Although only a few previous studies have reported the presence of small intestinal bacterial overgrowth (SIBO) in RLS, to the best of our knowledge this is the first study to highlight significant differences in the gut microbiota composition of RLS compared to both CTRL and INS, identifying a specific RLS metagenomic signature.
This study analyzed a newly built resource called curatedMetagenomicData (cMD) 3, a uniformly processed collection of over 22,000 human microbiome samples with manually curated metadata. The researchers combined data across 94 studies and 42 countries to make large-scale meta-analysis possible, something that had been difficult due to a lack of standardization across public datasets. Using this resource, they searched for microbial species and functions associated with host traits and disease status. They also developed a new metric, the oral enrichment score (OES), based on the relative abundance in the gut of bacteria that are typically found in the oral cavity rather than the gut.
The analysis drew on more than 22,000 human microbiome samples aggregated from 94 separate studies conducted across 42 countries. This is a public, pooled metagenomic dataset rather than a single original cohort recruited for this study. The abstract does not give specific demographic breakdowns beyond noting that sex, age, body mass index, and disease status were among the host variables examined across this large, internationally diverse sample collection.
The meta-analysis identified hundreds of microbial species and thousands of microbial functions that were significantly associated with a person's sex, age, body mass index, and disease status. The team catalogued these associations as a reference resource for the field. Most notably, they found that a higher oral enrichment score (OES), meaning greater relative abundance of oral-type bacteria in the gut, was a consistent feature of individuals with disease. The overall patterns identified across the dataset were described as modest but widely shared across the many studies pooled together.
The findings suggest that OES can serve as a simple, quantifiable signal of altered gut microbiome health, since oral bacteria showing up in the gut appears to track with disease status across many different conditions and populations. Because cMD 3 is described as reproducible and readily updatable, it offers an ongoing reference dataset that other researchers can use to validate microbiome-disease associations. This kind of large, standardized meta-analysis approach could help establish more generalizable, cross-study biomarkers of microbiome health rather than relying on findings from single, smaller cohorts.
This study examined how SARS-CoV-2 infection reshapes the gut microbiota in people living with HIV, and whether those changes track with COVID-19 severity. Researchers analyzed stool over time using 16S rRNA gene sequencing. Samples from infected patients were grouped by time since onset: within 8 days, 8 to 14 days, and one month or later. They compared diversity and composition against uninfected controls and used LEfSe and predicted metabolic function to identify shifts and their links to disease course.
The infected group was 12 hospitalized men living with HIV and confirmed COVID-19, with a median pre-infection CD4 count of 671 cells per microliter. Their median age was 47 years. Controls were 19 healthy adults and 25 uninfected people living with HIV, recruited in Tokyo, Japan. All patients had received antiretroviral therapy for over a year with suppressed HIV. Seven were mildly ill, four moderately, and one severely. Eight of the 12 had comorbidities such as asthma, diabetes, or dyslipidemia. All recovered and were discharged.
Overall diversity in infected patients did not differ significantly from controls, but diversity did separate by disease severity. Mild cases showed a greater rise in diversity in the second week than moderate to severe cases. After onset, the Clostridia class fell, including short-chain fatty acid producers, while Gammaproteobacteria and Negativicutes rose. This dysbiosis persisted at least one month, sometimes after recovery. By one month, Enterobacteriaceae, mainly Escherichia-Shigella, increased and were enriched in the two patients who developed post-acute sequelae. Predicted carbohydrate, amino acid, and xenobiotic metabolism pathways were enhanced in infected patients.
The findings suggest people living with HIV may show delayed recovery of the gut environment after COVID-19, even once the illness resolves. A persistent drop in short-chain fatty acid producers plus a rise in opportunistic pathogens could favor inflammation. The authors link this dysbiosis to COVID-19 severity and to post-acute sequelae, framing the gut as a potential contributor. The cohort was small, only 12 patients with just two developing long COVID, and lacked pre-infection samples. Conclusions are associative and need larger validation.
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.
The widespread availability of antiretroviral therapy (ART) has dramatically reduced mortality and improved life expectancy for people living with HIV (PLWH). However, even with HIV-1 suppression, chronic immune activation and elevated inflammation persist and have been linked to a pro-inflammatory gut microbiome composition and compromised intestinal barrier integrity. PLWH in urban versus rural areas of sub-Saharan Africa experience differences in environmental factors that may impact the gut microbiome and immune system, in response to ART, yet this has not previously been investigated in these groups. To address this, we measured T cell activation/exhaustion/trafficking markers, plasma inflammatory markers, and fecal microbiome composition in PLWH and healthy participants recruited from an urban clinic in the city of Harare, Zimbabwe, and a district hospital that services surrounding rural villages. PLWH were either ART naïve at baseline and sampled again after 24 weeks of first-line ART and the antibiotic cotrimoxazole or were ART-experienced at both timepoints.
Although expected reductions in the inflammatory marker IL-6, T-cell activation, and exhaustion were observed with ART-induced viral suppression, these changes were much more pronounced in the urban versus the rural area. Gut microbiome composition was the most highly altered from healthy controls in ART experienced PLWH, and characterized by both reduced alpha diversity and altered composition. However, gut microbiome composition showed a pronounced relationship with T cell activation and exhaustion in ART-naïve PLWH, suggesting a particularly significant role for the gut microbiome in disease progression in uncontrolled infection. Elevated immune exhaustion after 24 weeks of ART did correlate with both living in the rural location and a more Prevotella-rich/Bacteroides-poor microbiome type, suggesting a potential role for rural-associated microbiome differences or their co-variates in the muted improvements in immune exhaustion in the rural area.
Successful ART was less effective at reducing gut microbiome-associated inflammation and T cell activation in PLWH in rural versus urban Zimbabwe, suggesting that individuals on ART in rural areas of Zimbabwe may be more vulnerable to co-morbidity related to sustained immune dysfunction in treated infection. Video Abstract.
This study asked whether gut bacteria and their short-chain fatty acids shape gastric cancer, and by what mechanism. Researchers profiled fecal and blood bacteria and short-chain fatty acids in patients and controls. They then used antibiotic-treated mice, fecal transplants, butyrate supplementation, and GPR109A-knockout mice. Finally they tested butyrate on cultured cancer cells, on CD8 T cells, and on CAR-Claudin 18.2 CD8 T cells in vitro and in tumor-bearing mice.
The human sample was 20 gastric cancer patients and 20 healthy volunteers, aged 30 to 75, providing feces and blood in China. Tumor and adjacent tissue was analyzed from 50 to 60 patient pairs. Mouse work used C57BL/6J mice given H. pylori plus N-methyl-N-nitrosourea to induce cancer, with 10 to 12 animals per group. Cell work used human gastric cancer lines MGC-803, HGC-27, and SNU-216 versus the normal line GES-1.
Gastric cancer patients showed gut dysbiosis with fewer short-chain-fatty-acid-producing genera and markedly lower fecal acetate, butyrate, and total short-chain fatty acids, mirrored in serum. Tumor tissue had reduced GPR109A and GPR43. Mice given patient microbiota developed more gastric tumors and had lower butyrate than mice given healthy microbiota. Butyrate cut cancer-cell proliferation and raised apoptosis via GPR109A and HOPX. In mice, butyrate or a high-fiber diet reduced tumor number and raised IFN-gamma CD8 T cells, effects lost when GPR109A was knocked out. Butyrate at 0.5 mmol/L maximized IFN-gamma and boosted CAR-Claudin 18.2 CD8 T cell killing.
The findings suggest gut-derived butyrate helps restrain gastric cancer by sharpening CD8 T cell cytotoxicity through the GPR109A and HOPX axis. This points to microbiota or butyrate support as a possible adjunct to immunotherapy. Butyrate also enhanced CAR-Claudin 18.2 CD8 T cell activity, hinting at value for engineered cell therapy. The work is preclinical, using patient samples plus mouse and cell models, so human treatment benefit remains to be tested.
This study asked whether living with HIV accelerates biological aging in the intestines, and whether gut microbes drive it. It combined epigenetic aging clocks, tight junction imaging, 16S rRNA sequencing of the V1-V2 region, and metabolomics. Samples spanned colon and ileum biopsies, blood, and stool. Correlation networks linked microbes, metabolites, and aging. The design was a systems biology comparison of tissue and blood.
The cohort was 25 people with HIV on suppressive antiretroviral therapy and 23 people without HIV, at Rush University in the United States. Groups were matched for age, sex, BMI, and ethnicity. All HIV-positive participants had viral loads below 50 copies per milliliter. People on special diets or with celiac disease were excluded. Colon, ileum, blood, and stool were sampled from each participant.
Blood biological age was accelerated by 2.59 to 7.05 years in people with HIV on therapy. Aging also accelerated in the ileum (four clocks) and colon (two clocks). Tight junction proteins fell and microbial translocation markers rose, both tied to faster aging. Pro-inflammatory bacteria that catabolize tryptophan, enriched in the gut, correlated with accelerated aging. Depleted butyrate producers tracked with slower aging, alongside higher tryptophan catabolites and lower hippuric acid.
The work links intestinal microbial dysbiosis, a leaky gut, and specific metabolites to accelerated aging in people with HIV on therapy. Mucosal tissue signatures, not fecal ones, tracked most closely with aging. This reflects HIV, antiretroviral therapy, sexual practices, and other factors combined. It is a human association study, so mechanisms and causation remain unproven.
This crossover trial tested how a short-term pectin-enriched smoothie affects the gut microbiota and health markers. Participants alternated between two smoothies and washout periods. One smoothie was high in pectin (about 11.6 grams fiber per day) and one lower (about 4.8 grams). The high-pectin recipe added pectin, psyllium, and beta-glucan. Fecal microbiota were profiled by 16S rRNA sequencing of the V4 region. Weekly food diaries, blood tests, and body composition were also collected.
The study enrolled adults recruited as low-fiber, low-activity consumers with mild gastrointestinal complaints, and 31 completed it (3 men). It ran in Estonia from October to December 2022. Participants were split by habitual fiber intake from food diaries. The low-fiber group (22 people) ate under 23 grams of fiber daily, and the high-fiber group (9 people) ate more. Recent antibiotic users and those with chronic disease or special diets were excluded. Participants kept their usual diet aside from the smoothies.
The smoothie effects on gut bacteria were temporary and reverted to baseline after each washout period. Changes depended on habitual fiber intake at baseline. Low-fiber consumers (22) showed more up- and down-shifts in genera than high-fiber consumers (9). At baseline, Prevotella-9 dominated over Bacteroides in the low-fiber group, with the reverse in high-fiber consumers. In both groups, the pectin-enriched smoothie reduced one bacterial group. Several other genera differed between fiber-intake groups at study start, confirming diet-linked community structure.
The results suggest even a short pectin-rich intervention can shift gut bacteria, and that habitual low-fiber consumers respond more. This points to baseline diet as a key modifier of microbiota response. Because changes reverted after washout, sustained intake would likely be needed for lasting effects. The sample was small, especially the nine high-fiber controls. The authors conclude the short-term crossover design is a workable way to link specific food components to gut bacterial shifts.
Childhood obesity is linked to maternal smoking during pregnancy. Gut microbiota may partially mediate this association and could be potential targets for intervention; however, its role is understudied. We included 1,592 infants from the Canadian Healthy Infants Longitudinal Development Cohort. Data on environmental exposure and lifestyle factors were collected prenatally and throughout the first three years. Weight outcomes were measured at one and three years of age. Stool samples collected at 3 and 12 months were analyzed by sequencing the V4 region of 16S rRNA to profile microbial compositions and magnetic resonance spectroscopy to quantify the metabolites. We showed that quitting smoking during pregnancy did not lower the risk of offspring being overweight. However, exclusive breastfeeding until the third month of age may alleviate these risks. We also reported that maternal smoking during pregnancy significantly increased Firmicutes abundance and diversity. We further revealed that Firmicutes diversity mediates the elevated risk of childhood overweight and obesity linked to maternal prenatal smoking. This effect possibly occurs through excessive microbial butyrate production. These findings add to the evidence that women should quit smoking before their pregnancies to prevent microbiome-mediated childhood overweight and obesity risk, and indicate the potential obesogenic role of excessive butyrate production in early life.
This study asked whether gut bacteria causally influence six diabetes complications: hypoglycemia, ketoacidosis, nephropathy, neuropathy, retinopathy, and Charcot's foot. The authors used two-sample Mendelian randomization. This method uses genetic variants (single-nucleotide polymorphisms) as instruments to infer causation and reduce confounding. Inverse variance weighted analysis was the primary method. Inverse MR tested reverse effects, and multivariate MR adjusted for traditional risk factors.
The analysis used genome-wide summary data, not new patients, all from people of European ancestry. Gut microbiota data came from the MiBioGen consortium (18,340 participants across 24 cohorts) as discovery, with the Dutch Microbiome Project (7,738 participants) for replication. Complication data came from FinnGen (up to 377,277 samples). Case counts ranged from 473 for Charcot's foot to 7,841 for ketoacidosis. In total 196 bacterial taxa were tested.
After multiple-testing correction, the Bacteroidia class and Bacteroidales order were positively linked to diabetic hypoglycemia (OR 1.3541, 95% CI 1.1346-1.6160, P 0.0008). The Verrucomicrobiae class and Verrucomicrobiales order were positively linked to diabetic nephropathy (OR about 1.40, 95% CI 1.1336-1.7319, P 0.0018). Across all six complications, 65 causal associations emerged (4 strong, 61 suggestive). Reverse MR found the complications did not alter these taxa. Multivariate MR kept results stable after adjusting for alcohol, LDL, triglycerides, and smoking.
The findings offer genetic evidence that specific gut taxa may causally shape diabetes complications, pointing toward microbiome-based prevention. Because the method limits confounding and reverse causation, the associations are more robust than typical observational reports. The authors suggest possible targets for dietary therapy, probiotics, engineered microbes, and fecal transplantation. However, all data were European, no subgroup analysis by age or sex was possible, and suggestive links need further study.
The study examined how peripheral neurons connected to the gastrointestinal tract influence the gut microbiome and gut physiology. Researchers activated choline acetyltransferase (ChAT)-expressing or tyrosine hydroxylase (TH)-expressing gut-associated neurons in mice. They then measured effects on intestinal microbial communities, microbial metabolites (including bile acid profiles), and host physiological responses using multi-omics approaches.
The subjects were mice in which ChAT+ or TH+ gut-associated neurons were experimentally activated. The abstract does not give a specific sample size or strain detail, so no cohort numbers can be stated. This was an animal model study, not a human cohort, and it generated multi-omics datasets from these mice rather than drawing on a public metagenomic dataset.
Activating either ChAT+ or TH+ neurons reshaped the structure of the intestinal microbiome, including changes to bile acid profiles and fungal colonization. Physiologically, activation of either neuron type increased fecal output, showing a shared downstream effect on gut transit. Only ChAT+ neuron activation additionally increased colonic contractility and produced diarrhea-like fluid secretion, indicating that these two neuronal subtypes act through distinct physiological pathways despite some overlapping effects.
The findings show that distinct subsets of peripheral, gut-associated neurons can independently shape microbiome composition and gastrointestinal physiology without requiring signals from the brain. This suggests the enteric and peripheral nervous system directly sculpts microbial ecology, including bacterial and fungal populations and bile acid metabolism, rather than the microbiome being shaped only by diet or host genetics. Because different neuron subtypes produce different physiological outcomes (fecal output alone versus contractility and diarrhea-like secretion), this points to neuron-specific pathways as potential targets for understanding or treating GI motility and secretory disorders.
This study tested whether Parkinson's disease alters the periodontitis-associated oral microbiome. Researchers collected unstimulated saliva samples and stool samples and profiled microbial communities using next-generation sequencing of the 16S ribosomal RNA gene (V1-V3 regions). Clinical, periodontal, and neurological parameters were recorded, including the severity of Parkinson's disease motor dysfunction.
Three groups were enrolled: patients with periodontitis and Parkinson's disease (PA+P), patients with periodontitis but without Parkinson's disease (P), and systemically and periodontally healthy individuals used as controls (HC). The abstract does not give exact group sizes. The PA+P group had mild to moderate motor dysfunction, and plaque scores were comparable between the PA+P and P groups, 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 groups, showing that both periodontitis and the presence of Parkinson's disease reshape the oral microbial community. Saliva and fecal microbial profiles were distinct from each other. Mycoplasma faucium, Tannerella forsythia, Parvimonas micra, and Saccharibacteria (TM7) were increased in the P group, while Prevotella pallens, Prevotella melaninogenica, and Neisseria multispecies were more abundant in the PA+P group. In fecal samples from the P group, Ruthenibacterium lactatiformans, Dialister succinatiphilus, Butyrivibrio crossotus, and Alloprevotella tannerae were detected.
The findings support the hypothesis that Parkinson's disease is associated with a distinct periodontitis-related oral microbial signature, separate from periodontitis alone. Because oral and gut microbial profiles diverged between groups despite similar oral hygiene, the results suggest disease-associated shifts rather than simple hygiene differences drive these community changes. This points to the oral-gut microbiome axis as a potential area for further investigation in Parkinson's disease and periodontitis.
This study compared the gut microbiota of stunted and normal-length young children in Indonesia. It sequenced the V3-V4 region of the 16S rRNA gene from stool and measured fecal short-chain fatty acids by GC-MS. Microbiota were correlated with growth z-scores and sanitary conditions. Two sites, one urban and one rural, were sampled. The aim was to find microbial taxa associated with stunting.
The cohort was 200 children aged 36 to 45 months in East Nusa Tenggara, Indonesia. It included 100 stunted and 100 non-stunted children, split across Kupang (urban) and North Kodi (rural). Stunted children averaged about 8 cm shorter and were lighter, while ages did not differ (p = 0.62). The design was cross-sectional, with no intervention. Stunting was defined as a length-for-age z-score below minus two.
Bacteroidetes were higher in stunted children (23.9% versus 20.0%, p = 0.014), as were Cyanobacteria (p = 0.048). Three genera were consistently higher in stunted children at both sites: Lachnoclostridium, Faecalibacterium, and Veillonella. Faecalibacterium reached 13.3% in stunted versus 8.8% in non-stunted children (p = 3.1 x 10 to the minus 4). Fecal acetate (p = 0.003), propionate (p = 0.035), and total short-chain fatty acids (p = 0.011) were lower in stunted children. Butyrate did not differ significantly (p = 0.67).
Lower short-chain fatty acids suggest reduced energy extraction and possibly weaker gut barrier function in stunted children. Certain genera track with stunting, offering candidate targets for dietary and sanitation interventions. The signature differed from the same team's earlier study on Java, showing strong geographic variation. No causation is established, and these are cross-sectional correlations.
This study examined the early development of the human gut microbiome by comparing infants to their mothers and grandmothers within the same family lines. Researchers used a multi-omics approach combining metagenomics (16S rRNA gene and shotgun sequencing) with two independent metabolomics platforms, gas chromatography and capillary electrophoresis coupled to mass spectrometry. The goal was to characterize differences in microbial populations, function, and metabolite output across three generations.
Fecal samples were collected from 200 individuals spanning three generations of the same families. This included infants aged 0 to 12 months (55% female, 45% male) along with their respective mothers and grandmothers. The design allowed direct comparison of gut microbiota and metabolome across a shared generational line.
Infants showed markedly less diverse gut microbiota than their mothers and grandmothers, along with distinct microbial population and functional profiles. The infant metabolome also differed substantially from the adults, particularly in short- and branched-chain fatty acids. These metabolite shifts were linked to corresponding differences in bacterial populations between infants and elders.
The findings offer biochemical insight into how the gut microbiome is shaped during infancy within a single family lineage. Because dysregulation of the gut microbiome at this early stage may contribute to disease later in life, understanding these generational differences could inform strategies to support healthy microbiome development in infants. The authors suggest this multi-omics approach could ultimately help improve childhood health outcomes.
This study asked how urbanization and Western diets in South Africa reshape the gut microbiome and metabolome, and how that relates to colorectal cancer risk. It was a cross-sectional, observational pilot study comparing rural and urban communities. Researchers measured dietary intake, fecal 16S bacteriome, virome, and metabolome (short-chain fatty acids and bile acids), plus food and skin microbiota.
Participants were healthy middle-aged Black South Africans self-identifying as amaXhosa (Xhosa). The urban cohort (n=20) lived in Cape Town, and the rural cohort (n=24) lived in the Eastern Cape Province. Food samples came from 6 urban and 7 rural households. Virome analysis used 28 fecal samples (9 urban, 19 rural). Hand-swab skin sampling covered 6 urban and 7 rural participants.
Urban participants ate far more energy (3,578 versus 2,185 kcal/day) plus more fat and animal protein, while the rural diet gave 72% of calories from carbohydrate. Urban feces had lower bacterial diversity, a shift from fiber-fermenting genera like Prevotella toward taxa linked to bile acid metabolism and colorectal cancer, and higher deoxycholic acid. Short-chain fatty acids, including butyrate, were similar between groups. Of 900 viral contigs, only 176 were shared; virome composition differed by urbanization and correlated with bile acids and dietary nutrients.
The findings support the idea that dietary Westernization during urbanization pushes the gut microbiome toward patterns tied to non-communicable diseases like colorectal cancer. Higher deoxycholic acid and loss of fiber-degrading, butyrate-producing bacteria may raise cancer risk, even where fiber intake stays moderate. The authors propose restoring traditional diet components, such as diverse plant foods and fermentation. Limits include small sample size, two study sites, no colonic biopsies, and a cross-sectional design that cannot prove cause.
This pilot prospective cohort study examined whether ethnicity influences gut microbiome dysbiosis in pregnancies complicated by gestational diabetes mellitus (GDM). The researchers also investigated whether diet and lifestyle modifications made after a GDM diagnosis could modulate the gut microbiome. Fecal samples were collected at two time points, 24 to 28 weeks and 36 to 40 weeks of gestation, and analyzed using targeted 16S rRNA gene-based amplicon sequencing. Statistical comparisons between groups used PERMANOVA, differential abundance testing used DeSeq2, and functional predictions were generated with PICRUSt2.
The cohort included 53 women with GDM and 16 women without GDM, all residing in Singapore. Participants belonged to three Asian ethnic groups: Chinese, Malay, and Indian. This design allowed comparison of gut dysbiosis patterns both across GDM status and across ethnic background within the same population.
Among women with GDM, gut microbiomes from the different ethnic groups shared common features rather than diverging by ethnicity. This suggests that GDM-related dysbiosis is a relatively consistent phenomenon across the Chinese, Malay, and Indian groups studied. The abstract indicates that ethnicity was not a major driver of the microbiome differences observed in these GDM pregnancies.
If GDM-associated gut dysbiosis is largely independent of Asian ethnic background, microbiome-targeted strategies for GDM may generalize across these ethnic groups rather than needing ethnicity-specific approaches. This supports the idea that dietary and lifestyle interventions after a GDM diagnosis could be evaluated and applied similarly across diverse populations. As a pilot study, these findings point to the need for larger cohorts to confirm whether microbiome-based interventions can be standardized across ethnicities.
This study examined how a high-fat diet (HFD) alters the gut microbiota to promote cancer progression. The researchers focused on whether HFD-associated gut bacteria drive the generation of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs), an immune cell population linked to tumor immune evasion. They investigated the mechanism connecting microbial metabolism, specifically leucine production, to mTORC1 signaling and myeloid cell differentiation. The work combined mouse modeling with clinical correlation in breast cancer patients.
The study used tumor-bearing mice across several experimental models, including HFD feeding, fecal microbiota transplantation, antibiotic treatment, and direct bacterial gavage. Clinically, the researchers also studied female patients with breast cancer, examining associations between obesity, obesity-related gut microbiota, peripheral blood leucine levels, and clinical outcomes. Exact sample sizes for the human cohort are not stated in the abstract.
Obesity and obesity-related gut microbiota were associated with poor prognosis and more advanced clinicopathological status in female breast cancer patients. In mice, HFD-related gut microbiota promoted cancer progression by generating PMN-MDSCs. Mechanistically, the HFD microbiota released abundant leucine, which activated the mTORC1 signaling pathway in myeloid progenitors to drive PMN-MDSC differentiation. Elevated peripheral blood leucine linked to the HFD microbiota correlated with greater tumoral PMN-MDSC infiltration and worse clinical outcomes in patients.
The findings define a gut-bone marrow-tumor axis through which diet-altered microbiota can reprogram myeloid cell fate and suppress anti-tumor immunity. Targeting microbial leucine production or the mTORC1 pathway in myeloid progenitors could represent a new strategy to limit PMN-MDSC-driven immune suppression. This work also strengthens the rationale for dietary and microbiota-directed interventions as adjuncts in breast cancer management. Further research is needed to confirm these mechanisms and their clinical relevance in larger patient cohorts.
This study examined whether the traditional Chinese medicine formula Shenling Baizhu San (SLBZS) could prevent or treat non-alcoholic fatty liver disease (NAFLD) at the preclinical level. Researchers induced NAFLD using a western diet combined with CCl4 injection, then treated mice with SLBZS for six weeks. They measured body weight, energy intake, liver enzymes, pro-inflammatory factors, and hepatic steatosis. They also tracked gut microbiota and metabolite changes using 16S rRNA gene sequencing and untargeted metabolomics, alongside serotonin-pathway markers TPH1, 5-HT, HTR2A, and HTR2B.
The study used male C57BL/6J mice, a standard inbred laboratory mouse strain, divided into three groups. One group received a normal diet, a second received a western diet plus CCl4 injection to induce NAFLD, and a third received the same NAFLD-inducing regimen plus SLBZS intervention. No human subjects were studied; this was an animal model investigation.
SLBZS intervention for six weeks reduced serum and liver lipid levels, blood glucose, and pro-inflammatory factors, while improving insulin resistance and liver function indexes, effectively alleviating NAFLD in the mice. The treatment also produced significant changes in intestinal TPH-1, 5-HT, liver 5-HT, and the related receptors HTR2A and HTR2B. Gut microbiota analysis via 16S rRNA sequencing showed SLBZS altered the composition of the gut microbiota, linking these microbial shifts to the observed metabolic and serotonergic changes.
The findings suggest SLBZS may offer a multi-target approach to NAFLD prevention and treatment by simultaneously improving liver function, metabolic markers, gut microbiota composition, and gut-liver serotonin signaling. This supports further investigation of traditional Chinese medicine formulas as adjunct or alternative therapies for NAFLD. Because this work was conducted in mice, human clinical studies are needed before drawing conclusions about efficacy in people.
This study examined how the gut microbiota differs in polycystic ovary syndrome with dyslipidemia compared to PCOS alone and healthy women. It also linked bacteria to lipids and sex hormones. Fecal samples were profiled by 16S rRNA V3-V4 sequencing, with community diversity, taxonomy, and predicted function assessed. LEfSe identified differential genera, PICRUSt predicted metabolic pathways, and Spearman tests correlated bacteria with clinical parameters.
The cohort was 52 reproductive-aged women at a hospital in Hefei, China: 16 healthy controls, 18 with PCOS, and 18 with PCOS plus dyslipidemia (PCOS.D). PCOS was diagnosed by the 2003 Rotterdam criteria. Groups did not differ significantly in age or BMI. Women with insulin resistance, obesity, diabetes, or recent antibiotic, probiotic, or metformin use were excluded to reduce confounding.
Beta diversity did not separate the three groups. PCOS and PCOS.D showed decreased Proteobacteria, and PCOS.D uniquely showed increased Bacteroidota. At genus level, PCOS.D had higher Clostridium_sensu_stricto_1 and lower Faecalibacterium and Holdemanella than PCOS. Ruminococcaceae and Bifidobacteriaceae were also reduced in PCOS.D. Faecalibacterium and Holdemanella correlated negatively with lipid measures including triglycerides and total cholesterol, and Pseudomonas correlated negatively with luteinizing hormone.
The results suggest that dyslipidemia in PCOS is accompanied by a distinct gut microbial signature, especially loss of butyrate-producing Faecalibacterium. Because these genera track lipid levels, the authors propose them as possible targets for regulating cholesterol and triglycerides in PCOS. The sample was small and cross-sectional, so causation cannot be inferred and larger studies are needed to confirm whether dysbiosis drives dyslipidemia.
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 gut microbiota in young adults with schizophrenia showing prominent negative symptoms, a group that is poorly characterized. Stool samples underwent 16S rRNA gene sequencing, with sequences clustered into operational taxonomic units. Symptoms were rated with the positive and negative syndrome scale (PANSS). Analyses included diversity metrics, LEfSe, Spearman correlation, and random forest classification.
Participants were young adults aged 18 to 30 years in China, recruited at Xijing Hospital. After exclusions, the study analyzed 30 patients with prominent negative symptoms, 32 with prominent positive symptoms, and 36 healthy controls. Groups matched the negative-symptom patients on sex, age, smoking, alcohol, and BMI. People with obesity, metabolic disease, or recent antibiotic or probiotic use were excluded.
Beta-diversity separated the groups (Bray-Curtis P 0.001), but alpha-diversity did not differ significantly. Negative-symptom patients had higher Fusobacteria and Proteobacteria and lower Firmicutes at the phylum level, plus 27 genera differing from controls. A six-genus panel (Coprococcus, Monoglobus, Prevotellaceae NK3B31 group, Escherichia-Shigella, Dorea, and Butyricicoccus) distinguished patients from controls with an AUC of 0.939. Several short-chain-fatty-acid-producing genera were depleted in patients. The microbiota could not reliably separate negative-symptom from positive-symptom schizophrenia (minimum error rate 0.544).
The findings suggest gut dysbiosis may participate in schizophrenia with negative symptoms and could offer peripheral diagnostic markers. Enriched inflammation-linked phyla and depleted short-chain-fatty-acid producers hint at roles for inflammation and metabolism in negative symptoms. The authors propose probiotics or short-chain fatty acids as possible adjunct strategies. Limits include a small cross-sectional sample, past antipsychotic use, single stool sampling, and 16S sequencing that cannot resolve function.
This study examined the relationship between faecal microbiota and nutritional status in schoolchildren using a double-blinded cluster-randomized controlled trial. Researchers tested the impact of six months of consumption of rice fortified with two different levels of vitamins and minerals. The faecal microbiota was characterized using 16S rRNA sequencing and analyzed against nutritional, micronutrient, inflammatory, and parasitic infection markers. The trial was registered with ClinicalTrials.gov (NCT01706419).
The study population consisted of 380 Cambodian schoolchildren enrolled in a cluster-randomized trial. Participants were assessed for age, sex, nutritional status (including underweight and stunting), and micronutrient status covering iron, zinc, and vitamin A deficiencies. Additional measures included anaemia, iron deficient anaemia, hemoglobinopathy, systemic and gut inflammation, and parasitic infection status.
The faecal microbiota of these schoolchildren showed a surprisingly high proportion of Lactobacillaceae. Deficiencies in specific micronutrients, namely iron and vitamin A, correlated with particular microbiota profiles, while zinc deficiency showed no such association. The six-month rice fortification intervention altered both the composition and the predicted functions of the microbiota, with the two rice treatments producing different effects. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, or sulfur metabolism.
These findings suggest that specific micronutrient deficiencies, rather than micronutrient status broadly, are linked to distinct gut microbiota signatures in children. The differential response of microbiota composition and function to two fortification formulations indicates that the type of nutrient fortification matters, not just its presence. This work supports further investigation into how targeted nutritional interventions might be designed to favorably shape childhood gut microbiota and, in turn, nutritional and inflammatory outcomes.
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 a history of repeated, but not recent, antibiotic use has lasting effects on the gut microbiota and on microbiota-mediated intestinal mucus barrier function. Researchers used human-to-mouse fecal microbiota transplantation to transfer gut microbial communities from previously antibiotic-exposed and healthy individuals into mice. They then measured mucus growth rate and mucus penetrability using ex vivo analyses of viable colonic tissue explants, and characterized the transplanted microbiota using shotgun metagenomic sequencing and metabolite profiling.
The human source population was drawn from the deeply phenotyped Estonian Microbiome Cohort (EstMB), from which individuals with a history of repeated antibiotic use and healthy controls were selected for fecal sampling. The functional experiments were then carried out in mice that received fecal microbiota transplants from these human donors, so the mucus and microbiota outcomes reported reflect this humanized mouse model rather than direct measurements in the human donors themselves.
Mice transplanted with microbiota from humans with a history of repeated antibiotic use showed a reduced mucus growth rate and increased mucus penetrability compared to mice given microbiota from healthy controls. Shotgun metagenomic sequencing showed the antibiotic-shaped microbial community had a significantly altered composition, with mucus-utilizing bacteria, including Akkermansia muciniphila and Bacteroides fragilis, dominating the gut. This altered microbiota was also marked by a distinct metabolite profile.
The findings suggest that repeated antibiotic use can leave a lasting, microbiota-encoded imprint on the gut that impairs the mucus barrier long after the antibiotics themselves are gone. Because a healthy mucus layer normally protects the intestinal epithelium against infection and inflammation, this microbiota-driven thinning and increased penetrability could plausibly raise vulnerability to gut infection or inflammatory conditions. The dominance of mucus-utilizing organisms such as Akkermansia muciniphila and Bacteroides fragilis points to microbial mucus consumption as a candidate mechanism linking antibiotic history to barrier dysfunction, warranting further mechanistic study.
This study characterized the caecal gut microbiota of scavenging indigenous village chickens across Ethiopia's varied altitude-dependent agro-ecologies. Researchers used shotgun metagenomics on caecal content samples collected from many villages and districts. They built a non-redundant gene catalogue of over 33 million genes, assembled metagenome-assembled genomes, defined enterotypes, and linked microbiota to climate, topsoil, and farmer-supplied supplementary diets.
The samples came from 243 Ethiopian indigenous scavenging chickens, of which 240 passed quality control. Birds were sampled from 26 sites across 15 districts, spanning wide ranges of latitude, longitude, and altitude. Five climate zones were defined, with altitude and mean annual temperature as major predictors. These free-ranging birds differ sharply from grain-fed commercial breeds raised in biosecure facilities, giving a rare view of naturally adapted poultry microbiomes.
Bacteroidota was the most abundant phylum (48.0 percent), followed by Firmicutes (32.9 percent). The microbiota clustered into three enterotypes, with enterotype 3 dominating high-altitude zone 1 (62 percent of samples). Chickens above 3000 m carried more than 2.5-fold higher Bacteroides (17.6 percent). Diversity decreased significantly as altitude rose. The team assembled 9977 strain-level genomes; 9682 strains and 1242 species were absent from prior chicken datasets and the Genome Taxonomy Database. Most species-level genomes carried at least one antimicrobial resistance gene, most often for tetracycline.
The work greatly expands the known microbial diversity of poultry, showing scavenging village chickens host thousands of previously uncatalogued microbes. Altitude, temperature, precipitation, topsoil, and supplementary grains all shaped the gut microbiota, arguing that local environment drives microbial adaptation. The rich carbohydrate-active enzyme repertoire may support digestion of diverse scavenged fibers. These genomes are a resource for improving indigenous poultry nutrition and disease resistance, though the observational design cannot prove that specific microbes cause the observed adaptations.
This study investigated the relationship between periodontitis and the oral-gut axis in first-trimester pregnant women using integrative microbiome and metabolome profiling. Researchers combined 16S rRNA sequencing of subgingival plaque, saliva, and stool with untargeted metabolomics of serum and other sample types, alongside clinical traits. The goal was to characterize how oral dysbiosis linked to periodontitis translates into distal gut microbial and metabolic changes during early pregnancy.
The cohort consisted of 54 Chinese pregnant women sampled at the first trimester. Of these, 31 women had maternal periodontitis (the Perio group) and 23 women served as Non-Perio controls. Subgingival plaque, saliva, serum, and stool samples were collected from each participant for multi-omics analysis.
The study identified a novel bacterial distinguisher, Coprococcus, in the feces of women with periodontitis, and this genus was associated with subgingival periodontopathogens. Notably, Coprococcus behaved differently from other fecal genera within the Lachnospiraceae family. The ratio of fecal Coprococcus to Lachnoclostridium was able to discriminate between the Perio and Non-Perio groups, indicating a measurable gut-level signature tied to oral disease status.
The findings support the existence of a functional oral-gut axis through which periodontitis in early pregnancy is reflected in distinct gut microbial and metabolic alterations. Identifying the fecal Coprococcus to Lachnoclostridium ratio as a discriminating feature suggests potential translational value as a biomarker linking oral and gut health in pregnant women. This integrative multi-omics approach may help clarify how periodontitis contributes to adverse pregnancy outcomes via systemic, gut-mediated pathways.
This study tested whether the traditional Chinese medicine formula Xuanfei Baidu (XFBD) treats systemic inflammatory response syndrome (SIRS) by remodeling the gut microbiome. It combined animal experiments, fecal microbiota transplantation, and in-vitro compound screening. Researchers screened 51 compounds isolated from the formula for their ability to shift dysbiotic gut communities toward a healthy structure. High-scoring compounds were then combined into gut microbiome remodeling compound (GMRC) cocktails and tested for anti-inflammatory efficacy.
The main model was six-week-old male C57BL/6 mice with SIRS induced by lipopolysaccharide injection, using 12 mice per group. Groups received the formula, dexamethasone, or vehicle. Fecal microbiota transplantation used XFBD-treated mice as donors, with recipients given live or heat-killed fecal material. In-vitro screening used cultured mouse cecal contents. The work also cultured fecal samples from 8 human SIRS patients and compared them with 10 healthy volunteers.
XFBD at 1.95 g/kg improved survival, reduced spleen and lung injury, and lowered serum TNF-alpha, IL-1beta, and IL-6. It reduced Proteobacteria and raised beneficial taxa in the gut. Transplanting the remodeled microbiota reproduced the benefit, while heat-killed material did not, confirming a microbiota-dependent effect. Cocktail C, containing aucubin, gentiopicroside, syringic acid, gallic acid, p-hydroxybenzaldehyde, para-hydroxybenzoic acid, and isoimperatorin, outperformed single compounds and other cocktails. In SIRS patient fecal cultures, cocktail C raised the Firmicutes to Bacteroidetes ratio and shifted composition toward healthy volunteers.
The work supports gut microbiome remodeling as a mechanism for herbal treatment of severe systemic inflammation. It shows a rational path from a complex formula to a defined small-molecule cocktail. The in-vitro screening approach let the team quantify and cluster 51 compounds efficiently, faster than animal trials alone. Findings remain preclinical. The in-vitro culture reduced microbial diversity, and human data were limited to fecal cultures, so clinical efficacy and safety still require testing.
This study characterized the gut microbiome and fecal immune profiles of infants in a rural, under-studied region of Cambodia. Stool was analyzed by 16S rRNA amplicon sequencing, with faecal cytokine concentrations measured across a multi-marker panel. Selected bacteria were cultured and whole-genome sequenced. The team also compared two storage methods, freezing versus a DNA preservation solution, because immediate freezing is hard in rural settings, and linked microbiome data to infant diet, growth, and illness.
The cohort was 32 infants from the rural Kampong Cham province of Cambodia, part of the NHAM birth cohort, mostly in small-scale farming families. Three stool samples were collected per infant, 96 in total, at mean ages of 201, 216, and 236 days. This was a human observational study. Metadata covered breastfeeding, recent diarrhea, antibiotic use, growth, and household hygiene. Most families had poor access to hygiene facilities and used unregulated antibiotics.
The microbiome was dominated by Bifidobacterium, with a median relative abundance of 48.7 percent, and Bifidobacterium longum was the most abundant species. Breastfeeding was the single strongest driver of composition, raising Bifidobacterium abundance. Recent diarrhea within 7 days tracked with higher Shigella and Klebsiella. Many isolates carried antimicrobial resistance genes, including in Bifidobacterium, while B. longum and B. breve carried human milk oligosaccharide gene clusters. Fecal IL-1alpha and VEGF were higher in breastfed infants.
The study provides some of the first detailed gut microbiome data from rural Cambodian infants, showing that breastfeeding shapes both bacteria and fecal immune signals even amid heavy pathogen exposure. Antibiotic use showed no clear effect, hinting at widespread resistance or ineffective drugs. DNA preservation solution better retained Bifidobacterium, a practical lesson for field sampling. With only 32 infants and few stunted cases, growth links could not be tested robustly, so findings are exploratory.
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.
The study asked how two human-targeted drugs disturb whole gut microbiomes and by what mechanism. Researchers incubated fresh human faecal samples ex vivo with entacapone (a Parkinson's disease treatment) or loxapine succinate (a schizophrenia treatment) at physiologically relevant colon concentrations. They combined quantitative microbiome profiling, 16S amplicon and long-read metagenomic sequencing, heavy-water single-cell activity imaging, and chemical imaging of drug uptake. They then tested whether iron chelation drove the effects, using iron rescue experiments and siderophore mutants.
This was an ex vivo human faecal study, not a clinical trial. Faecal samples came from nine healthy adults (three men and six women aged 22 to 39) who had taken no antibiotics in the prior three months. Most experiments pooled samples from six of these donors, incubated anaerobically at 37 degrees Celsius. Entacapone was tested at an estimated colon concentration of 1,965 micromolar. Some findings were confirmed in pure bacterial cultures and Escherichia coli mutants.
High-dose entacapone had a much stronger effect than loxapine. It significantly altered 29.4% of all bacterial amplicon variants after 24 hours and reduced total microbial cell numbers, while loxapine altered 11.8%. Entacapone's catechol group complexed iron, and this activity was not affected by nitroreduction. Adding iron reversed the growth inhibition across most affected taxa. Iron starvation selected for siderophore-producing Enterobacteriaceae, chiefly an Escherichia coli strain whose genome encodes 14 resistance and virulence genes plus enterobactin machinery.
The work identifies metal sequestration as a mechanism by which a human-targeted drug disturbs the gut microbiome. Entacapone depletes iron, a limiting nutrient, favouring potentially harmful iron-scavenging bacteria. This may relate to reported increases in Enterobacteriaceae and diarrhoea in some Parkinson's patients taking entacapone. The authors propose that delivering iron to the colon could help preserve microbiome balance. These are short-term ex vivo results from healthy donors, so long-term patient cohorts are still needed.
This study examined the gut microbiome in people who inject drugs, comparing those with and without HIV-1 infection. Researchers used amplicon-based 16S rDNA sequencing to identify amplicon sequence variants (ASVs) and detect shifts in bacterial community composition. The goal was to disentangle how HIV status and injection drug use, separately and together, shape the gut microbiota. Effects of multiple drug use on the microbiome were also assessed in both HIV-infected and non-infected participants.
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 disproportionately linked to it. Participants included both HIV-positive and HIV-negative individuals, and both drug-injecting and non-injecting individuals, allowing comparison across these groups. The abstract does not give an exact sample size.
HIV-positive individuals had 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 compared to non-injectors, regardless of HIV status. The study also found that using multiple drugs significantly affected the composition of the gut microbial community. These patterns show that HIV status and drug use each leave distinct, identifiable signatures on the gut microbiome.
The findings suggest that HIV infection and injection drug use independently reshape the gut microbiome, producing distinguishable bacterial signatures rather than a single combined effect. Identifying HIV-associated genera separately from drug-use-associated genera could help researchers understand how each factor contributes to health outcomes in this population. Recognizing that multiple drug use further alters the microbial community underscores the need to account for drug use patterns in microbiome research on people with HIV. This work supports using gut microbiota profiling as a tool to better understand the intersecting effects of infection and substance use.
This study asked whether gut microbiome composition can identify latent tuberculosis infection (LTBI) in patients with poorly controlled diabetes and whether it tracks host immune cytokines. Stool and blood were collected at enrollment. Gut bacteria were profiled by 16S rRNA gene sequencing of the V3-V4 region. A random forest classifier was built from the most discriminating genera, and plasma cytokines were measured by ELISA to link taxa to immunity.
The cohort was 130 patients with poorly controlled type 2 diabetes (HbA1c above 9.0 percent within the prior year), recruited in Kaohsiung, Taiwan. Latent tuberculosis status was set by QuantiFERON-TB Gold: 43 were LTBI-positive and 87 negative. Mean age was 67.1 years and 51 percent were male. Baseline features, including age, sex, BMI and antidiabetic drug use, were similar between the LTBI and non-LTBI groups.
Alpha diversity was similar between groups, but beta diversity differed significantly (unweighted UniFrac p equals 0.007). The LTBI group had a lower Prevotella-to-Bacteroides ratio (0.251 versus 0.724). LTBI patients were enriched in Bacteroides, Alistipes and Blautia and depleted in Prevotella, Streptococcus and Actinomyces. Bacteroides rose from 29.72 to 37.79 percent. A six-genus random forest model predicted LTBI with 0.872 accuracy and 0.834 AUROC. LTBI patients had lower plasma IL-17F (p equals 0.025) and TNF-alpha (p equals 0.038).
The results suggest gut microbial signatures may reflect immune status and tuberculosis risk in diabetes, offering a possible adjunct to standard interferon-release assays for latent infection. Linking specific genera to lower Th1 and Th17 cytokines points toward microbiome-directed strategies to bolster host defense. This was a cross-sectional study, so it cannot establish causation. It used 16S rather than shotgun sequencing and needs external validation across other populations before clinical use.
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 investigated the mucosal microbiota at multiple biopsy sites across the spectrum of colorectal cancer (CRC) progression. Researchers used Illumina Miseq sequencing of the 16S rRNA V4 region to profile microbial composition and dynamics in biopsy samples. They also used MinION nanopore sequencing of Fusobacterium-specific amplicons to characterize tumor-associated Fusobacterium nucleatum at the species and subspecies level. The goal was to map how microbial communities shift as tissue progresses from healthy to adenomatous polyp to cancer.
The abstract describes three groups of biopsy patients from Norway: cancer patients, patients with adenomatous polyps, and healthy controls. Biopsy samples from these groups were sequenced and compared to identify microbiota alterations associated with CRC progression. Fusobacterium-positive tumor biopsies were further subjected to targeted nanopore sequencing. Exact sample sizes for each group are not given in the abstract.
Cancer patients showed enrichment of oral biofilm-associated bacteria compared to adenomatous polyp and control patients, including Fusobacterium, Gemella, Parvimonas, Granulicatella, Leptotrichia, Peptostreptococcus, Campylobacter, Selenomonas, Porphyromonas, and Prevotella. Cancer-associated samples also showed higher abundance of amplicon sequence variants classified as Phascolarctobacterium, Bacteroides vulgatus, Bacteroides plebeius, Bacteroides eggerthii, Tyzzerella, Desulfovibrio, Frisingicoccus, and Eubacterium among others. The presence of Desulfovibrio, a sulfate-reducing bacterial genus capable of producing hydrogen sulfide, was notably elevated alongside these oral pathobionts in cancer tissue. The study further characterized Fusobacterium subspecies within Fusobacterium-positive tumor biopsies using nanopore sequencing.
These findings support a model in which oral biofilm-associated bacteria, together with sulfate-reducing organisms like Desulfovibrio, colonize and accumulate in colorectal tissue as it progresses toward malignancy. Mapping these site-specific microbial shifts across polyp and cancer stages could help identify microbial markers of CRC progression. Characterizing Fusobacterium at the subspecies level may also refine understanding of which strains are most relevant to tumorigenesis. Together, this work strengthens the rationale for using mucosal microbiota profiles, including sulfide-producing taxa, as part of CRC risk assessment.
This study examined whether dimethyl itaconate (DI), an anti-inflammatory derivative of the immune metabolite itaconate, could prevent cognitive impairment caused by a high-fat diet (HFD) in mice. The researchers focused on the gut-brain axis, testing whether DI's effects on intestinal immunity and inflammation could translate into protection of hippocampal function. DI was administered intraperitoneally alongside the high-fat feeding regimen to assess its impact on both colonic and brain outcomes.
The subjects were mice fed a high-fat diet to induce cognitive impairment, compared against mice treated with dimethyl itaconate during HFD feeding. The abstract does not specify exact group sizes, sex, or age of the animals, so no further cohort detail can be honestly reported. This was an animal model study rather than a human or clinical cohort.
DI treatment attenuated HFD-induced cognitive decline across object location, novel object recognition, and nest building tests, and it improved hippocampal gene transcription profiles tied to cognition and synaptic plasticity. It also reduced synaptic ultrastructural damage, restored levels of BDNF, SYN, and PSD95, and lowered microglial activation and neuroinflammation. In the colon, DI decreased macrophage infiltration and pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6) while boosting immune homeostasis markers IL-22, IL-23, and the antimicrobial peptide Reg3gamma. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so this study is summarized on its own gut-immune and neuroinflammatory terms.
The findings suggest that targeting itaconate-related anti-inflammatory pathways in the gut could offer a therapeutic route to protect cognition against diet-induced metabolic stress. By linking intestinal immune homeostasis and antimicrobial peptide expression to hippocampal synaptic health, the study reinforces the gut-brain axis as a mechanistic bridge between diet, gut inflammation, and neurodegeneration risk. This positions DI and similar itaconate derivatives as candidate agents for further investigation in obesity-associated cognitive decline.
The human microbiome plays an important role in modulating the host metabolism and immune system. Connections and interactions have been found between the microbiome of the gut and oral pharynx in the context of SARS-CoV-2 and other viral infections; hence, to broaden our understanding of host-viral responses in general and to deepen our knowledge of COVID-19, we performed a large-scale, systematic evaluation of the effect of SARS-CoV-2 infection on human microbiota in patients with varying disease severity.
We processed 521 samples from 203 COVID-19 patients with varying disease severity and 94 samples from 31 healthy donors, consisting of 213 pharyngeal swabs, 250 sputa, and 152 fecal samples, and obtained meta-transcriptomes as well as SARS-CoV-2 sequences from each sample. Detailed assessment of these samples revealed altered microbial composition and function in the upper respiratory tract (URT) and gut of COVID-19 patients, and these changes are significantly associated with disease severity. Moreover, URT and gut microbiota show different patterns of alteration, where gut microbiome seems to be more variable and in direct correlation with viral load; and microbial community in the upper respiratory tract renders a high risk of antibiotic resistance. Longitudinally, the microbial composition remains relatively stable during the study period.
Our study has revealed different trends and the relative sensitivity of microbiome in different body sites to SARS-CoV-2 infection. Furthermore, while the use of antibiotics is often essential for the prevention and treatment of secondary infections, our results indicate a need to evaluate potential antibiotic resistance in the management of COVID-19 patients in the ongoing pandemic. Moreover, a longitudinal follow-up to monitor the restoration of the microbiome could enhance our understanding of the long-term effects of COVID-19. Video Abstract.
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 how the gut microbiome shifts as chronic kidney disease advances toward end-stage renal disease, and how those shifts relate to clinical blood markers. It builds on the gut-kidney axis concept. Fecal samples underwent 16S rRNA gene V3-V4 sequencing. Community composition, alpha and beta diversity, and differential abundance were analyzed alongside many clinical indicators. Correlation methods including Spearman analysis, canonical correspondence analysis, Mantel tests, and network analysis linked specific genera to renal and inflammatory measures.
The cohort was 13 hospitalized patients at the Third Xiangya Hospital in Changsha, China, sampled in 2022. Seven had chronic kidney disease and 6 had end-stage renal disease. Participants were aged 22 to 76 years (mean about 55), with 10 males and 3 females. Groups were matched for gender and age. Patients taking laxatives, probiotics, antibiotics, immunosuppressants, or several other drug classes were excluded. The two groups differed significantly in eGFR, creatinine, blood urea nitrogen, lymphocytes, and beta-2 microglobulin.
Alpha and beta diversity did not differ significantly between stages, though alpha diversity trended downward. Firmicutes dominated, followed by Proteobacteria, Bacteroidota, and Actinobacteriota. In end-stage disease, 8 genera rose significantly and 9 fell versus chronic kidney disease. Community structure simplified, with single genera exceeding 50% relative abundance in some samples. Butyrate-producing genera declined, reducing anti-inflammatory butyrate. Beta-2 microglobulin explained the most variation in community structure and correlated with intermediate and rare genera.
The results suggest the gut microbiome simplifies and stabilizes in advanced kidney disease, offering candidate non-invasive markers for tracking progression toward end-stage disease. The loss of butyrate producers may remove a protective, anti-inflammatory influence on the kidney, and beta-2 microglobulin appears tied to specific microbial shifts. The sample size was only 13 patients with no healthy control group, so the authors stress that larger validation cohorts and metabolomic studies are needed before clinical use.
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 study tested how a ketogenic diet affects the gut microbiome and metabolites in polycystic ovary syndrome (PCOS). It also asked whether hormone changes relate to microbiota shifts. PCOS was induced in rats using letrozole plus a high-fat diet. A ketogenic diet was then fed for eight weeks. Serum was collected for biochemical analysis. Faecal samples underwent 16S ribosomal RNA sequencing and metabolomic analysis to link microbes with metabolites and sex hormones.
The subjects were rats, not humans. PCOS was induced with letrozole and a high-fat diet, then a ketogenic diet was applied for eight weeks. This is a controlled animal model designed to study mechanisms of diet on PCOS. Serum, faeces, and hormone measures were compared across dietary conditions. Because it is a rodent model, the findings describe biology under controlled induction rather than clinical outcomes in women with PCOS.
The ketogenic diet suppressed body weight gain and lowered luteinizing hormone and androgen levels. It also improved insulin levels in the PCOS rats. The diet reversed gut microbiota dysregulation by adjusting the ratio of Firmicutes to Bacteroidetes. Microbiome changes tracked with hormonal metabolic pathways. Several metabolites closely related to gut microbes decreased, including testosterone and 7-alpha-hydroxytestosterone. These shifts connected the microbiome to androgen metabolism. The authors also noted contradictory microbiome effects needing further study.
The results suggest the ketogenic diet may improve PCOS partly by reshaping the gut microbiome and androgen-related metabolites. This offers a possible mechanism for its clinical benefit. Improved insulin resistance and lower androgens matched changes in microbiota and metabolites tied to steroid hormone biosynthesis. The study was in rats, so results may not translate directly to women. The authors reported contradictory microbiome effects and stressed that further research is required before clinical conclusions.
Diagnosis of essential tremor (ET) at an early stage can be difficult, especially when distinguishing it from healthy controls (HCs) and Parkinson's disease (PD). Recently, stool sample analysis of gut microbiota and its metabolites provides new ways to detect novel biomarkers for neurodegenerative diseases. Short-chain fatty acids (SCFAs), as the main metabolites of gut microbiota, were reduced in the feces of PD. However, fecal SCFAs in ET have never been investigated. We aimed to investigate the fecal SCFA levels in ET, assess their relationships with clinical symptoms and gut microbiota, and identify their potential diagnostic abilities. Fecal SCFAs and gut microbiota in 37 ET, 37 de novo PD and 35 HC were measured. Constipation, autonomic dysfunction and tremor severity were evaluated by scales. ET had lower fecal propionic, butyric and isobutyric acid levels than HC. Combined propionic, butyric and isobutyric acid distinguished ET from HC with an AUC of 0.751 (95% CI: 0.634-0.867). ET had lower fecal isovaleric and isobutyric acid levels than PD. Isovaleric and isobutyric acid differentiated ET from PD with an AUC of 0.743 (95% CI: 0.629-0.857). Fecal propionic acid was negatively correlated with constipation and autonomic dysfunction. Isobutyric and isovaleric acid were negatively associated with tremor severity. Lowered fecal SCFAs were related to a decreased abundance of Faecalibacterium and Catenibacterium in ET. In conclusion, fecal SCFAs were decreased in ET and correlated with clinical severity and gut microbiota changes. Fecal propionic, butyric, isobutyric and isovaleric acid might be potential diagnostic and differential diagnostic biomarkers for ET.
Crohn's diseases and ulcerative colitis, both of which are chronic immune-mediated disorders of the gastrointestinal tract are major contributors to the overarching Inflammatory bowel diseases. It has become increasingly evident that the pathological processes of IBDs results from interactions between genetic and environmental factors, which can skew immune responses against normal intestinal flora.
The aim of this study is to assess and analyze the taxa diversity and relative abundances in CD and UC in the Saudi population. We utilized a sequencing strategy that targets all variable regions in the 16 S rRNA gene using the Swift Amplicon 16 S rRNA Panel on Illumina NovaSeq 6000.
The composition of stool 16 S rRNA was analyzed from 219 patients with inflammatory bowel disease and from 124 healthy controls. We quantified the abundance of microbial communities to examine any significant differences between subpopulations of samples. At the genus level, two genera in particular, Veillonella and Lachnoclostridium showed significant association with CD versus controls. There were significant differences between subjects with CD versus UC, with the top differential genera spanning Akkermansia, Harryflintia, Maegamonas and Phascolarctobacterium. Furthermore, statistically significant taxa diversity in microbiome composition was observed within the UC and CD groups.
In conclusion we have shown that there are significant differences in gut microbiota between UC, CD and controls in a Saudi Arabian inflammatory bowel disease cohort. This reinforces the need for further studies in large populations that are ethnically and geographically diverse. In addition, our results show the potential to develop classifiers that may have add additional richness of context to clinical diagnosis of UC and CD with larger inflammatory bowel disease cohorts.
This case-control study tested whether the link between cigarette smoking and colorectal tumor risk depends on gut microbiota type. Fecal microbiota was profiled by 16S rDNA sequencing. Cancer and adenoma cases were each split into two enterotypes (type I and type II) using a Dirichlet multinomial mixture model. Multivariate logistic regression tested smoking associations by subtype. Alpha and beta diversity, differential genera, and predicted functional pathways (Tax4FUN) were compared between subtypes.
Participants were Han Chinese adults aged 40 or older enrolled at Changhai Hospital in Shanghai, China, from 2015 to 2016. The study included 130 colorectal cancer patients, 120 adenoma patients, and 130 healthy controls. All underwent complete colonoscopy from cecum to rectum. People with recent antibiotics, prior colorectal neoplasm, inflammatory bowel disease, or a family history of CRC were excluded. Cancer cases split into type I (n=77) and type II (n=53); adenoma cases into type I (n=66) and type II (n=54). Smoking was self-reported in pack-years.
Smoking raised the odds of type II tumors but not type I. For type II CRC the adjusted odds ratio was 2.30 (95% CI 1.16-4.55, p=0.017); for type II adenoma it was 3.23 (95% CI 1.34-7.78, p=0.009). Odds rose with pack-years (trend p=0.025 for CRC, 0.046 for adenoma). The association differed significantly by enterotype (p less than 0.05 for heterogeneity). Type II (smoking-related) enterotypes had lower diversity and more of the pathogen Escherichia-Shigella, plus fewer short-chain-fatty-acid-producing Lachnospiraceae and Ruminococcaceae. Type II tumors showed enriched p53 signaling and higher PLD1/2, cytochrome C, and PTGS2 expression.
The findings suggest gut microbiota may mediate why smoking raises colorectal cancer risk for some people and not others, helping explain inconsistent past epidemiology. Smoking appears tied to a specific microbial and molecular tumor subtype. The proposed mechanism links smoking to more pro-inflammatory bacteria and fewer protective short-chain-fatty-acid producers, activating oncogenic and inflammatory pathways. This was a retrospective, single-center study using only 16S sequencing of fecal samples, so reverse causation and lack of replication limit conclusions. Prospective cohorts collecting stool before diagnosis are needed.
This study investigated how rare, low-abundance bacterial phylotypes contribute to the microbial communities associated with urinary stone disease (USD), rather than focusing only on dominant, common taxa. The researchers conducted a meta-analysis of existing 16S rRNA sequencing datasets derived from kidney stone, stool, and urine samples. They separated bacterial taxa into rare and common groups based on the frequency and abundance of amplicon sequence variants, then compared how each group related to disease status across the three sample types. The aim was to clarify the distinct contribution of rare phylotypes to the gut, upper urinary, and lower urinary tract microbiomes in USD.
The analysis drew on previously generated 16S rRNA datasets from participants with and without urinary stone disease, pooled across stone, stool, and urine sample types. The abstract does not specify exact participant numbers, ages, or geographic origin, so this appears to be a secondary meta-analysis of existing public or previously published cohort data rather than a newly recruited cohort. What can be said with confidence is that the population included both USD patients and comparison individuals without the disease.
Consistent with prior work, the gut, upper urinary tract, and lower urinary tract microbiomes were each found to be distinct microbial communities. Rare phylotypes, those present at low frequency and abundance, comprised the majority of the taxa detected across kidney stone, stool, and urine samples. This indicates that the low-abundance portion of these communities is numerically dominant even though it is often overlooked in favor of common, high-abundance taxa. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings suggest that rare phylotypes deserve dedicated attention in future USD microbiome research, since they make up most of the taxonomic diversity across stone, stool, and urine niches. Because bacteriotherapies for urologic health are being developed based on microbiome composition, ignoring rare taxa could mean missing organisms relevant to disease onset or progression. This work supports a shift toward analytical approaches that explicitly separate rare from common phylotypes when characterizing the kidney stone, gut, and urinary tract microbiome relationship to USD.
This study sought intestinal microbiome and metabolome signatures that distinguish patients with chronic granulomatous disease (CGD) and CGD-associated inflammatory bowel disease (CGD-IBD). CGD is caused by defects in the NOX2 enzyme complex. Researchers profiled the fecal microbiome by 16S rRNA amplicon sequencing and the stool metabolome by liquid chromatography-mass spectrometry. Diversity, LEfSe, random forest, and PICRUSt2 functional prediction were applied. Confounders such as antibiotics, steroids, and azathioprine were identified and controlled. Findings were validated in a second cohort.
This cross-sectional study enrolled patients at the NIH Clinical Center (primary cohort) and through the Primary Immune Deficiency Treatment Consortium (validation cohort), recruited between 2012 and 2018. The primary cohort included 79 CGD patients, 8 pathogenic variant carriers, and 19 healthy controls. The validation cohort added 36 pre-transplant CGD patients from 11 centers across the USA and Canada. The validation cohort was mostly pediatric, with a median age of 2.1 years, versus 23 years in the primary cohort. Most CGD patients had X-linked gp91 defects and were male.
CGD patients had significantly lower bacterial alpha diversity than healthy controls and their samples were enriched for Proteobacteria. Beta diversity separated CGD from healthy (p less than 0.003). Stool from CGD patients was enriched for Erysipelatoclostridium, Sellimonas, and Lachnoclostridium species, while butyrate-producing genera were depleted. Active or prior CGD-IBD clustered separately (p less than 0.009) with lower diversity. CGD-IBD showed severe reductions in the anti-inflammatory 1,4-DHNA pathway. Several taxa correlated significantly between the two cohorts, supporting reproducibility.
As the largest microbiome-metabolome study in CGD to date, the findings point to candidate biomarkers and therapeutic targets. Restoring butyrate producers or bacteria that make aryl hydrocarbon receptor ligands may help treat CGD-IBD. The severe loss of 1,4-DHNA, an anti-inflammatory microbial metabolite, in CGD-IBD suggests a mechanism that could be therapeutically restored. Limitations include sex imbalance, an age gap between cohorts, and reliance on 16S sequencing. The observational design means associations do not establish causation.
This study asked whether curing hepatitis C virus (HCV) with direct-acting antivirals (DAAs) produces lasting improvement in gut dysbiosis and microbial translocation. It followed patients long after treatment. Fecal samples at baseline and 72 weeks after treatment completion were analyzed by 16S rRNA sequencing. Butyryl-CoA:acetate CoA transferase (BCoAT), a butyrate-production gene, was measured by real-time PCR. Plasma lipopolysaccharide binding protein (LBP) and intestinal fatty acid binding protein (I-FABP) were measured by ELISA as markers of translocation and gut damage.
The prospective longitudinal cohort was 69 HCV-infected adults treated with DAAs at King Chulalongkorn Memorial Hospital in Bangkok, Thailand. This included 50 patients with HCV monoinfection and 19 with HCV/HIV coinfection, plus 20 healthy controls. HCV/HIV patients were on antiretroviral therapy with undetectable HIV RNA. Patients were grouped by liver fibrosis stage, from no or early fibrosis (F0-F1) to significant fibrosis or cirrhosis (F2-F4). Sustained virological response reached 94 percent in monoinfection and 100 percent in coinfection.
Among treatment responders, gut microbial richness improved and stayed improved at 72 weeks. Chao1 rose from a baseline of about 99 to about 128, while non-responders showed no improvement. Fourteen short-chain fatty acid producing genera increased, including Blautia, Fusicatenibacter, Subdoligranulum, and Bifidobacterium. BCoAT expression rose to levels comparable with healthy controls. Plasma LBP fell significantly in responders, from about 17,700 to about 13,900, matching healthy levels, and its change correlated inversely with BCoAT (r=-0.315, p=0.011). Gains were strongest in HCV-monoinfected patients with mild fibrosis. I-FABP did not decline significantly.
The results indicate HCV cure can durably restore gut microbiota and butyrate production and reduce microbial translocation, supporting guidelines that recommend early DAA treatment regardless of fibrosis stage. Because improvement was limited in HCV/HIV coinfection and in advanced fibrosis, coinfected patients may retain residual dysbiosis and need additional gut-directed strategies. The unchanged I-FABP suggests translocation reduction is tied to microbiota composition more than to repaired gut barrier. The study reports associations, not proven causation, and had few coinfected patients.
This study examined the gut microbiota and short-chain fatty acids (SCFAs) in children with constipated autism spectrum disorder (C-ASD). Researchers used an integrated approach combining 16S rRNA gene sequencing with gas chromatography-mass spectrometry-based metabolomics to characterize bacterial community composition and SCFA levels. The aim was to clarify the relationship between constipation, autism spectrum disorder, gut microbiota, and SCFAs, an area the authors describe as still debated.
The study enrolled 80 Chinese children, divided into a constipated autism spectrum disorder (C-ASD) group of 40 children and a typically developing (TD) group of 40 children. Both groups were compared directly using the same 16S rRNA sequencing and metabolomics methods. The abstract does not provide further demographic details such as age range or sex distribution.
Gut microbial community diversity, measured by the Observed, Chao1, and ACE indices, was significantly lower in the C-ASD group than in the TD group. Several taxa, including Ruminococcaceae_UCG_002, Phascolarctobacterium, Megamonas, Parabacteroides, Fusobacterium, and Prevotella species, were enriched in C-ASD children, while Anaerostipes, Lactobacillus, Ruminococcus_gnavus_group, and related taxa were enriched in TD children. Propionate levels were higher in the C-ASD group and were negatively correlated with other measured parameters, indicating altered SCFA metabolism alongside the shifted microbial community.
The findings suggest that constipation in children with autism spectrum disorder is accompanied by a distinct, less diverse gut microbiota and altered short-chain fatty acid production, particularly elevated propionate. This supports the idea that gut microbial and metabolic changes are linked to gastrointestinal comorbidity in autism spectrum disorder rather than being incidental. These microbiota and SCFA signatures could inform future research into microbiome-targeted approaches for managing constipation in this population.
This study examined whether rifaximin, a poorly absorbed antibiotic known for regulating gut microbiota, could improve loperamide-induced constipation. The researchers assessed effects on serum neurotransmitters and neuropeptides, water-channel gene expression, inflammation-related gene expression, gut microbiota composition, and serum metabolomics. The goal was to clarify how rifaximin might act on the gut-microbiota axis to relieve constipation.
The study used Sprague-Dawley (SD) rats in which constipation was experimentally induced with loperamide. No human cohort was involved, as this was a preclinical animal model study. Sample size and group numbers were not specified in the abstract.
Rifaximin improved constipation by increasing serum 5-HT and substance P (SP) and by raising mRNA expression of the water-channel genes AQP3 and AQP8, while reducing expression of the inflammation-related genes TLR2 and TLR4. It also reshaped the gut microbiota of constipated rats, increasing potentially beneficial bacteria Akkermansia muciniphila and Lactobacillus murinus while reducing Bifidobacterium pseudolongum. Metabolomics analysis showed that serum metabolites altered by constipation, including bile acids and steroids, were restored toward normal levels after rifaximin treatment.
The findings suggest rifaximin could serve as a multi-target therapy for functional constipation, acting through gut microbiota modulation, water metabolism, neurotransmitter and neuropeptide signaling, and reduced intestinal inflammation. The multi-omics approach highlights specific bacterial taxa and metabolite classes, such as bile acids, as potential mechanistic links between microbiota changes and constipation relief. These results support further investigation of rifaximin as a microbiome-targeted intervention for constipation, pending confirmation in human studies.
This study asked whether gut microbiota composition correlates with leukopenia (low white blood cell count) after chemotherapy in colorectal cancer (CRC) patients. Leukopenia reflects chemotherapy-induced bone marrow suppression. Fecal microbiota was profiled by 16S rRNA sequencing of the V3-V4 region on a MiSeq platform, with alpha-diversity, LEfSe, and correlation analyses. Six machine-learning algorithms, including logistic regression, random forest, neural network, support vector machine, gradient boosting, and CatBoost, were used to build prediction models.
The cohort was 55 CRC patients receiving first-time chemotherapy and 56 healthy volunteers at Huzhou Central Hospital in China, sampled between 2019 and 2021. By post-chemotherapy white blood cell level, patients were split into a hypoleukocytes group (n=13, below 3.5 x10^9/L) and a normal leukocytes group (n=42). CRC was pathologically confirmed, and patients with prior chemotherapy, other tumors, or recent microbiota preparations were excluded. Healthy controls skewed younger than patients.
CRC patients had significantly lower gut microbial diversity than healthy controls, though total abundance did not differ. Fifteen differential taxa were found, including Bacteroides, Faecalibacterium, and Streptococcus. Within CRC, the hypoleukocytes group had significantly lower diversity than the normal group, and Escherichia-Shigella was reduced. Nine differential taxa separated the groups, such as Fusicatenibacter and Cetobacterium. For leukopenia prediction, random forest reached AUC 0.995 and CatBoost gave the best accuracy (sensitivity 85.17 percent, specificity 100 percent). The most predictive taxa were Fusicatenibacter, Cetobacterium, and Paraeggerthella.
The results suggest gut microbiota is associated with chemotherapy-induced leukopenia in CRC and could help predict which patients are at high risk, enabling earlier preventive measures like leukocyte support or dose adjustment. Distinct microbial signatures for CRC and for post-chemotherapy leukopenia may offer non-invasive biomarkers. The authors note the small sample, the age gap between younger controls and older patients, and that whether these bacterial shifts cause or result from low white cell counts remains unknown. Larger studies are needed.
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 study characterized the gut microbiome in people with HIV who also have metabolic dysfunction-associated steatotic liver disease (MASLD). It used 16S rRNA sequencing of the V3-V4 region on stool. Investigators compared three groups to separate the effect of MASLD from HIV. They measured alpha diversity, beta diversity, and genus-level markers. The aim was to find a microbiome signature specific to MASLD in this population.
The cohort was 80 adults recruited in Madrid, Spain. It included 30 with HIV plus MASLD, 30 with HIV without MASLD, and 20 with MASLD without HIV. All HIV-positive participants were on stable antiretroviral therapy, averaging about six years, with more men than the MASLD-only group. MASLD severity was matched by FibroScan. The design was a multicenter prospective cohort with strict exclusions for active viral hepatitis and heavy alcohol use.
Major butyrate producers, including Faecalibacterium, Ruminococcus, and Lachnospira, dominated all three groups. Shannon and Simpson diversity were higher in MASLD-positive participants (Kruskal-Wallis p = 0.047). Beta diversity separated by MASLD, with MASLD-positive people overlapping regardless of HIV status (ADONIS R squared = 0.166, p < 0.001). MASLD, not HIV, drove community structure (q = 0.002 versus q = 0.930). The Firmicutes/Bacteroidetes ratio did not differ (p = 0.203).
The findings indicate MASLD influences the gut microbiome more than HIV status alone. Some shifts previously blamed on HIV may instead reflect the high prevalence of fatty liver in this group. The study is cross-sectional and small, so it cannot prove the microbiome causes MASLD. It lacked a fully healthy control group and assessed composition, not microbial function.
This study characterized the gut microbiota of Chinese children with autism spectrum disorder (ASD) and compared it to healthy children. It also sought candidate microbial biomarkers for early diagnosis. Researchers used 16S rRNA gene sequencing of the V3-V4 region on faecal samples. They analyzed alpha and beta diversity, taxonomic composition, and co-occurrence networks. LEfSe and KEGG pathway analyses identified differentially abundant taxa and predicted metabolic functions between the ASD and control groups.
The cohort was 1,118 children from 12 provinces of China: 957 with clinically diagnosed ASD and 161 healthy controls. Both groups were aged 2 to 12 years. Mean ages were 4.6 years for ASD and 4.8 years for controls. ASD diagnosis followed DSM-5 criteria before enrollment. No participant had taken antibiotics, antipsychotics, probiotics, or prebiotics in the prior month. Children with other major psychiatric or inflammatory conditions were excluded.
Alpha diversity was significantly lower in ASD children than controls, and beta diversity separated the groups. The Bacteroidetes to Firmicutes ratio was 0.54 in ASD versus 0.89 in controls. Genera enriched in ASD included Faecalibacterium, Blautia, Eubacterium eligens group, Parasutterella, Lachnospiraceae NK4A136 group, and Veillonella. Prevotella 9 and Agathobacter were higher in controls. Bacteroides fragilis increased in ASD, while Bacteroides plebeius, stercoris, coprocola, and Parabacteroides merdae decreased. The ASD co-occurrence network was more complex, with average degree 49.78 versus 26.71 in controls.
This is one of few large studies of gut microbiota in Chinese children with autism, adding evidence of gut dysbiosis in ASD. It also flags candidate biomarkers for early diagnosis. Predicted functions differed in ASD, especially folate, fatty acid, amino acid, and aromatic compound metabolism, plus some neurotransmitter pathways. These may link microbes to autism biology. The design was cross-sectional and observational, so it shows association, not causation. The distinctive taxa could support non-invasive diagnostic tools pending validation.
Researchers in Ghana compared the gut microbiome of tuberculosis (TB) patients, including subgroups with diabetes mellitus (TB-DM) or HIV (TB-HIV) comorbidity, against healthy household controls. They assessed changes before treatment and again after the two-month intensive phase of anti-TB therapy.
Ninety participants (60 TB-only, 23 TB-DM, 7 TB-HIV) provided stool samples at baseline, and 50 of them were resampled after two months of HRZE antibiotic therapy. Gut microbiota were profiled by 16S rRNA gene sequencing, with taxonomic diversity and PICRUSt2-predicted functional pathways compared across groups.
All three TB cohorts showed significantly lower alpha diversity and altered composition versus healthy controls, with enrichment of inflammatory genera Escherichia-shigella, Streptococcus, Enterococcus and Erysipelatoclostridium, and depletion of Faecalibacterium, Bifidobacterium and Clostridium. TB-only patients were enriched with Streptococcus and Erysipelatoclostridium, TB-DM with Bacteroides, and TB-HIV with Escherichia-shigella, Dialister and Erysipelatoclostridium. After two months of anti-TB therapy, Erysipelotrichaceae UCG-003, Veillonella and Fusobacterium became more enriched across cohorts.
The findings suggest tuberculosis itself, independent of diabetes or HIV status, drives gut dysbiosis and expansion of inflammation-associated microbes, which may have implications for immune function and treatment response during anti-TB therapy.
This study investigated whether gut microbiota dysbiosis associates with Henoch-Schonlein purpura nephritis, also called IgA vasculitis with nephritis, in adults. Fecal bacteria were profiled by 16S ribosomal RNA gene sequencing of the V3-V4 region on the Illumina MiSeq platform, analyzed at genus level. Diversity, community structure, and differential taxa were compared between patients and controls. A receiver operating characteristic model assessed diagnostic value, and genera were correlated with clinical indices.
The study enrolled 52 adults at West China Hospital, Sichuan University, in Chengdu, China, between June 2018 and November 2019. It compared 26 patients with clinically and pathologically diagnosed Henoch-Schonlein purpura nephritis against 26 healthy controls matched for sex and age. Samples were collected at diagnosis before immunosuppressive therapy, with a unified diet 3 days beforehand and no antibiotics within 4 weeks. Kidney-damage markers were clearly worse in patients.
Patients showed lower gut diversity, with ace index 288.06 and chao index 294.71 versus 366.04 and 371.36 in controls. Three genera were increased in patients: Bacteroides (p = 0.016), Escherichia-Shigella (p = 0.021), and Streptococcus (p = 0.012), while Prevotella_9 was reduced (p = 0.016). A four-genus classifier reached an area under the curve of 0.86. Streptococcus correlated positively with urinary red blood cells (r = 0.492, p = 0.011) and negatively with serum albumin (r = -0.474, p = 0.014).
The results suggest adult Henoch-Schonlein purpura nephritis features gut dysbiosis marked by fewer beneficial bacteria and more potential pathogens. Higher Streptococcus tracked with hematuria, hypoalbuminemia, and severe pathology, and correlated with abnormal Gd-IgA1-to-IgA ratios, hinting at a role in disease severity through mucosal immunity. The authors propose fecal bacteria as a possible diagnostic aid and microbiome modulation as a therapeutic direction. As a cross-sectional observational study, it cannot establish that dysbiosis causes or drives the disease.
Researchers compared gut microbiota in 90 thyroid carcinoma patients and 90 healthy controls, using stool samples analyzed by 16S rRNA gene sequencing.
An exploratory cohort of 60 patients and 60 controls was used to build a microbial signature via LEfSe, stepwise logistic regression, lasso regression, and random forest modeling. An independent cohort of 30 patients and 30 controls validated the findings, and Tax4Fun plus PICRUSt2 predicted functional pathway changes.
Thyroid carcinoma patients had reduced gut microbiota richness and diversity, though phylum-level abundances did not differ significantly overall. A 10-genus signature distinguished patients from controls, with AUCs of 0.809 in the exploration cohort and 0.746 in validation, and predicted functional changes included declines in aminoacyl-tRNA biosynthesis, homologous recombination, mismatch repair, DNA replication, and nucleotide excision repair. A separate four-genus signature distinguished patients with metastatic lymphadenopathy from those without.
These findings support gut microbiota dysbiosis as a feature of thyroid carcinoma and suggest stool-based microbial signatures could aid non-invasive diagnosis and staging.
This large population study asked whether yoghurt consumption is linked to gut microbiome composition, faecal metabolites, and metabolic health. It combined dietary questionnaires with sequencing. Gut microbiota were profiled by 16S rRNA gene sequencing and whole shotgun metagenomic sequencing. Faecal metabolomics measured 1116 metabolites. Models adjusted for age, sex, BMI, family structure, and habitual diet using a Healthy Eating Index. Findings were tested for replication in a separate Dutch cohort, and 24-hour food records checked whether effects were transient.
Participants were from the TwinsUK registry, a predominantly older, white, female British cohort of adult twins aged 18 to 89 years. In total 4117 completed a food frequency questionnaire. Of these, 1092 never ate yoghurt and 3025 ate it at least weekly, averaging 4.67 times per week. Microbiome subsets included 1057 and 400 yoghurt eaters for 16S and shotgun data. Replication used 1103 volunteers from the LifeLines-DEEP cohort in the Netherlands, where 1010 were yoghurt consumers and 93 were not.
Yoghurt eaters had lower visceral fat mass (beta = -28.18 g, p = 0.016 after diet adjustment) and a healthier eating pattern. 16S data showed higher alpha diversity (Shannon beta = 0.05, p = 0.004). Two species rose with consumption: Streptococcus thermophilus (beta = 0.41, p = 6.14e-14) and Bifidobacterium animalis subsp. lactis (beta = 0.30, p = 1.49e-8), both dose-dependent. S. thermophilus replicated in LifeLines-DEEP. B. animalis subsp. lactis correlated with 13 faecal metabolites, including 3-hydroxyoctanoic acid, an HCA3 receptor agonist linked to reduced gut inflammation. Food records showed the bacterial increase was transient.
Yoghurt consumption tracks a healthier diet, lower visceral fat, and detectable gut increases in the live bacteria contained in the product. These yoghurt bacteria appear transient, not durable colonizers. Because the increase depended largely on eating yoghurt within the prior 24 hours, detection of these species mainly signals recent intake rather than lasting engraftment. The metabolite link, especially 3-hydroxyoctanoic acid, hints at how yoghurt bacteria might influence gut inflammation. This is a cross-sectional observational study, so it cannot prove that yoghurt causes the metabolic benefits.
This study examined whether dysbiosis of the skin microbiome and the gut microbiome is associated with melanoma growth and progression. The researchers used the MeLiM porcine model, which spontaneously develops melanoma that can progress or regress, to study this relationship. They performed parallel analysis of cutaneous (skin) microbiota and faecal microbiota from the same animals, comparing melanoma tissue to healthy skin and comparing MeLiM piglets to control piglets. Bacterial composition was profiled using high throughput sequencing of the V4-V5 region of the 16S rRNA gene.
The subjects were MeLiM piglets aged 8 to 12 weeks, a porcine model of melanoma progression and spontaneous regression. Skin swabs from melanoma tissue and healthy skin, along with faecal samples, were collected from the same individual animals. A control group of piglets without melanoma was also included for comparison of the faecal microbiome. The abstract does not specify the exact number of animals sampled.
There was a significant difference in microbiome diversity and richness between melanoma tissue and healthy skin, and between the faecal microbiome of MeLiM piglets and control piglets. Principal Coordinate Analysis and Non-metric multidimensional scaling both showed clear dissimilarities between these different bacterial communities. Linear discriminant analysis was used to identify specific bacterial taxa distinguishing the groups, though the abstract text is cut off before naming these taxa. Overall, the findings indicate that melanoma progression is accompanied by detectable shifts in both cutaneous and gut bacterial community composition.
The findings support the idea that skin microbiome alterations, not just gut microbiome alterations, may be relevant to the tumor microenvironment in melanoma. This suggests a potential link between local skin dysbiosis and systemic gut dysbiosis during melanoma progression, an area the authors note had not been previously investigated. Because the gut microbiome has already been shown to modulate response to melanoma immunotherapy, these results raise the possibility that skin microbiota could also influence tumor behavior or serve as an additional biomarker. This porcine model may offer a useful system for further mechanistic study of microbiome-melanoma interactions relevant to human disease.
Researchers gave Sprague-Dawley rat pups oral ferrous sulfate, ferrous bis-glycinate chelate, or a vehicle control from postnatal day 2 to 14. They tracked gut microbiome composition and metabolome changes, and followed a second cohort supplemented through weaning into young adulthood.
Pups received one of the three postnatal treatments and were profiled for microbiome alpha-diversity and metabolites including short-chain fatty acids and trimethylamine. A separate cohort was supplemented until postnatal day 21, weaned onto standard chow, then re-assessed at about 8 weeks of age.
Iron supplementation reduced alpha-diversity and altered SCFA and trimethylamine levels in a form-dependent way. Lactobacilli abundance dropped 10,000-fold with iron exposure in both pre-weanling and young adult animals. In young adulthood, ferrous sulfate raised microbiome diversity above control while ferrous bis-glycinate chelate lowered it.
The chemical form of supplemental iron, not just the dose, shapes how the infant gut microbiome develops and recovers. Effects on Lactobacilli and diversity persisted long after supplementation ended, suggesting early iron form choices could have lasting consequences.
This study asked whether the colonic microbiome returns to normal after surgical removal of colorectal cancer, or stays abnormal. Researchers profiled colonic biopsies using 16S rRNA gene amplicon sequencing of the V3-V4 region. They compared four groups: patients after CRC resection, controls, patients with newly diagnosed CRC, and patients with polyps. Analyses included beta diversity, differential abundance by linear regression and ANCOMBC, co-abundance group clustering, and links between microbiota, diet, and medication.
The cohort was adults recruited in Cork, Ireland, from 2017 to 2019. It included 63 patients after CRC resection during surveillance endoscopy, compared with 52 to 58 controls, 93 patients with newly diagnosed CRC, and 28 with polyps. Post-resection patients had a mean age of 64.5 years and were 58.7 percent male. Two biopsies were taken per patient, proximal and distal to the anastomosis. Findings were validated against published fecal datasets from France, Canada, the United States, and Japan, using dietary questionnaires for lifestyle data.
The colonic microbiota stayed significantly different from controls in 65 percent of post-resection patients. Clustering split them into two groups: one CRC-like (41 subjects) and one normal-like (22 subjects, about 35 percent). The normal-like group had significantly higher Shannon diversity (p less than 0.0001). Post-resection microbiomes had fewer CRC-associated pathobionts (Fusobacterium, Parvimonas) and more beneficial fiber-fermenting genera. Seven cross-study markers, including Fusobacterium, Parvimonas, Peptostreptococcus, and Porphyromonas, tracked the same split. Higher intake of cruciferous vegetables, fruiting vegetables, peanuts, vegetable soup, and cardiovascular drugs co-varied with the normal-like microbiome.
The results suggest the microbiome could serve as a risk marker, not just a diagnostic one, identifying which CRC survivors carry a cancer-like microbiota and may warrant closer surveillance. Because diet and cardiovascular drugs co-varied with a more normal microbiome, the authors raise the possibility that lifestyle factors modulate microbiome recovery after surgery. This is correlational, not proven cause. The study was cross-sectional with modest size and variable time since surgery. The authors call for longitudinal studies, ideally with structured dietary intervention, before clinical application.
This study compared the gut microbiome of children with ulcerative colitis to healthy children using two sequencing methods on the same samples. Researchers ran both 16S rRNA gene sequencing (V4 region) and whole metagenomic shotgun sequencing. They analyzed three data types: 16S genus abundance, shotgun species abundance, and shotgun pathway abundance. Outcomes were alpha diversity, beta diversity, differentially abundant taxa, and machine-learning prediction of disease status by random forests.
The main cohort was 19 pediatric ulcerative colitis cases and 23 healthy controls, aged 7 to 21 years, with mild to moderate active disease. All participants were Caucasian, and none used antibiotics, probiotics, or proton pump inhibitors. A few cases were on steroids, biologics, immunomodulators, or 5-aminosalicylate therapy. Age and sex did not differ between groups. Conclusions were confirmed in an independent set of 7 pediatric cases and 8 controls.
Children with ulcerative colitis had lower alpha diversity than healthy controls, significant by Shannon index for both data types. Beta diversity within cases was more variable, and disease status contributed significantly to it. Families including Akkermansiaceae, Clostridiaceae, Eggerthellaceae, Lachnospiraceae, and Oscillospiraceae contained species depleted in cases. Christensenellaceae species were depleted and Enterobacteriaceae species enriched. Random forests predicted disease status with an AUROC close to 0.90 using either 16S or shotgun data.
The findings show children with ulcerative colitis harbor a dysbiotic, less diverse gut community that overlaps substantially with adult ulcerative colitis signatures. This supports shared microbial features across ages. Importantly, 16S data predicted disease as accurately as shotgun data, which is more costly and labor-intensive. For classification, cheaper 16S sequencing may suffice. The authors caution that sample sizes remain small and that the study is observational, so it identifies associations rather than causes.
This study examined how delivery mode shapes the early gut microbiota of newborns using high-resolution shotgun sequencing. Researchers tracked the composition and dynamics of the neonatal gut microbiome over the first month of life. The design specifically compared elective cesarean section against vaginal delivery to sidestep the confounding effect of emergency cesareans, which can muddy conclusions about delivery mode's true influence.
The cohort consisted of Tunisian newborns, with stool samples collected from 5 infants born by elective cesarean section and 5 born vaginally. Samples were taken longitudinally at Day 0, Day 15, and Day 30 after birth. This is a small, delivery-mode-stratified newborn cohort rather than a large population sample.
Bacterial richness and diversity were similar between the elective cesarean and vaginally delivered groups, and both showed a shift in microbiota community composition during the first two weeks regardless of delivery mode. Both groups were dominated by Proteobacteria, Actinobacteria, and Firmicutes. However, starting from the second week, cesarean-delivered infants showed an underrepresentation of Bacteroides alongside an enrichment of opportunistic pathogenic species belonging to the ESKAPE group.
The findings suggest that even elective, non-emergency cesarean delivery is associated with a distinct early gut microbiota signature marked by Bacteroides depletion and ESKAPE pathogen enrichment, not merely overall diversity differences. This points to delivery mode as an independent driver of neonatal microbiome composition beyond confounding clinical circumstances. The emergence of opportunistic ESKAPE species by two weeks of age raises questions about potential vulnerability to opportunistic infection in cesarean-born infants that merit further, larger-scale investigation.
Researchers compared gut microbiota in 44 colorectal cancer (CRC) patients versus 20 healthy controls, and linked microbial patterns to tumor gene mutations.
Fecal samples underwent 16S rRNA gene sequencing for all participants. Targeted next-generation sequencing of formalin-fixed paraffin-embedded tumor tissue identified somatic mutations in 39 of the CRC patients.
CRC patients had lower microbial diversity and higher levels of Bifidobacterium, Bacteroides, and Megasphaera, while healthy controls showed more Collinsella, Faecalibacterium, and Agathobacter. APC mutations occurred in 77 percent (30 of 39) of CRC patients, the highest rate observed. KRAS mutant tumors were associated with Faecalibacterium, Roseburia, Megamonas, Lachnoclostridium, and Harryflintia, with KRAS status negatively correlated with Bifidobacterium and positively correlated with Faecalibacterium.
This is among the first studies directly linking specific tumor gene mutations to gut microbiota composition in colorectal cancer. The authors suggest targeted CRC therapy response may relate to gut flora, warranting further investigation.
This study investigated the ocular surface microbiome in patients with unilateral or asymmetric glaucoma who were using 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 tested whether differences in microbial composition were related to 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 were patients with asymmetric or unilateral glaucoma who used topical glaucoma therapy in only one eye, allowing comparison between their treated and untreated eyes. Seven were age-matched healthy controls with no history of ocular disease or eyedrop use, and samples were grouped into three categories: treated glaucomatous eyes, untreated contralateral eyes, and healthy control eyes.
Both the treated and the untreated eyes of glaucoma patients showed significantly greater alpha-diversity and a greater relative abundance of gram-negative organisms compared to healthy control eyes. This pattern occurred even in the contralateral eye that received no eyedrops, suggesting a systemic or bilateral effect rather than one confined to the treated eye alone. The microbial composition of patient eyes was also associated with decreased tear meniscus height and decreased tear break-up time, linking microbiome alterations to signs of ocular surface disease.
The findings suggest that topical glaucoma therapy is associated with ocular surface microbiome shifts that extend beyond the directly treated eye, potentially through systemic exposure or shared tear film dynamics. Because these microbial changes correlated with impaired tear film stability, the results implicate the ocular surface microbiome as a factor in medication-related ocular surface disease among glaucoma patients. This raises the possibility that microbiome monitoring could inform strategies to reduce ocular surface complications in long-term glaucoma treatment.
This study examined the composition, structure, and function of gut microbiota in patients with diabetic retinopathy (DR), a common complication of type 2 diabetes mellitus. Researchers used 16S ribosomal RNA gene sequencing on stool samples to characterize microbial community differences. They also explored correlations between gut microbiota features and the clinical characteristics of DR.
The study included 50 total participants who provided stool samples: 25 patients with diabetic retinopathy and 25 healthy controls. DNA was extracted from the fecal samples and analyzed using the MiSeq sequencing platform. No further demographic details were given in the abstract.
The gut microbial structure and composition of DR patients differed from that of healthy controls, and microbial richness was higher in the DR group. These alterations were associated with disrupted levels of the Firmicutes, Bacteroidetes, Synergistota, and Desulfobacterota phyla. At the genus level, Bacteroides, Megamonas, Ruminococcus_torques_group, Lachnoclostridium, and Alistipes were increased, while Blautia, Eubacterium_hallii_group, Collinsella, Dorea, Romboutsia, Anaerostipes, and Fusicatenibacter were decreased in DR patients. Notably, the Desulfobacterota phylum, which includes sulfate-reducing bacteria capable of hydrogen sulfide production, was among the disrupted taxa in DR.
These findings suggest that gut microbiota alterations, including shifts in sulfate-reducing Desulfobacterota, may be linked to the development or progression of diabetic retinopathy. The distinct microbial signature identified in DR patients raises the possibility that gut microbiota could serve as a biomarker or contributing factor in this diabetic complication. Further research building on the stochastic forest model mentioned in the abstract could help clarify whether specific taxa have diagnostic or mechanistic relevance to DR.
Maintaining the health of seafarers is a difficult task during long-term voyages. Little is known about the corresponding changes in the gut microbiome-host interaction. This study recruited 30 seafarers undertaking a 6-month voyage and analyzed their gut microbiota using 16S rRNA gene sequencing. Fecal untargeted metabolomics analysis was performed using liquid chromatography-mass spectrometry. Significant changes in the composition of the gut microbiota and an increased ratio of Firmicutes/Bacteroidetes at the end (day 180) of the 6-month voyage, relative to the start (day 0), were observed. At the genus level, the abundances of Holdemanella and Plesiomonas were significantly increased, while the abundance of Bacteroides was decreased. Predicted microbial functional analysis revealed significant decreases in folate biosynthesis and biotin metabolism. Furthermore, 20 differential metabolites within six differentially enriched human metabolic pathways (including arginine biosynthesis, lysine degradation, phenylalanine metabolism, sphingolipid metabolism, pentose and glucuronate interconversions, and glycine, serine, and threonine metabolism) were identified by comparing the fecal metabolites at day 0 and day 180. Spearman correlation analysis revealed close relationships between the 14 differential microbiota members and the six differential fecal metabolites that might affect specific human metabolic pathways. This study adopted a multi-omics approach and provides potential targets for maintaining the health of seafarers during long-term voyages. These findings are worthy of more in-depth exploration in future studies. IMPORTANCE Maintaining the health of seafarers undertaking long-term voyages is a difficult task. Apart from the alterations in the gut microbiome and fecal metabolites after a long-term voyage, our study also revealed that 20 differential metabolites within six differentially enriched human metabolic pathways are worthy of attention. Moreover, we found close relationships between the 14 differential microbiota members and the six differential fecal metabolites that might impact specific human metabolic pathways. Accordingly, preventative measures, such as adjusting the gut microbiota by decreasing potential pathobionts or increasing potential probiotics as well as offsetting the decrease in B vitamins and beneficial metabolites (e.g., d-glucuronic acid and citrulline) via dietary adjustment or nutritional supplements, might improve the health of seafarers during long-term sea voyages. These findings provide valuable clues about gut microbiome-host interactions and propose potential targets for maintaining the health of seafarers engaged in long-term sea voyages.
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 bacteriome, mycobiome (fungal community), and serum metabolome in people with polycystic ovary syndrome (PCOS) compared to healthy individuals, across both normal-weight and overweight/obese body types. Researchers used 16S rRNA sequencing to profile bacteria, ITS2 gene sequencing to profile fungi, and metabolome analysis to profile serum metabolites. The goal was to characterize multi-omic differences between PCOS and healthy states and to explore whether microbiota-based markers could support a diagnostic method for PCOS. Classifiers combining bacterial, fungal, pathway, and metabolite markers were built to distinguish PCOS from healthy controls.
The analysis drew on 88 fecal samples for the 16S rRNA and ITS2 sequencing and 87 serum samples for metabolome analysis. Participants included both PCOS patients and healthy volunteers, and both groups were further divided into normal-BMI and overweight/obese subgroups (PCOS-LB, Healthy-LB, PCOS-HB, Healthy-HB). No further demographic details such as age range or geographic origin are given in the abstract.
Significant differences in bacterial, fungal, and metabolite profiles were found between PCOS patients and healthy controls in both normal-weight and overweight/obese groups. Healthy overweight/obese individuals showed less abnormal metabolism than PCOS patients and a uniquely higher abundance of the fungal genus Mortierella. Nine bacterial genera, four predicted functional pathways, eleven fungal genera, and the top 30 metabolites were identified as distinguishing features, with classification accuracies (AUC) of 0.84, 0.64, 0.85, and 1.0 respectively. The metabolite-based model outperformed the microbe-based model at distinguishing PCOS from healthy controls within both BMI strata, and featured bacteria, fungi, pathways, and metabolites showed strong associations with the free androgen index in a cooccurrence network.
The findings suggest that serum metabolites, more than gut bacterial or fungal composition alone, may offer the most accurate biomarker signal for distinguishing PCOS from healthy states regardless of body weight. The strong links between featured multiomic markers and the free androgen index point to a mechanistic connection between gut microbiota, metabolism, and androgen excess in PCOS. This multiomics approach could support development of non-invasive diagnostic tools for PCOS that account for BMI status rather than treating all patients uniformly.
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.
Researchers tested whether curcumin, at three doses (40, 80, 160 mg/kg), could improve motor impairment, dopamine neuron loss, and gut microbiota disruption in the MPTP mouse model of Parkinson's disease.
Six groups of mice (control, solvent control, MPTP, and three curcumin doses) underwent pole, hanging, and open-field tests after 14 days. Tyrosine hydroxylase immunohistochemistry and electron microscopy assessed dopamine neuron survival and ultrastructure, and 16S rRNA sequencing profiled gut microbiota.
All curcumin doses reduced pole-climbing time and increased suspension scores and movement distance dose-dependently, with better dopamine neuron survival and less cell degeneration at higher doses. The MPTP group showed higher relative abundance of Patescibacteria, Proteobacteria, and Verrucomicrobia, while Patescibacteria, Enterobacteriaceae, and Enterococcaceae abundance decreased in all curcumin groups. Medium and high curcumin doses also reduced a KEGG pathway for N-acetylneuraminate degradation.
This preliminary mouse study suggests curcumin may offer neuroprotective benefits in Parkinson's disease partly through modulating gut microbiota composition, supporting further research into microbially targeted therapies.
This study tested whether a water extract of Cannabis sativa seed, a key ingredient in the traditional formula MaZiRenWan, relieves chronic constipation. It examined the role of gut microbiota. Researchers used a loperamide-induced constipation mouse model. They measured intestinal transit, fecal water content, gut barrier and inflammation markers, and anxiety and depression behaviors. A microbiota-depletion experiment tested whether the laxative effect depended on gut bacteria, using 16S ribosomal RNA sequencing to profile the microbiome.
The model used mice divided into three groups of eight: a blank control, a loperamide constipation group, and a group pretreated with the cannabis seed extract. Constipation was induced by subcutaneous loperamide at 10 milligrams per kilogram twice daily for two weeks. The extract was given by gavage at 1 gram per milliliter. This is a preclinical animal study. A separate arm added antibiotics to deplete the gut flora and test whether the extract still worked.
The extract improved intestinal motility and water-electrolyte metabolism, reduced inflammation, protected the gut barrier, and eased anxiety and depression behaviors in constipated mice. It reversed the loss of barrier molecules and lowered inflammatory factor expression. It also restructured the microbiota, altering bacteria linked to inflammation. Crucially, once the gut flora was depleted by antibiotics, the extract no longer relieved constipation, showing the effect depended on the microbiota.
The findings support cannabis seed extract as a microbiota-dependent option for constipation, offering a rationale for the traditional MaZiRenWan formula. The benefit tracked with shifts in the gut microbiota. Because flora depletion abolished the effect, gut microbiota appear necessary for the laxative action. This is a mechanistic finding in mice, not a human treatment claim. The authors call for further investigation of the extract for constipation, and human relevance remains to be established in clinical settings.
This case-control study asked whether gut microbiota differ between HIV patients who recover CD4 T-cells on therapy and those who do not. Researchers linked bacterial composition to markers of immune activation, inflammation, and bacterial translocation. Fecal microbiota were characterized by 16S ribosomal RNA gene V3-V4 region sequencing on the Illumina MiSeq platform. T-cell activation and senescence were measured by flow cytometry. Plasma lipopolysaccharide, soluble CD14, and twelve cytokines were quantified. Bacteria were correlated with immune measures using Spearman analysis.
The study enrolled 94 adults in Hangzhou, China: 28 immunological responders, 30 immunological non-responders, and 36 healthy controls. Responders had CD4 counts of 500 cells per microliter or more, and non-responders under 200, after two years of viral suppression on antiretroviral therapy. All HIV-positive participants had undetectable viral loads and no comorbidities. People with hepatitis, opportunistic infections, recent antibiotics, or inflammatory bowel disease were excluded. Groups were matched for age, sex, and body mass index.
Both responder and non-responder groups showed persistent gut dysbiosis versus controls, with reduced diversity that did not differ between the two patient groups. Fusobacterium, Ruminococcus gnavus, and Megamonas were enriched, while Faecalibacterium, Alistipes, Bifidobacterium, Eubacterium rectale, and Roseburia were depleted. Ruminococcaceae and Alistipes correlated positively with nadir and current CD4 counts and negatively with CD8+CD57+ T-cells. Inflammation markers and LPS rose with Ruminococcus and Fusobacterium but fell with Faecalibacterium. Escherichia-Shigella and Blautia were significantly higher in responders than non-responders.
The findings suggest gut dysbiosis persists despite successful viral suppression and may be one factor shaping how well immune function recovers on therapy. Specific genera tracked with CD4 recovery, immune activation, and translocation. Because samples were taken only after treatment and the design is correlational, the study cannot show whether microbiota drive immune outcomes or reflect them. Diet and living conditions may have biased results. The authors point to Escherichia-Shigella and Blautia as candidate genera linked to differing treatment outcomes, warranting direct manipulation studies.
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.
Gastric adenocarcinoma is associated with H. pylori infection and inflammation that can result in the dysbiosis of gastric microbiota. The association of intestinal microbiota with gastric adenocarcinoma subtypes or with gastric gastrointestinal stromal tumors (GIST) is however not well known. Therefore, we performed 16S rRNA gene sequencing on DNA isolated from stool samples of Finnish patients and controls to study differences in microbiota among different histological subtypes of gastric adenocarcinoma, gastric GIST and healthy controls.
We found that gut microbiota alpha diversity was lowest in diffuse adenocarcinoma patients, followed by intestinal type and GIST patients, although the differences were not significant compared to controls. Beta-diversity analysis however showed significant differences in microbiota composition for all subtypes compared to controls. Significantly higher abundance of Enterobacteriaceae was observed in both adenocarcinoma subtypes, whereas lower abundance of Bifidobacteriaceae was seen only in diffuse adenocarcinoma and of Oscillibacter in intestinal adenocarcinoma. Both GIST and adenocarcinoma patients had higher abundance of Enterobacteriaceae and lower abundance of Lactobacillaceae and Oscillibacter while lower abundance of Lachnoclostridium, Bifidobacterium, Parabacteroides and Barnesiella was seen only in the adenocarcinoma patients.
Our analysis shows association of higher Enterobacteriaceae abundance with all types of gastric tumors. Therefore it could be potentially useful as a marker of gastric malignancies. Lower gut microbiota diversity might be indicative of poorly differentiated, invasive, advanced or aggressive tumors and could possibly be a prognostic marker for gastric tumors.
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 examined the composition and functional potential of the gut microbiota in people with type 2 diabetes (T2D) across two distinct populations, Denmark and South India. The researchers used 16S ribosomal RNA gene amplicon sequencing on stool samples to compare the gut microbiota between countries and between people with and without T2D. A central goal was to determine whether any microbiome signature of T2D is universal across ethnicities and diets, or whether such signatures are instead country-specific. The study also looked at microbial associations with treatment using the anti-hyperglycemic drug metformin.
The study population consisted of 279 Danish study participants and 294 Indian study participants, for a total of 573 people. Stool samples were collected from both cohorts and profiled using 16S rRNA gene amplicon sequencing. The abstract does not specify additional demographic details such as age or sex distribution within these two national cohorts.
The gut microbiota differed measurably between the Danish and Indian populations, reflecting country-specific patterns in diversity and composition. Samples were stratified to look for both global (trans-ethnic) and country-specific microbial signatures associated with T2D and with metformin treatment. This approach allowed the researchers to separate microbial features that might be universal markers of T2D from those that are shaped by local diet or ethnic background. The abstract does not report specific taxa, effect sizes, or statistical values for these comparisons.
By directly comparing two ethnically and geographically distinct populations, this study helps clarify whether gut microbiota changes linked to type 2 diabetes represent a truly universal signature or are instead dependent on diet and ethnic origin. This distinction matters for whether microbiome-based diagnostics or interventions for T2D could be applied globally or would need to be tailored to specific populations. Separating country-specific findings from trans-ethnic ones also helps prevent overgeneralizing microbiome associations discovered in a single population. The findings support continued large-scale, multi-population microbiome research as a foundation for any future universal T2D biomarkers.
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 the nasal and oropharyngeal (NOP) microbial community using 16S rRNA gene sequencing. Researchers compared the microbiota composition and diversity across groups differing in COVID-19 status and severity. The goal was to characterize how SARS-CoV-2 infection alters the local respiratory microbiome, since no reliable markers exist to predict disease prognosis in these patients.
The cohort included 21 patients affected by COVID-19, some paucisymptomatic and others admitted to the Intensive Care Unit (ICU). They were compared against 10 controls who tested negative for COVID-19, as well as 8 patients infected with other human coronaviruses (HKU1, NL63, and OC43). All samples were drawn from nasal/oropharyngeal swabs analyzed by 16S rRNA sequencing.
Chao1 index, a measure of microbial richness, was significantly lower in ICU COVID-19 patients compared to paucisymptomatic patients. Chao1 was also decreased across ICU, paucisymptomatic, and other-coronavirus groups relative to controls. Shannon diversity index, which accounts for both richness and evenness, was significantly reduced only in ICU patients compared to controls and paucisymptomatic patients. At the phylum level, Deinococcus-Thermus was detected only in controls and was absent in SARS-CoV-2 and other-coronavirus patient groups.
The progressive loss of microbial diversity in the nasal/oropharyngeal tract, most pronounced in ICU patients, suggests that upper respiratory microbiome disruption tracks with COVID-19 severity. These findings raise the possibility that 16S rRNA-based diversity indices, such as Chao1 and Shannon, could serve as candidate biomarkers to help stratify disease severity. Further research could clarify whether restoring microbial diversity or targeting specific taxa like Deinococcus-Thermus has prognostic or therapeutic relevance in COVID-19 management.
The gut microbiota of preterm infants is affected by perinatal factors and, in turn, may impact upon infant health. In this study, we collected fecal samples at Day-10 (D10) and 4-months corrected-age (4M) from 227 moderate-late preterm (MLPT) babies enrolled in a randomized controlled trial of nutritional management. A total of 320 samples underwent 16S amplicon sequencing, and shotgun metagenomic sequencing was performed on 94 samples from the 4M time point. The microbiome of babies whose families lived in lower socioeconomic status (SES) areas exhibited a significantly higher microbial alpha diversity at D10 (Wilcoxon test, p = 0.021), greater abundance of Bifidobacterium (linear model, q = 0.020) at D10 and Megasphaera (q = 0.031) at 4M. Hospital of birth explained 5.2% of the observed variance in 4M samples (PERMANOVA, p = 0.038), with Staphylococcus aureus more abundant in fecal samples from babies born in Middlemore hospital (linear model, q = 0.016). Maternal antibiotic (Wilcoxon test, p = 0.013) and probiotic (p = 0.04) usage within the four-week period before sample collection was associated with a reduction in the alpha diversity of D10 samples. Infant probiotic intake explained 2.1% (PERMANOVA, p = 0.021) of the variance in the D10 microbial profile with increased Lactobacillus (linear model, q = 1.1 × 10-10) levels. At 4M, the microbiome of infants who were breastmilk fed had reduced alpha diversity when compared to non-breastmilk fed infants (Wilcoxon test, p < 0.05). Although causality cannot be inferred within our study, we conclude that in MLPT babies, maternal socioeconomic factors, as well as the perinatal medical environment and nutrition impact on the development of the newborn microbiome.
The importance of sun exposure on human health is well recognized, and a recent trend in the avoidance of sun exposure has led to the risk of missing the beneficial effects such as vitamin D3 biogenesis. Vitamin D3 insufficiency is one of the risk factors for the development of food allergies (FAs), and vitamin D3 status controls gut homeostasis by modulating the microbiota. This study aimed to explore the impact of daily full spectrum light exposure (phototherapy) on the pathogenesis of FAs. Phototherapy ameliorated allergic diarrhea and improved FA-associated vitamin D3 insufficiency and dysbiosis. Fecal microbiota transplantation (FMT) of FA donor feces induced allergic diarrhea with OVA-specific IgE elevation in naïve mice. In contrast, FMT of naïve donor feces ameliorated allergic diarrhea in established FA mice, suggesting the involvement of the microbiota composition in FA. Phototherapy is an alternative approach for the prevention of FA-like allergic diarrhea through the modulation of vitamin D3 status and microbiota composition.
This study aims to determine differences in the on- and off-tumor microbiota between patients with right- and left-sided colorectal cancer. Microbiome profiling of tumor and tumor-adjacent biopsies from patients with right-sided (n = 17) and left-sided (n = 7) colorectal adenocarcinoma was performed using 16S ribosomal RNA sequencing. Off-tumor alpha and beta diversity were significantly different between right- and left-sided colorectal cancer patients. However, no differences in on-tumor diversity were observed between tumor locations. Comparing the off-tumor microbiota showed the right colon to be enriched with species of the Lachnoclostridium, Selenomonas, and Ruminococcus genera. Whereas the left colon is enriched with Epsilonbacteraeota phylum, Campylobacteria class, and Pasteurellales and Campylobacterales orders, in contrast, the on-tumor microbiota showed relatively fewer differences in bacterial taxonomy between tumor sites, with left tumors being enriched with Methylophilaceae and Vadin BE97 families and Alloprevotella, Intestinibacter, Romboutsia, and Ruminococcus 2 genera. Patients with left-sided colorectal cancer had large taxonomic differences between their paired on- and off-tumor microbiota, while patients with right-sided colorectal cancer showed relatively fewer taxonomic differences. Collectively, this suggests that the right and left colon show distinctive bacterial populations; however, the presence of a colonic tumor leads to a more consistent microbiota between locations.
Researchers examined whether gut microbiota composition changes as patients recover from asymptomatic or mild COVID-19. They followed 12 quarantined patients in Korea longitudinally and compared them with 36 pre-pandemic healthy controls.
Paired fecal samples were collected from each patient at two time points: while SARS-CoV-2 RNA was still detectable in the respiratory tract, and again after it converted to negative. Samples underwent 16S rRNA amplicon sequencing (V3 to V4 region) with diversity and taxonomic analysis.
Bacteroidetes was depleted during infection (5.8% relative abundance) and rebounded after recovery (31.8%), a 3.34 fold increase in odds (FDR 9.17×10⁻⁵). The Firmicutes/Bacteroidetes ratio dropped from a mean of 215.02 during infection to 6.01 after recovery, and microbial evenness rose significantly (p = 0.003), all within a median 10 day interval.
Even asymptomatic or mild COVID-19 caused measurable gut dysbiosis, but the microbiota reverted toward a healthier, control-like composition quickly after viral clearance. The authors suggest modifying gut microbes could be a therapeutic avenue during COVID-19 recovery.
This study examined whether an ileal bile acid transporter inhibitor (IBATi), a drug developed to treat chronic idiopathic constipation, could improve nonalcoholic fatty liver disease (NAFLD) by acting on the gut microbiota. IBATi increases delivery of bile acids to the colon, and the researchers tested whether this shift in colonic bile acid exposure could alter gut bacteria in a way that benefits the liver. They measured body weight, liver function markers, serum lipids, NAFLD activity scores, and expression of bile-acid-related genes (Cyp7a1 in liver, Fgf15 in ileum) in high-fat diet (HFD) mice treated with IBATi.
The subjects were mice fed a high-fat diet to induce a NAFLD model, with some receiving IBATi treatment alongside the HFD. Gut microbiota composition was assessed from fecal samples using 16S rRNA sequencing. A separate cohort of antibiotic-treated mice was recolonized through fecal microbiome transplantation (FMT) using stool from either HFD or HFD-plus-IBATi donor mice, allowing the researchers to test whether the microbiota itself could transfer the treatment effect.
IBATi treatment significantly suppressed body weight gain, improved liver dysfunction, lowered serum LDL levels, and reduced NAFLD activity scores compared to untreated HFD mice. It also reversed HFD-induced decreases in hepatic Cyp7a1 and increased ileal Fgf15 expression, both markers of altered bile acid signaling. IBATi changed gut microbiota alpha-diversity that had been reduced by the high-fat diet, and this altered microbiota profile was able to be transferred to antibiotic-treated recipient mice via fecal transplantation.
The findings suggest that redirecting bile acids to the colon with an ileal bile acid transporter inhibitor can improve hepatic steatosis largely through correction of gut microbiota dysbiosis, rather than through direct liver-only mechanisms. Because the FMT experiments show the microbiota changes themselves reproduce benefits, this supports the gut-liver axis as a therapeutic target for NAFLD. This positions IBATi, an already-used constipation drug, as a potential repurposed candidate for NAFLD treatment pending further research.
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.
Differences in the microbiota in populations over age and geographical locations complicate cross-study comparisons, and it is therefore essential to describe the baseline or control microbiota in each population. This includes the determination of the influence of demographic, clinical and environmental factors on the microbiota in a setting, and elucidates possible bias introduced by these factors, prior to further investigations. Little is known about the microbiota of children in South Africa after infancy. We provide a detailed description of the gut microbiota profiles of children from urban Cape Town and describe the influences of various clinical and environmental factors in different age groups during the first 5 years of life. Prevotella was the most common genus identified in the participants, and after infancy, the gut bacteria were dominated by Firmicutes and Bacteroidetes. In this setting, children exposed to antibiotics and indoor cooking fires were at the most risk for dysbiosis, showing significant losses in gut bacterial diversity.
This 24-week follow-up study looked for gut microbial biomarkers that diagnose schizophrenia and predict antipsychotic treatment response. Stool samples underwent 16S rRNA gene sequencing of the V3-V4 regions. Treatment response was measured by change in the Positive and Negative Symptoms Scale total score after risperidone. A random forest model was built to distinguish patients from controls. Inflammatory markers, hypersensitive C-reactive protein and homocysteine, were also measured.
The sample was 107 first-episode, drug-naive schizophrenia patients and 107 healthy controls from China. Controls were matched by age, gender, education, smoking, and body mass index. Patients were treated with risperidone monotherapy titrated to 4 to 6 mg per day. Samples were collected at baseline and after treatment, with 60 patients completing the full 24 weeks.
Patients showed lower alpha-diversity than controls at baseline, on both the Shannon and Simpson indices, and a significant beta-diversity difference. A 10-microbe model separated patients from controls with an area under the curve of 0.867 in the verification set. Nineteen genera differed at baseline, and 14 of them belonged to the Firmicutes phylum. After 24 weeks, Lachnoclostridium decreased and Romboutsia increased. Baseline Lachnoclostridium and Romboutsia levels were significantly associated with treatment response.
The results suggest schizophrenia patients carry a characteristic gut microbiota, and that certain microbes may predict how well risperidone works. Baseline levels of specific genera were tied to symptom improvement. Because the design was observational, it cannot prove the microbiota causes schizophrenia or drives the drug response. Findings apply to risperidone and may not generalise to other antipsychotics. Microbiota-targeted strategies were proposed as a future direction.
This study examined how the gut microbial community changes along different regions of the gastrointestinal tract, comparing the small intestine, cecum, colon, and rectum. It also compared these gut regions across three closely related, co-occurring wild rodent species. The goal was to determine how much of the variation in gut microbiota is explained by gut region versus host species.
The study sampled three sympatric species of wild rodents: Apodemus speciosus, Apodemus argenteus, and Myodes rufocanus. These animals were presumably collected from the wild and sampled at multiple gastrointestinal sites (small intestine, cecum, colon, and rectum) per individual. The abstract does not give an exact number of animals sampled.
The small intestine harbored a microbial community that was distinct from that of the lower gastrointestinal tract (cecum, colon, and rectum) in all three rodent species. The genus Lactobacillus was notably more abundant in the small intestine than in lower gut regions across all three species. This pattern held consistently regardless of host species, suggesting gut region has a strong and generalizable effect on microbiome composition.
The findings indicate that gut region is an important driver of microbiome variation, meaning fecal or colon samples alone may not represent the full gastrointestinal microbial community. This has implications for how wild animal microbiome studies are designed, since relying only on fecal samples could miss important small-intestinal features like Lactobacillus enrichment. Comparative host-microbiome research may need to sample multiple gut regions to draw accurate conclusions about host-microbe interactions.
This is a phase Ib/II study of regorafenib plus toripalimab for colorectal cancer. The objective response rate (ORR) is 15.2% and the disease control rate is 36.4% in evaluable patients with recommended phase II dose (80 mg regorafenib plus toripalimab). The median progression-free survival (PFS) and the median overall survival are 2.1 months and 15.5 months, respectively. Patients with liver metastases have lower ORR than those without (8.7% versus 30.0%). All patients (3/3) with lung-only metastasis respond, whereas no patients (0/4) with liver-only metastasis respond. 94.9% and 38.5% of patients have grade 1 and grade 3 treatment-related adverse events, respectively. Gut microbiome analysis of the baseline fecal samples shows significantly increased relative abundance and positive detection rate of Fusobacterium in non-responders than responders. Patients with high-abundance Fusobacterium have shorter PFS than those with low abundance (median PFS = 2.0 versus 5.2 months; p = 0.002).
This study examined the gut microbiome composition of patients with young-onset colorectal cancer (yCRC), a form of sporadic colorectal cancer whose incidence is rising. Researchers used 16S rRNA gene sequencing to identify microbial markers distinguishing yCRC, then validated these findings in an independent cohort. Metagenome sequencing was also performed to characterize species-level and functional differences in bacterial communities associated with yCRC.
The discovery analysis drew on 728 samples analyzed by 16S rRNA gene sequencing. An independent validation cohort of 310 samples was used to confirm the identified microbial markers. A further subset of 200 samples underwent metagenome sequencing for species-level and functional analysis.
Gut microbial diversity was increased in yCRC compared to other groups studied. Flavonifractor plautii emerged as an important bacterial species associated with yCRC, whereas the genus Streptococcus contained the key phylotype linked to old-onset colorectal cancer. Functional analysis showed that yCRC-associated bacterial communities were distinguished by a dominance of DNA binding and RNA-dependent DNA biosynthetic processes, and a random forest classifier built on these microbial features achieved strong classification performance.
The findings suggest that gut microbiota biomarkers, particularly Flavonifractor plautii abundance and associated functional signatures, could serve as a non-invasive tool for detecting and distinguishing yCRC. This approach could help address the diagnostic gap for younger patients as sporadic colorectal cancer incidence rises in this age group. The distinct microbial and functional profile of yCRC versus old-onset colorectal cancer also points to potentially different underlying disease biology between the two age groups.
This study examined whether jasmine tea can ease depressive-like behavior through the brain-gut-microbiome axis. Researchers built a chronic unpredictable mild stress (CUMS) rat model to induce depression-like symptoms and then treated the animals with jasmine tea. They tracked depression-related behavioral indicators alongside changes in the gut microbiota using 16S rRNA sequencing. The goal was to connect microbial shifts to neurochemical changes in the brain.
The subjects were rats subjected to a chronic unpredictable mild stress protocol designed to produce depressive-like symptoms. The abstract does not report a specific number of animals, strain, sex, or age. This was an animal (rodent) model study rather than a human cohort, and no human population was involved.
Jasmine tea treatment improved depressive-like behaviors and normalized neurotransmitter levels in the CUMS rats. It also increased gut microbiota diversity and richness compared to untreated depressed rats. Spearman correlation analysis linked differential bacterial taxa, including Patescibacteria, Firmicutes, Bacteroidetes, Spirochaetes, Elusimicrobia, and Proteobacteria, to depression-related markers such as BDNF, GLP-1, and 5-HT in the hippocampus and cerebral cortex. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so this study did not address that angle.
The findings support the idea that jasmine tea's antidepressant-like effects operate at least partly through modulation of the gut microbiome, not solely through direct brain effects. This strengthens the broader case for the brain-gut-microbiome axis as a target for managing depression. It also suggests dietary or beverage-based interventions could complement other approaches to mood disorders. Because this is a rat model, further work would be needed before drawing conclusions about human depression treatment.
The diabetic autonomic neuropathy is one of the most common complications in type 2 diabetes mellitus (T2DM), especially gastrointestinal autonomic neuropathy (GAN), which occurs in up to 75% of patients. The study aimed to investigate the gut microbiota composition, structure, and function in T2DM patients with GAN (T2DM_GAN) and set up a link between gut microbiota and clinical characteristics of patients.
DNA was extracted from fecal samples of three groups using the kit method: healthy volunteers (n = 19), the patients with T2DM (n = 76), and T2DM_GAN (n = 27). Sequencing of 16S ribosomal DNA was performed using the MiSeq platform.
According to the clinical data, higher age, lower triglyceride, and lower body mass index were the main features of patients with T2DM_GAN. The gut microbiota analysis showed that Bacteroidetes, Firmicutes, and Proteobacteria constituted the three dominant phyla in healthy individuals. In addition, the gut microbiota structure and function of T2DM_GAN patients were clearly different from that of T2DM patients. T2DM patients were characterized by Fusobacteria, Fusobacteriia, Fusobacteriales, Fusobacteriaceae, Fusobacterium, Lachnoclostridium, and Fusobacterium_mortiferum. Those gut microbiota may be involved in carotenoid and flavonoid biosyntheses. Relatively, the Gammaproteobacteria, Enterobacteriales, Enterobacteriaceae, Escherichia-Shigella, Megasphaera, Escherichia_coli, and Megasphaera_elsdenii were characteristic in the T2DM_GAN patients. Those may be involved in bacterial invasion of epithelial cells and pathogenic Escherichia coli infection.
GAN exacerbated gut microbiota dysbiosis in adult patients with T2DM. The findings indicated that phyla Fusobacteria and class Gammaproteobacteria were closely related to the occurrence of T2DM. Especially the latter may promote T2DM_GAN.
This study examined whether gut microbiome composition differs in people with biopsy-proven nonalcoholic steatohepatitis (NASH), the more severe, inflammatory form of nonalcoholic fatty liver disease (NAFLD) that can progress to cirrhosis. Researchers characterized microbial diversity and specific genus-level abundances in NASH patients, both with and without cirrhosis, and compared these to healthy controls. They also tested whether the most NASH-associated genus correlated with blood lipid markers such as triglycerides and cholesterol.
The study included UK patients with biopsy-confirmed NASH, split into those without cirrhosis (n = 40) and those with cirrhosis (n = 25), for a combined NASH group of 65 patients. These were compared against 76 healthy controls. All participants had their gut microbiome composition assessed, alongside fasting lipid measurements in at least some individuals.
NASH patients without cirrhosis showed a 7% lower Shannon alpha diversity than controls, and this dropped further to 14% lower in NASH patients with cirrhosis, indicating progressively reduced microbial diversity with disease severity. Beta diversity (unweighted UniFrac distance) was also significantly reduced in both NASH groups compared to controls. The genus Collinsella was most strongly associated with NASH, rising from 0.29% abundance in controls to 3.45% in NASH without cirrhosis and 4.38% in NASH with cirrhosis. Collinsella abundance was also positively correlated with fasting triglycerides and total cholesterol, and negatively correlated with high-density lipoprotein cholesterol.
These findings strengthen the case that reduced gut microbial diversity and enrichment of specific proinflammatory taxa, particularly Collinsella, are linked to NASH severity and associated lipid abnormalities. Because Collinsella has previously been tied to obesity and atherosclerosis, its elevation in NASH suggests a potentially shared microbial pathway across these metabolic conditions. This supports gut microbiome composition, and Collinsella abundance specifically, as a candidate biomarker or contributor to NASH pathogenesis worth further mechanistic investigation.
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.
This study examined the relationship between the gut microbiota and psychiatric symptom severity among inpatients with serious mental illness. Researchers used 16S rRNA gene sequencing and whole genome shotgun sequencing to characterize fecal samples collected early in hospitalization. They then tested whether microbial richness and alpha diversity were associated with depression, anxiety, trauma, and suicide severity measures, and whether these microbial features predicted treatment outcome at discharge.
The study population consisted of 111 adult inpatients with serious mental illness. Diagnoses, suicide severity, trauma, depression, and anxiety were assessed shortly after admission. Participants self-collected fecal swabs early in the course of their hospital stay for microbiota analysis.
Depression and anxiety severity shortly after admission were negatively associated with bacterial richness and alpha diversity, meaning more severe symptoms corresponded to a less rich and less diverse gut microbiota. Specific bacterial taxa were identified as associated with depression and anxiety severity. Gut microbiota richness and alpha diversity measured early in hospitalization also significantly predicted depression remission by the time of discharge.
The findings support a link between gut microbial diversity and psychiatric symptom severity in a clinical inpatient population, extending prior evidence from animal models and small human studies. Because early microbiota measures predicted depression remission at discharge, gut microbiota composition may hold value as a marker of treatment response in serious mental illness. This strengthens the rationale for further investigating the brain-gut relationship as a factor in psychiatric care and outcomes.
The study characterised the relationships between gut microbiome composition, serum and faecal metabolites (including uraemic toxins and secondary bile acids), and clinical symptoms in end-stage renal disease (ESRD). Researchers used multidimensional data integration across microbiome, metabolome, and phenotype datasets to identify links between microbial functions and toxin accumulation. They then tested these relationships mechanistically using chronic kidney disease (CKD) rodent models, transplanting patient-derived microbiota into germ-free mice and antibiotic-treated rats to assess effects on toxin production and disease severity.
The human portion of the study included a cohort of 223 patients with end-stage renal disease (ESRD) and 69 healthy controls. Gut microbiome, serum, and faecal metabolome data were collected from these individuals. The mechanistic portion of the study used renal-injured germ-free mice and antibiotic-treated rats as recipients of human-derived microbiota, rather than additional human subjects.
A specific group of microbial species was enriched in ESRD patients and correlated tightly with clinical variables, and these species encoded functions involved in synthesizing uraemic toxins and secondary bile acids. The abundance of these microbial functions correlated with the serum and faecal concentrations of the corresponding metabolites. When microbiota from ESRD patients were transplanted into renal-injured germ-free mice or antibiotic-treated rats, the animals showed higher serum uraemic toxin production and more severe renal fibrosis and oxidative stress compared to animals receiving control microbiota. Two specific species, including Eggerthella lenta, were highlighted among those enriched in ESRD.
The findings support a causal role for specific gut microbial species and their toxin-synthesizing functions in driving uraemic toxin accumulation and worsening renal injury, rather than the microbiome shift being merely a byproduct of kidney failure. This suggests that targeting these microbial species or their metabolic pathways could be a strategy to reduce toxin burden and slow renal fibrosis in ESRD patients. The transplantation experiments in rodents strengthen the case that gut-derived microbial functions have a direct, testable effect on host kidney disease severity.
Researchers compared gut microbial composition among 165 people with major depressive disorder (MDD), 217 with bipolar disorder (BD), and 217 healthy controls. The goal was to find microbial features that could distinguish MDD from BD, a distinction that is often difficult clinically.
Stool samples from 599 subjects underwent 16S rRNA gene sequencing to profile bacterial operational taxonomic units (OTUs). Findings from a discovery set were then tested in an independent validation set using a random forest classifier.
Compared to controls, MDD showed altered covarying OTUs in the Bacteroidaceae family, while BD showed disturbed covarying OTUs in Lachnospiraceae, Prevotellaceae, and Ruminococcaceae. A 26 OTU signature separated the groups with AUCs of 0.961 to 0.986 in the discovery set and 0.702 to 0.741 in validation, and 4 of the 26 markers correlated with depression severity.
Misdiagnosis between MDD and BD can lead to the wrong treatment, since antidepressants and mood stabilizers are used differently for each. A validated gut microbial panel could offer a noninvasive tool to support differential diagnosis.
This study examined the gut microbiota structure of children with Autism Spectrum Disorder (ASD) across different ages and its relationship to fecal metabolites. Researchers used 16S rRNA sequencing to characterize the gut microbial population, then applied metagenomics and liquid chromatography-mass spectrometry to investigate a subset with chronic constipation. The goal was to clarify how gut microbial composition and its metabolic activity relate to ASD and to the gastrointestinal symptoms that commonly accompany it.
The primary cohort consisted of 143 children aged 2 to 13 years old, evaluated using 16S rRNA sequencing and grouped into ASD and typically developing (TD) categories. A subset of 30 children with ASD and co-occurring chronic constipation (C-ASD), along with their age-matched TD counterparts, was selected for more detailed metagenomic and metabolomic analysis. No further demographic or geographic details were provided in the abstract.
The ASD group showed no significant increase in gut microbial diversity with age, unlike the TD group, whose diversity increased as children got older, indicating a divergent developmental trajectory of the gut microbiota in ASD. Among children with constipation, the C-ASD group had decreased microbial diversity and depletion of Sutterella, Prevotella, and Bacteroides compared to matched TD children. These compositional changes were accompanied by dysregulated metabolism activities, and metabolomic analysis using liquid chromatography-mass spectrometry supported the metagenomic findings, though the abstract text was truncated before further detail.
The findings suggest that gut microbiota development in ASD does not follow the same age-related maturation seen in typically developing children, pointing to a distinct trajectory that may reflect or contribute to disease biology. The depletion of specific genera and disrupted metabolic activity in constipated ASD children implicate the gut microbiome in the pathogenesis of gastrointestinal symptoms that frequently co-occur with ASD. These results support the gut microbiota and its metabolic output as a potential area for further mechanistic study and biomarker development in ASD subgroups with GI involvement.
Acute graft-versus-host disease (aGVHD) is the main complication of hematopoietic stem cell transplantation (HSCT). Changes in gut microbiota composition have been associated with subsequent aGVHD, and reconstitution of healthy microbiota is currently being explored as a therapeutic approach. However, the specific actors in the intestinal ecosystem involved in the pathologic process at the time of aGVHD onset are not yet fully known. We prospectively collected stool samples from patients who underwent allogeneic HSCT. Patients sampled at aGVHD onset were compared with non-GVHD patients. To identify phylogenetic and functional signatures of the disease process, we determined fecal short-chain fatty acid (SFCA) profiles and used high-throughput DNA sequencing and real-time quantitative polymerase chain reaction to assess the microbiota composition. Microbiota alterations were highly specific of gastrointestinal (GI) aGVHD severity. Bacterial biomass and α-diversity were lower in severe aGVHD. We identified several bacterial signatures associated with severe aGVHD at disease onset; a negative correlation was observed with anaerobic bacteria of the Lachnospiraceae, especially the Blautia genus, and Ruminococcaceae families. In parallel, in severe aGVHD patients, we showed a dramatic decrease in the levels of the main SFCAs: acetate (75.8%), propionate (95.8%), and butyrate (94.6%). Mild aGVHD patients were characterized by conserved levels of propionate and Blautia propionate producers. Butyrate was significantly decreased in all GI aGVHD stages, representing a potential diagnostic marker of the disease. Specific microbiota and metabolic alterations were thus associated with aGVHD severity and may be useful for diagnostic and pathophysiologic purposes.
This study examined whether gut microbiome changes occur before the onset of brain pathology in a mouse model of Alzheimer's disease. Researchers compared gut microbiota composition between APP/PS1 transgenic mice and their wild-type littermates across multiple ages using 16S ribosomal RNA gene amplicon sequencing. The goal was to determine when microbiota divergence begins relative to amyloid deposition and microglial activation in the brain.
The subjects were APP/PS1 transgenic mice, a widely used Alzheimer's disease mouse model, compared against their wild-type littermates. Animals were sampled at several time points, including young ages of 1 to 3 months and later ages of 6 and 9 months. No human cohort was involved, as this was an animal model study of gut microbiota and neuropathology.
Gut microbiota composition began diverging between APP/PS1 and wild-type mice as early as 1 to 3 months of age, before any obvious amyloid plaque formation or plaque-localized microglial activation appeared in the cerebral cortex. By 6 and 9 months, distinct shifts emerged in inflammation-related bacterial taxa, including increases involving Escherichia-Shigella, Desulfovibrio, Akkermansia, and Blautia. Desulfovibrio, a sulfate-reducing bacterial genus capable of producing hydrogen sulfide, was among the taxa whose abundance changed alongside these other inflammation-linked microbes in the AD model mice.
The findings suggest that gut microbiota alterations precede, rather than merely follow, the development of hallmark Alzheimer's disease pathology such as amyloidosis and neuroinflammation. This raises the possibility that early microbiome changes, including shifts in sulfate-reducing bacteria like Desulfovibrio, could serve as diagnostic biomarkers for detecting AD risk before brain pathology becomes evident. It also points to the gut microbiota as a potential avenue for early intervention strategies targeting Alzheimer's disease before major neuropathological damage occurs.
This pilot study examined whether gut microbiome disturbances, gut barrier dysfunction, bacterial translocation, and resulting inflammation are associated with cognitive dysfunction in dementia. Researchers assessed gut microbiome composition, gut barrier integrity, bacterial translocation markers, and inflammatory markers using stool and serum samples. Microbiome composition was profiled through 16S rRNA sequencing, with analysis performed using QIIME 2 and Calypso 7.14 tools. Nutritional status and medication use were also documented to characterize the study population.
The study included 23 patients with dementia and 18 age and sex matched controls without cognitive impairment. Nutritional status was assessed in participants using the Mini Nutritional Assessment Short Form (MNA-SF). Detailed information on drug use was also collected from the cohort. This was a relatively small, matched case control pilot study rather than a large population based investigation.
Dementia was associated with dysbiosis, reflected in differences in beta diversity and shifts in taxonomic composition of the gut microbiome compared to controls. Gut permeability was increased in dementia patients, as shown by elevated serum diamine oxidase (DAO) levels. Systemic inflammation was also confirmed, evidenced by increased soluble cluster of differentiation 14 levels. The abstract does not report findings specific to Faecalibacterium prausnitzii, butyrate, or anti-inflammatory commensals.
These findings support the hypothesis that gut microbiome disturbances, impaired gut barrier function, and resulting systemic inflammation may contribute to cognitive dysfunction in dementia. The results suggest a potential gut-brain axis mechanism linking dysbiosis and barrier dysfunction to the inflammatory processes implicated in cognitive decline. As a pilot study with a modest sample size, these findings point toward the need for larger studies to confirm causal relationships and explore microbiome-targeted interventions for dementia.
Researchers examined protein lysine acetylation (Kac), a post-translational modification, across the gut microbiome as a whole, rather than in single organisms. They then compared Kac patterns between Crohn's disease patients and controls.
The team used a peptide immuno-affinity enrichment strategy coupled with Orbitrap mass spectrometry to capture Kac peptides from gut microbiome samples. An integrated metaproteomics and lysine acetylomics bioinformatic workflow, developed for this study, identified and quantified both microbial and human protein Kac sites.
The approach identified 35,200 Kac peptides from microbial and human proteins in gut microbiome samples. Kac was widespread across microbial metabolic pathways, including anaerobic fermentation that generates short-chain fatty acids. In Crohn's disease patients versus controls, 52 host and 136 microbial protein Kac sites were differentially abundant.
This is the first characterization of protein Kac at the whole-microbiome level, establishing that acetylation is altered in disease. The microbiome-wide acetylomic approach opens a new layer for studying functional dysregulation in Crohn's disease and other conditions.
The study examined whether acupuncture could improve Parkinsonism and correct gut microbial dysbiosis in mice treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a standard model of Parkinson's disease (PD). Researchers applied acupuncture at the acupoints GB34 and ST36 and assessed motor function, anxiety-like behavior, dopaminergic neuron and fiber levels, neuroinflammatory and apoptotic markers, and gut microbiota composition via 16S rRNA sequencing. The work rests on the premise that the gut-brain axis is a promising therapeutic target for PD.
The subjects were mice given MPTP to induce a Parkinson's disease phenotype, then treated with acupuncture at GB34 and ST36 or left untreated for comparison. The abstract does not report an exact number of animals, strain, sex, or age, so no specific cohort size can be stated. This was a controlled animal model study rather than a human clinical trial.
Acupuncture improved motor function and comorbid anxiety in the PD mice and increased dopaminergic fibers in the striatum and dopaminergic neurons in the substantia nigra. It also reduced the overexpression of microglia and astrocytes and normalized the Bax to Bcl-2 expression balance in both brain regions, indicating that acupuncture blocked inflammatory responses and apoptosis. Using 16S rRNA sequencing, the researchers found that acupuncture altered the relative abundance of 18 bacterial genera compared to untreated PD mice, including changes in Butyricimonas and Holdemania, showing that acupuncture also corrected gut microbial dysbiosis.
The findings support acupuncture as a strategy that can act on both the brain and the gut microbiome in Parkinson's disease, reinforcing the gut-brain axis as a viable therapeutic target. By simultaneously reducing neuroinflammation, protecting dopaminergic neurons, and reshaping microbial community structure, acupuncture may offer a non-pharmacological complement to existing PD treatments. Further work in human populations would be needed to confirm whether these mouse-model effects translate to patients.
Researchers examined whether gut microbiome composition tracks with clinical response to anti-PD-1/PD-L1 immunotherapy in gastrointestinal cancer. This association had previously been shown in melanoma, non-small cell lung cancer, and renal cell carcinoma but not GI cancers.
The team recruited 74 patients with advanced-stage GI cancer receiving anti-PD-1/PD-L1 treatment, collecting fecal samples before and during immunotherapy alongside clinical evaluations. Samples underwent 16S rRNA taxonomy surveying and shotgun metagenomic sequencing.
Responders showed an elevated Prevotella/Bacteroides ratio, and a responder subgroup had significantly higher Prevotella, Ruminococcaceae, and Lachnospiraceae. Short-chain fatty acid producing bacteria, including Eubacterium, Lactobacillus, and Streptococcus, were positively associated with response across GI cancer types, alongside differential microbial pathways in nucleoside, lipid, and sugar metabolism.
The identified bacterial taxa predicted patient stratification in both this GI cancer cohort and in melanoma patients from two prior published studies. This suggests the gut microbiome could serve as a marker for immune-checkpoint blockade response across cancer types.
This study characterized the gut microbiome in children with autism spectrum disorder. It compared stool bacterial profiles between affected and healthy children. Autism severity was rated using the Childhood Autism Rating Scale. A random forest model tested whether specific bacteria could distinguish autism from controls. Predicted microbial functions were also compared between groups.
The study enrolled 77 children with autism spectrum disorder and 50 age-matched healthy children. Among the autism cases, 33 had mild and 44 had severe autism by rating scale score. The children were recruited in China. Stool samples were analyzed to profile the gut microbiota. This was a human case-control study in a pediatric population.
Children with autism showed higher biomass, richness, and biodiversity of gut bacteria and an altered community structure. Bacteroides, Faecalibacterium, Parasutterella, and Paraprevotella were significantly lower than in controls. Several genera rose in autism. These included unidentified Lachnospiraceae, Clostridiales, Erysipelotrichaceae, Dorea, Collinsella, and Lachnoclostridium. Erysipelotrichaceae, Faecalibacterium, and Lachnospiraceae correlated positively with autism severity. Three markers, Faecalitalea, Caproiciproducens, and Collinsella, classified cases with an area under the curve of 0.94, validated at 0.98.
The findings add evidence that gut bacteria differ measurably in children with autism. A small set of genera classified affected children with high accuracy, suggesting possible diagnostic value. Altered functions such as galactose and glutathione metabolism hint at biological links to symptoms. The design is cross-sectional and cannot show whether bacteria cause autism traits. The authors frame microbiome modulation as a hypothesis for future therapeutic study.
Researchers compared gut microbiota in 80 people with type 2 diabetes: 45 with diabetic peripheral neuropathy (DPN), 21 with diabetes but no DPN, and 14 healthy controls. They tested whether flora composition tracked with clinical markers like insulin resistance and bile acid levels.
Fecal microbiota composition was profiled and compared across the three groups at the phylum and genus level. Correlations between bacterial taxa and clinical indicators, including the HOMA insulin resistance index and specific bile acids, were then analyzed.
In the DPN group, Firmicutes and Actinobacteria were more abundant while Bacteroidetes was reduced at the phylum level. At the genus level, Bacteroides and Faecalibacterium were depleted, while Escherichia-Shigella, Lachnoclostridium, Blautia, Megasphaera, and Ruminococcus torques group were enriched. Insulin resistance (HOMA-IR) correlated positively with Megasphaera, and glycine and tauroursodeoxycholic acids correlated positively with Ruminococcus gnavus group and related genera.
The findings point to a distinct gut microbiota disorder in diabetic peripheral neuropathy, linked to insulin resistance and bile acid metabolism. This suggests intestinal flora imbalance may contribute mechanistically to DPN development in type 2 diabetes.
This study investigated whether BDB, a natural bromophenol isolated from the marine red alga Rhodomela confervoides, could alleviate type 2 diabetes mellitus (T2DM) by modulating the gut microbiota. Researchers used 16S rRNA gene pyrosequencing of the V3-V4 regions along with metagenomic analysis to characterize microbial community changes during BDB treatment. The study compared BDB against metformin, a standard antidiabetic drug, and a vehicle control to assess effects on fasting blood glucose and gut microbial composition.
The study used 24 diabetic BKS db mice, randomly assigned in a blinded manner to receive BDB (n = 6), metformin (n = 6), or vehicle (n = 6) for seven weeks. Non-diabetic BKS mice (n = 6) served as a normal control group. This was an animal model study, not a human cohort.
Diabetic mice treated with BDB or metformin showed significant reductions in fasting blood glucose by the seventh week compared with vehicle-treated diabetic mice. Gut microbiota analysis revealed that short-chain fatty acid (SCFA) producing bacteria, including Lachnospiraceae and Bacteroides, were significantly more abundant in the BDB and metformin groups than in the vehicle group. Notably, Akkermansia was significantly elevated at the genus level in the BDB-treatment group specifically. No sulfate-reducing bacteria, Desulfovibrio, hydrogen sulfide, or sulfur metabolism findings were reported in this abstract.
These findings suggest that BDB's antidiabetic effects in this mouse model may be linked to favorable shifts in gut microbiota composition, particularly increases in SCFA-producing bacteria and Akkermansia. This positions BDB as a candidate natural compound worth further investigation for T2DM management through a gut-microbiota-mediated mechanism. The metagenomic data point toward specific microbial pathways that could be explored in future mechanistic and translational studies.
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 study characterized the gut and genital microbial ecosystems of wild vervet monkeys naturally infected with simian immunodeficiency virus (SIV). Researchers profiled fecal, rectal, vaginal, and penile microbiomes to examine shifts in microbial diversity, composition, and functionality during natural SIV infection. Unlike HIV-infected humans, SIV-infected vervet monkeys do not experience gut dysfunction, microbial translocation, or chronic immune activation, so the study aimed to describe this nonprogressing host-pathogen relationship at the microbiome level for the first time.
The subjects were wild vervet monkeys from populations across diverse locations in South Africa that were heavily infected with SIV. Fecal, rectal, vaginal, and penile samples were collected from these free-ranging animals rather than from a laboratory cohort. The abstract indicates the population varied by geographic site, age, and sex, all of which were examined as factors affecting the microbiome.
Geographic site, age, and sex all affected the vervet microbiome across different body sites. The fecal microbiome showed marked stratification into three enterotypes, and the vaginal microbiome stratified into two vagitypes, each predicted to be functionally distinct within its respective body site. External bioclimatic factors, biome type, and environmental temperature also influenced the microbiome locally, indicating that environment plays a substantial role alongside host factors in shaping microbial community structure.
By characterizing the gut and genital microbiome of a natural, nonprogressing SIV host, this study provides a comparative framework for understanding why vervet monkeys avoid the gut dysfunction, microbial translocation, and immune activation seen in HIV-infected humans. The identification of distinct, functionally stratified enterotypes and vagitypes suggests that microbiome composition and function, not just viral dynamics, may contribute to disease outcome in lentivirus infection. These findings support further investigation into host, environmental, and microbial factors that distinguish nonpathogenic SIV infection from progressive HIV disease in humans.
Researchers examined how cecal microbiota relate to feed efficiency in Xiayan chickens, an indigenous Chinese breed from Guangxi province. They compared 173 males and 167 females split into high and low feed efficiency groups by residual feed intake.
Cecal contents from chickens at the extremes of feed efficiency, 3 highest and 3 lowest residual feed intake per sex, were profiled by shotgun metagenome sequencing. Linear discriminant analysis effect size (LEfSe) identified taxa distinguishing high versus low feed efficiency groups, and predicted gene functions were compared between groups.
Bacteroides, Prevotella, and Alistipes were the most abundant genera overall. LEfSe found 6 biomarkers in males and 14 in females; Lactobacillus was consistently higher in high efficiency birds of both sexes, while Campylobacter avium (females) and Helicobacter pullorum (males) were enriched in low efficiency birds. High efficiency males also showed greater predicted capacity for xenobiotic biodegradation and metabolism.
The findings link specific cecal taxa, notably Lactobacillus enrichment and pathogen depletion, to better feed efficiency, and show that sex shapes these microbiome-performance relationships. This points to candidate microbial biomarkers for improving efficiency in indigenous chicken breeds.
We sought to characterize and assess differences in compositions of intestinal flora between patients with rheumatoid arthritis (RA) and their respective spouses. Eighty volunteers were recruited, including 30 pairs of RA patients and their spouses, and 20 healthy individuals. Fresh stool samples were collected, processed, and 16S rRNA-sequencing was performed. Data were analyzed using an operational taxonomic units-based method, and community structure assessments were performed. Community composition analysis indicated that there were similar intestinal microbiota structures in RA and in their respective spouses. Gut microbiota in spouses of RA were different from those of the healthy controls group, but these differences were not significant. We found that Blautia spp. and Streptococcus spp. were two most associated species in RA and these taxa were significantly higher in comparison to healthy controls. In contrast, our findings suggested that Roseburia spp. and Lachnoclostridium spp. were significantly lower in the RA in comparison to healthy controls. In conclusion, RA patients shared similar gut microbiota pattern with their spouses which were different from healthy individuals. The findings suggest that disturbance of the balance of gut microbiota may play an important role in the dynamics of pathogenesis of RA.
This study asked whether early diarrhea after kidney transplantation is linked to gut dysbiosis rather than infection. Researchers profiled the gut microbiota in serial stool samples using 16S ribosomal RNA gene V4-V5 deep sequencing. They also ran a multiplex PCR panel testing 22 bacterial, viral, and protozoan gut pathogens on diarrheal samples. PICRUSt was used to predict metabolic gene functions from the sequencing data. A hierarchical Bayesian logistic regression adjusted for repeated samples and clinical variables.
The cohort was 71 adult kidney transplant recipients at a New York hospital, followed during the first 3 months after transplant. They provided 199 stool samples in total. Twenty-five recipients developed post-transplant diarrhea. Analysis compared 28 diarrheal samples from 18 subjects against 112 samples from 46 recipients without diarrhea. The study also followed 2 recipients with recurrent Clostridioides difficile who underwent fecal microbial transplantation.
Diarrheal samples had significantly lower diversity than non-diarrheal samples (median Shannon index 2.4 vs 3.1, P below 0.001). Community structure separated clearly by ordination. Thirteen commensal genera were significantly less abundant during diarrhea, many from the Lachnospiraceae and Ruminococcaceae families (butyrate-producing Clostridia). Three genera were higher. Of 28 diarrheal samples, 26 were negative for all 22 tested pathogens; only 2 were positive. Diarrheal samples also showed lower predicted metabolic genes, including sugar-degrading pathways.
The findings suggest early post-transplant diarrhea usually reflects loss of beneficial commensal bacteria, not common infections. This challenges routine assumptions that immunosuppressant dosing alone explains it. Dysbiosis persisted across mycophenolate mofetil dose groups, arguing the drug dose is not the sole driver. In two fecal transplant cases, diarrhea resolved as depleted taxa recovered. Being observational, the study cannot prove whether dysbiosis causes diarrhea or results from it. Restoring commensal bacteria is a plausible avenue for future treatment research.
This cross-sectional study examined whether the gut microbiota is associated with extraintestinal joint inflammation in patients with inflammatory bowel disease (IBD). Stool samples were collected and DNA was sequenced on the Illumina platform, with reads quality-controlled using SHI7 and processed with SHOGUN. Microbial abundance and diversity were assessed with QIIME, and compositional biomarkers distinguishing groups were identified using LEfSe. The study also evaluated microbial functional pathways, including tyrosine degradation, and examined history of bowel surgery as a possible source of variability.
One hundred eighty patients were included in the analysis, divided into four groups: those with IBD-associated arthropathy (IBD-A), IBD without arthropathy (IBD-N), rheumatoid arthritis (RA), and non-IBD, nonarthritis controls. The abstract does not give a numeric breakdown of how many patients fell into each of the four groups. This design allowed direct comparison of gut microbial composition across intestinal and joint-related inflammatory phenotypes.
IBD-A was associated with an increased abundance of microbial tyrosine degradation pathways compared with IBD-N (P = 0.02). IBD-A and RA patients both showed an increased abundance of Clostridiaceae compared with controls (P = 0.045), suggesting a shared microbial signature across two distinct arthritis-associated conditions. History of bowel surgery was also identified as a significant source of variability among IBD patients (P = 0.001) and was linked to decreased alpha diversity.
The shared enrichment of Clostridiaceae in both IBD-associated arthritis and rheumatoid arthritis suggests a common gut microbial feature may underlie joint inflammation across different autoimmune and inflammatory contexts. Altered tyrosine degradation pathways in IBD-A point to a possible metabolic mechanism linking gut microbes to extraintestinal disease manifestations. The findings also highlight bowel surgery history as an important confounder to account for in future microbiome studies of IBD patients. Together, these results support further investigation of Clostridiaceae and related microbial pathways as potential targets or biomarkers for arthritis in IBD.
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.
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.
Resistant starch (RS) has been reported to reduce body fat in obese mice. However, this effect has not been demonstrated in humans. In this study, we tested the effects of RS in 19 volunteers with normal body weights. A randomized, double-blinded and crossover design clinical trial was conducted. The study subjects were given either 40 g high amylose RS2 or energy-matched control starch with three identical diets per day throughout the study. The effect of RS was evaluated by monitoring body fat, glucose metabolism, gut hormones, gut microbiota, short-chain fatty acids (SCFAs) and metabolites. The visceral and subcutaneous fat areas were significantly reduced following RS intake. Acetate and early-phase insulin, C-peptide and glucagon-like peptide-1 (GLP-1) secretion were increased, and the low-density lipoprotein cholesterol (LDL-C) and blood urea nitrogen (BUN) levels were decreased after the RS intervention. Based on 16S rRNA sequencing, certain gut microbes were significantly decreased after RS supplementation, whereas the genus Ruminococcaceae_UCG-005 showed an increase in abundance. Other potential signatures of the RS intervention included Akkermansia, Ruminococcus_2, Victivallis, and Comamonas. Moreover, the baseline abundance of the genera Streptococcus, Ruminococcus_torques_group, Eubacterium_hallii_group, and Eubacterium_eligens_group was significantly associated with the hormonal and metabolic effects of RS. These observations suggest that a daily intake of 40 g of RS is effective in modulating body fat, SCFAs, early-phase insulin and GLP-1 secretion and the gut microbiota in normal-weight subjects.
The link between gut microbes and autism spectrum disorders (ASD) has been already observed in some studies, but some bacterial families/species were found to be inconsistently up or down regulated. This issue has been rarely explored in the Chinese population. In this study, we assessed whether or not gut microbiota dysbiosis was associated with children with ASD in China. We enrolled 45 children with ASD (6-9 years of age; 39 boys and 6 girls) and 45 sex- and age-matched neurotypical children. Dietary and other socio-demographic information was obtained via questionnaires. We characterized the composition of the fecal microbiota using bacterial 16S ribosomal RNA (16S rRNA) gene sequencing. The ASD group showed less diversity and richness of gut microbiota than the neurotypical group, as estimated by the abundance-based coverage estimator index and the phylogenetic diversity index. The analysis of beta diversity showed an altered microbial community structure in the ASD group. After adjustment for confounders and multiple testing corrections, no significant group difference was found in the relative abundance of microbiota on the level of the phylum. At the family level, children with ASD had a lower relative abundance of Acidaminococcaceae than the healthy controls. Moreover, a decrease in the relative abundance of genera Lachnoclostridium, Tyzzerella subgroup 4, Flavonifractor, and unidentified Lachnospiraceae was observed in ASD group. This study provides further evidence of intestinal microbial dysbiosis in ASD and sheds light on the characteristics of the gut microbiome of autistic children in China.
This meta-analysis asked whether gut microbiome signatures of colorectal cancer are consistent worldwide. Researchers pooled eight fecal shotgun metagenomic case-control studies and reprocessed all raw data the same way. They controlled for confounders such as study origin, age, sex and colonoscopy. They then identified cancer-associated species, trained machine-learning classifiers, and tested them on studies not used for training.
The pooled data covered 768 adults, 386 with colorectal cancer and 392 tumor-free controls, from eight studies across seven countries on three continents. Samples were feces collected before any cancer treatment. Five studies (from France, Austria, China, the USA and Germany) formed the discovery set. Three further populations from Italy and Japan served as independent validation cohorts.
The analysis found 29 core species enriched in cancer at a very strict significance cutoff. These included known markers such as Fusobacterium and Bacteroides, plus a diverse set of Clostridiales. Classifiers reached an AUROC of at least 0.8 in seven of eight datasets. Cancer metagenomes showed more protein and mucin breakdown genes and fewer carbohydrate-degrading genes. Genes producing secondary bile acids were highly enriched (p = 1.6E-9), matching a fat and meat rich diet.
The work establishes that gut microbiome signatures of colorectal cancer generalize across countries and sequencing methods, supporting their use in future diagnostics. Accuracy approached that of the fecal occult blood test. By training across studies, the classifiers stayed specific to cancer and did not misfire on diabetes or inflammatory bowel disease. The bile-acid gene marker was confirmed by qPCR, a step toward a practical assay. The design is associative, not proof of causation.
This prospective cohort study asked how the gut microbiome differs in Alzheimer's disease and whether it disrupts intestinal homeostasis. Researchers collected monthly stool samples and ran shotgun metagenomic sequencing. They used machine learning (random forest) to find taxa that separate Alzheimer's from other groups. They also tested whether stool could alter P-glycoprotein, a mediator of gut anti-inflammatory balance. Stool supernatants were applied to T84 intestinal epithelial cells to measure P-glycoprotein and MRP2 protein expression.
The cohort was 108 nursing home elders in central Massachusetts, all aged 65 or older, followed up to 5 months. Of these, 51 had no dementia, 24 had Alzheimer's disease, and 33 had other dementia types. Across groups, 300 longitudinal stool samples were collected, one per elder per month. Elders exposed to antimicrobials, hospitalization, or medication changes were excluded. Elders with dementia, including the Alzheimer's group, had higher malnutrition and frailty scores and more often took atypical antipsychotics than elders without dementia.
Stool from Alzheimer's elders induced significantly lower functional P-glycoprotein expression than stool from other groups (p = 0.017). Lower P-glycoprotein signals a more proinflammatory gut epithelial state. Alzheimer's microbiomes had lower proportions of butyrate-producing species and fewer butyrate biosynthesis genes across four pathways. Proinflammatory and neurologically linked taxa were enriched in Alzheimer's elders. Frailty and malnutrition, plus specific taxa, accurately classified Alzheimer's versus no dementia in random forest models.
The results suggest the Alzheimer's gut microbiome may promote intestinal inflammation by lowering P-glycoprotein, a possible link in the gut-brain axis. This moves association studies toward a plausible mechanism. Butyrate-producing bacteria emerge as a candidate for study and future intervention in dementia. This is observational work in frail elders, so causation is not established. Confounders like malnutrition and medications were modeled but cannot be fully excluded.
This pilot study tested whether fecal microbial metabolites could serve as practical surrogates for gut microbiome composition after stem cell transplant. Standard 16S sequencing is too slow for clinical decisions. Researchers measured fecal indole and butyrate by liquid chromatography tandem mass spectrometry. Gut microbiota were profiled by 16S ribosomal RNA V4 sequencing. Metabolite and diversity measures were correlated with transplant outcomes including graft-versus-host disease, infection, and survival.
The cohort was 44 adult hematopoietic stem cell transplant recipients at a Texas cancer center, with 6 additional enrollees withdrawing. Most had acute myeloid leukemia or myelodysplastic syndrome (65.9%). Longitudinal stool samples (451 total) were collected from before transplant through day 100. Eighteen healthy adult volunteers gave one-time control samples. Median recipient age was 58.5 years. Most received myeloablative conditioning and matched unrelated donor grafts.
Both fecal indole and butyrate correlated with the Shannon diversity index at baseline (P = 0.02 and P = 0.002) and after transplant (P = 0.006 and less than 0.001). High-butyrate samples were enriched for Clostridiales; high-indole samples also for Bacteroidales. Lower diversity at engraftment was linked to more acute intestinal graft-versus-host disease (P = 0.02) and transplant-related deaths (P = 0.03). Patients who developed bloodstream infection within 30 days had significantly lower fecal butyrate at week 2 (P = 0.03).
The findings suggest fecal butyrate and indole could act as fast surrogate markers for gut microbial diversity and specific taxa after transplant. This could sidestep the delays of sequencing in the clinic. Low butyrate shortly after transplant flagged patients at risk of bloodstream infection, hinting that diet or prebiotic approaches might help. Metabolites were not significantly tied to graft-versus-host disease or overall survival, likely due to small size. Larger multi-center studies are needed before clinical use.
This study examined whether gut microbiome composition differs in people with fibromyalgia (FM), a syndrome marked by chronic widespread pain, fatigue, and impaired sleep. Researchers compared microbiome profiles using both 16S rRNA gene amplification and whole-genome sequencing. They also measured serum levels of the short-chain fatty acids butyrate and propionate to see whether metabolite changes tracked with any bacterial shifts. The design combined differential abundance analysis, variance analysis against clinical and environmental variables, and machine-learning classification.
The study population consisted of 77 women diagnosed with fibromyalgia and 79 control participants who were unrelated to the patients. Microbiome data came from stool samples analyzed by 16S rRNA sequencing and whole-genome sequencing, paired with targeted serum metabolite testing in the same participants. No further demographic or geographic details were given in the abstract.
Differential abundance analysis revealed significant differences in several bacterial taxa between FM patients and controls. Variance in microbiome composition was explained by FM-related variables more than by any other innate or environmental factor, and this variance correlated with clinical indices of FM. Consistent with alterations in butyrate-metabolizing bacterial species, serum levels of butyrate and propionate also differed in FM patients. Using machine-learning algorithms, microbiome composition alone classified patients versus controls with a receiver operating characteristic area under the curve of 87.8%.
This is described as the first demonstration of gut microbiome alteration in a nonvisceral pain condition, extending microbiome-disease links beyond gut-localized disorders. The strong classification performance suggests the microbiome could potentially serve as a diagnostic aid for fibromyalgia, a syndrome that is otherwise difficult to diagnose. The link to altered butyrate and propionate levels points toward specific metabolic pathways that may warrant further mechanistic study. The authors frame these findings as a foundation for future work on FM pathophysiology and possible new treatment approaches.
Researchers examined whether prenatal antibiotic exposure was linked to infant adiposity and gut microbiome composition, using the Nurture birth cohort (454 mother infant pairs recruited 2013 to 2015 in Durham, North Carolina).
Antibiotic exposure was captured by timing, number of courses, and type, then linked to infant weight-for-length z score (WFL-z) and skinfold thicknesses at 12 months. A subsample of infants (68 at 3 months, 50 at 12 months) had stool analyzed by 16S rRNA sequencing to assess gut microbial composition.
Any prenatal antibiotic exposure was linked to a 0.21 higher WFL-z at 12 months, with a dose-dependent trend (P for trend = 0.006) up to 0.41 higher WFL-z for 3 or more courses. After adjusting for delivery method, only second-trimester exposure remained associated with higher WFL-z (0.27) and greater subscapular skinfold thickness (0.49 mm). Second-trimester exposure was also linked to differing abundance of 13 bacterial amplicon sequence variants at 3 months and 17 at 12 months.
The findings suggest the second trimester may be a sensitive window where antibiotics could simultaneously reshape the infant gut microbiome and influence early adiposity, though the authors call for larger cohorts to confirm the link.
This study used next-generation 16S ribosomal RNA gene sequencing to characterize the salivary (oral) microbiota associated with throat cancer. Researchers compared microbial community diversity and composition among throat cancer patients, vocal cord polyp patients, and healthy controls. They also built a diagnostic model based on constituent bacteria and verified select findings with real-time quantitative PCR.
The study analyzed 70 oral (salivary) samples collected from three groups: 32 patients with throat cancer, nine patients with a vocal cord polyp, and 29 healthy individuals serving as normal controls. All participants were drawn from a clinical setting where throat cancer and vocal cord polyp diagnoses had been made, alongside disease-free comparison subjects.
The salivary microbiota of throat cancer patients was significantly different from that of polyp patients and healthy individuals, with beta diversity clearly divergent in the cancer group. Alpha diversity was significantly reduced in cancer patients, as shown by the Chao1 estimator (P = 8.1e-05), Simpson index (P = 0.0045), and Shannon index (P = 0.0071). The genera Aggregatibacter, Pseudomonas, Bacteroides, and Ruminiclostridium were significantly enriched in throat cancer patients compared with the other two groups, a result confirmed by qPCR. A diagnostic model built from these bacterial constituents achieved 87.5% accuracy in distinguishing cancer patients from the other groups.
These findings suggest that reduced salivary microbial diversity and enrichment of specific bacterial genera may serve as biological indicators associated with throat cancer. The strong diagnostic accuracy of the bacteria-based model points to the potential for salivary microbiota profiling as a non-invasive tool to help distinguish throat cancer from benign vocal cord polyps and healthy states. Because this is an association-based study, further research is needed to determine whether these microbial shifts are causal, secondary to tumor presence, or influenced by other factors before clinical application.
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 the Yanomami, a semi-nomadic hunter-gatherer group in the Amazon rainforest, using shotgun metagenomic sequencing. Researchers compared the taxonomic composition and functional gene content of the Brazilian Yanomami gut microbiome against the Venezuelan Yanomami, other traditional Amazonian groups, and an urban-industrialized population. The goal was to identify taxonomic and functional biomarkers that distinguish these groups and to understand how traditional, non-industrialized lifestyles shape the gut microbiome.
The subjects were members of the Yanomami, the largest semi-nomadic hunter-gatherer group in the Americas, sampled from populations in Brazil and Venezuela. The study also drew on comparison groups consisting of other traditional Amazonian populations and an urban-industrialized group. The abstract does not give specific sample sizes or additional demographic details for these cohorts.
Distinct taxonomic biomarkers were identified for each South American traditional group studied, including separate signatures for the Brazilian and Venezuelan Yanomami. Broad functional categories did not strongly distinguish traditional groups from the urban-industrialized group, but when these categories were stratified into finer detail, clear segregation between groups emerged. The Brazilian Yanomami gut microbiome showed unique functional features, including a higher abundance of gene families related to regulation and cell signaling, motility and chemotaxis, and virulence, setting it apart from the other groups compared.
The findings suggest that even within a single traditional hunter-gatherer group, geography and local ecological niches can shape distinct gut microbiome taxonomic and functional profiles. This indicates that broad category-level functional comparisons may obscure meaningful differences between populations, and that finer-grained analysis is needed to capture true microbiome variation. These results contribute to a baseline understanding of non-industrialized human gut microbiomes that can inform how urbanization and lifestyle change affect microbiome structure and function.
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.
Researchers compared the fecal gut microbiota of Hashimoto's thyroiditis (HT) patients against healthy controls, then tested whether microbiota patterns could serve as diagnostic biomarkers.
A cross-sectional cohort of 28 HT patients and 16 matched healthy controls had fecal samples analyzed by 16S ribosomal RNA gene sequencing. An independent validation cohort of 22 HT patients and 11 healthy controls tested the diagnostic value of biomarkers identified in the first cohort.
Overall bacterial richness and diversity did not differ between groups. HT patients had higher Blautia, Roseburia, Ruminococcus_torques_group, Romboutsia, Dorea, Fusicatenibacter, and Eubacterium_hallii_group, and lower Fecalibacterium, Bacteroides, Prevotella_9, and Lachnoclostridium. Linear discriminant analysis found 27 differing genera correlated with clinical parameters, and a 10-species biomarker panel achieved AUC values of 0.91 in the exploration cohort and 0.88 in validation.
Gut microbiota composition tracked with clinical parameters in HT patients, suggesting microbiome data could support diagnosis and warrants further study of its role in HT pathogenesis.
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 examined patterns of gut microbiota composition in people living with HIV/AIDS compared to HIV-uninfected healthy individuals. Stool samples were profiled by sequencing bacterial 16S rRNA genes to characterize community structure and abundance of specific taxa. The researchers also compared microbiota differences between treated and untreated HIV patients, and between patients grouped by mode of HIV transmission (homosexual versus heterosexual).
The study enrolled 33 patients with HIV/AIDS from a population in South China, including 14 participants who had received highly active antiretroviral therapy (HAART) for more than 3 months and 19 who had not received treatment. A comparison group of 35 healthy controls was also enrolled. This was a cross-sectional design using stool samples collected from these participants.
Dysbiosis was more common in patients with AIDS than in healthy controls, marked by decreased alpha-diversity. Patients with AIDS had lower mean counts of Bacteroidetes, Faecalibacterium, Prevotella, Bacteroides vulgatus, Dialister, and Roseburia inulnivorans, alongside higher mean counts of Proteobacteria, Enterococcus, Streptococcus, Lactobacillus, Lachnoclostridium, Ruminococcus gnavus, and Streptococcus vestibularis. Bacilli abundance was increased specifically in homosexual patients, while Proteobacteria abundance was higher among heterosexual patients with HIV.
These findings reinforce that HIV/AIDS is associated with a distinct, reproducible gut dysbiosis signature involving both reduced beneficial commensals and increased pro-inflammatory or opportunistic taxa. The differences observed by transmission route and treatment status suggest that host behavioral and clinical factors may shape the gut microbiome in HIV infection beyond the virus itself. Characterizing these shifts could help identify microbial targets relevant to the gastrointestinal disease and systemic immune activation seen in AIDS.
Although increasing evidence suggests a role for the gut microbiota in neurodevelopment, the actual structure and composition of microbiota in children with attention-deficit/hyperactivity disorder (ADHD) remain unclear.
Thus, the present study aimed to define the characteristics of gut microbiota in treatment-naive children with ADHD and to assess their relationship with the severity of ADHD symptoms. High-throughput pyrosequencing was used to investigate the microbiota composition in fecal matter from 51 children with ADHD and 32 healthy controls (HC).
An operational taxonomical unit (OTU)-level analysis revealed a significant decrease in the fractional representation of Faecalibacterium in children with ADHD compared to HC. In individuals with ADHD, the abundance of Faecalibacterium was negatively associated with parental reports of ADHD symptoms. However, there was no significant difference in alpha diversity between the ADHD and control groups.
This present findings support the involvement of microbiota alteration in psychiatric diseases and Faecalibacterium may represent a potential novel marker of gut microbiota in ADHD. Future studies are needed to validate these findings and to elucidate the temporal and causal relationships between these variables.
Animal models have indicated that intestinal microbiota influence acute graft-versus-host disease (aGVHD) by modulating immune homeostasis. But, in humans, the mechanism by which the microbiota induces aGVHD remains unclear. In this study, we investigated the relationship between the intestinal microbiota and T cell subsets in patients who undergo allogeneic hematopoietic stem cell transplantation (allo-HSCT) to explore the mechanism by which microbiota induced aGVHD. Based on aGVHD, this study was categorized into two groups: grades II-IV aGVHD (aGVHD group, n = 32) and grade 0-I aGVHD (non-aGVHD group, n = 49). The intestinal microbiota was detected by 16S rRNA gene sequencing, and the T cell subsets and histone 3 (H3) acetylation in CD4+ T cells in the peripheral blood was assayed by flow cytometry at the time of engraftment. The aGVHD group had greater low microbial diversity than the non-aGVHD group (56.3 versus 24.5%, p = 0.004). The bacterial community was depleted of Clostridia (e.g., the Lachnospiraceae and Ruminococcaceae families) and enriched for Gammaproteobacteria (e.g., the Enterobacteriaceae family) in the aGVHD group compared with the non-aGVHD group. The relative abundance of Lachnospiraceae and Ruminococcaceae was positively correlated with the Treg/Th17 ratio counts (r = 0.469 and 0.419; p < 0.001 and <0.001, respectively), whereas Enterobacteriaceae was negatively correlated with the Treg/Th17 ratio (r = -0.277; p = 0.012). The level of acetylated H3 in CD4+ T cells was not only correlated with Lachnospiraceae/Ruminococcaceae, but also with the Treg/Th17 ratio (r = 0.354; p = 0.001). In conclusions, our results suggest that decreased Lachnospiraceae and Ruminococcaceae and increased Enterobacteriaceae, correlate with a Treg/Th17 imbalance, which might be through acetylated H3 in CD4+ T cells. These findings suggest that intestinal microbiota might induce aGVHD by influencing the Treg/Th17 balance.
Researchers compared gut microbiota composition between patients with Alzheimer's disease (AD) and cognitively normal controls. The goal was to determine whether gut bacteria differ in AD, a link already shown for other neuropsychiatric disorders.
Fecal samples were collected from 43 AD patients and 43 age- and gender-matched cognitively normal controls. 16S ribosomal RNA sequencing was used to characterize the microbiota composition in each sample.
Overall gut microbiota composition differed between AD patients and controls. Several bacterial taxa were altered in AD, including Bacteroides, Actinobacteria, Ruminococcus, Lachnospiraceae, and Selenomonadales.
The findings suggest gut microbiota alterations may be involved in the pathogenesis of Alzheimer's disease. This supports gut microbiota as a potential area of investigation for AD, alongside its established role in other neuropsychiatric conditions.
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 the association between gut microbiota composition and Helicobacter pylori-related gastric lesions in a population at high risk for gastric cancer. Researchers used deep sequencing of the microbial 16S ribosomal RNA gene in fecal samples to characterize gut bacterial communities. The work was motivated by concern that H. pylori eradication, while effective for gastric cancer prevention, may carry adverse consequences such as microbial dysbiosis.
The study included 47 subjects from a high-risk population for gastric cancer. Participants were grouped by H. pylori infection status (negative, past infection, or current infection) and by gastric lesion category, including normal, gastritis, and metaplasia. Fecal samples from these subjects were used for the microbiota analysis.
Bacteroidetes, Firmicutes, and Proteobacteria dominated the fecal microbiota, with average relative abundances of 54.77%, 31.37%, and 12.91% respectively. Microbial diversity, measured by observed species and the Shannon index, was higher in subjects with past or current H. pylori infection than in H. pylori-negative subjects. Bacteroidetes abundance significantly decreased from H. pylori-negative subjects (66.16%) to those with past infection (33.01%), and also declined progressively from normal (76.49%) to gastritis (56.04%) to metaplasia (46.83%). Firmicutes and Proteobacteria showed elevated trends in the past infection group compared with the negative group, though these differences did not reach statistical significance.
The findings suggest that H. pylori infection history and the severity of associated gastric lesions are linked to measurable shifts in gut bacterial diversity and composition, particularly reductions in Bacteroidetes. This raises the possibility that gut microbial dysbiosis accompanies both H. pylori infection and its downstream gastric pathology, which is relevant to concerns about consequences of eradication therapy. The results support further investigation into how gut microbiota patterns might serve as markers or contributors to gastric lesion progression in high-risk populations.
Researchers compared gut microbiota in 14 infants with refractory epilepsy against 30 healthy infants. They then tested whether one week of ketogenic diet (KD) therapy reshaped the epileptic infants' microbiota.
Stool samples underwent 16S rDNA sequencing on the Illumina MiSeq platform, with community composition analyzed in MOTHUR and compared across groups using R.
Epileptic infants showed lower microbial diversity and a distinct community structure from healthy infants, dominated by Proteobacteria (24.3%) and Cronobacter (23.3%), which was near-absent in healthy infants. After one week of KD, 64% of epileptic infants had improved seizure control with a 50% average drop in frequency. Proteobacteria fell to 10.8%, Cronobacter dropped to 10.4%, while Bacteroidetes rose from 26.8% to 38.7% and Bacteroides, Prevotella, and Bifidobacterium increased.
The findings suggest ketogenic diet rapidly corrects gut dysbiosis in refractory pediatric epilepsy alongside clinical improvement, supporting the gut-brain axis as a mechanism worth further study.
2026-07-04
Lachnoclostridium majorTaxon page created: genus biology (morphology, ecological role, biomarker features), its clinical associations in colorectal neoplasia, the data-derived Conditions table across 136 conditions, and the full research feed.
Liang JQ, Li T, Nakatsu G, Chen YX, Yau TO, Chu E, Wong S, Szeto CH, Ng SC, Chan FKL, Fang JY, Sung JJY, Yu J.
A novel faecal Lachnoclostridium marker for the non-invasive diagnosis of colorectal adenoma and cancer.Gut. 2020
Liang JQ, Wong SH, Szeto CH, Chu ES, Lau HC, Chen Y, Fang J, Yu J, Sung JJ.
Fecal microbial DNA markers serve for screening colorectal neoplasm in asymptomatic subjects.J Gastroenterol Hepatol. 2020
Liang JQ, Zeng Y, Kwok G, Cheung CP, Suen BY, Ching JYL, To KF, Yu J, Chan FKL, Ng SC.
Novel microbiome signatures for non-invasive diagnosis of adenoma recurrence after colonoscopic polypectomy.Aliment Pharmacol Ther. 2022
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