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Desulfovibrio breathes sulfate the way we breathe oxygen, and its exhaust is hydrogen sulfide: the rotten-egg gas that at high gut levels can damage the colon lining.
Desulfovibrio is a genus of sulfate-reducing gut bacteria that turn dietary sulfate into hydrogen sulfide. Normal at low levels, a bloom (favored by high-animal-protein Western diets) floods the colon with genotoxic sulfide, linking it to inflammatory bowel disease and colorectal cancer.
Microbiome-targeted interventions (MBTIs) are validated using a dual-evidence logical framework. First, the intervention must realign the condition’s microbiome signature by increasing beneficial taxa that are consistently depleted and reducing pathogenic taxa that are consistently enriched. Second, the intervention must demonstrate measurable clinical benefit. Concordance of these effects in the same context validates the intervention as an MBTI and supports the clinical relevance of the microbiome signature.
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreDesulfovibrio is a genus of Gram-negative, strictly anaerobic, sulfate-reducing bacteria and a normal, low-abundance member of the human gut microbiota.[1] Its defining activity is turning sulfate into hydrogen sulfide, and it is one of the main sulfidogenic residents of the colon.[2][1] On this database it appears as a differentially abundant taxon across many human microbiome studies, where its meaning is tied to the gut's sulfur economy.
What makes Desulfovibrio distinctive is dissimilatory sulfate reduction: it respires sulfate and related sulfur compounds, using hydrogen or organic acids as electron donors, and releases hydrogen sulfide as the end product.[3][1] At the concentrations reached in the colon that sulfide is a double-edged molecule, a signaling gas at low levels but genotoxic to the gut lining at high levels, which is why Desulfovibrio blooms are linked to inflammatory bowel disease and colorectal cancer.[4][2] A Western, high-animal-protein diet that raises colonic sulfate favors these sulfidogenic bacteria.[2]
Members of Desulfovibrio are Gram-negative, strictly anaerobic bacteria, typically curved or vibrioid motile rods, in the class Deltaproteobacteria.[1] They are chemoorganotrophic sulfate reducers: they use sulfate as a terminal electron acceptor rather than fermenting sugars, and are among the dominant sulfate-reducing bacteria of the human colon.[1][3]
Desulfovibrio's core chemistry is dissimilatory sulfate reduction. Sulfate is activated and stepwise reduced through sulfite to hydrogen sulfide, with hydrogen or short-chain organic acids such as lactate as electron donors.[3] Unlike the assimilatory pathway that builds sulfur into amino acids, this dissimilatory route releases free hydrogen sulfide as a waste product.[3] Because colonic sulfate and organic sulfur rise with diet, the size of the Desulfovibrio population and its sulfide output track what the host eats.[2][1]
Desulfovibrio behaves as a pathobiont rather than a classic invader: harmless at low levels, but harmful when it blooms and floods the colon with hydrogen sulfide.[2] Elevated sulfidogenic bacteria and sulfide are associated with ulcerative colitis, Crohn's disease, and irritable bowel syndrome, and sulfide is implicated in colorectal cancer.[1][2] As with any differential-abundance signal, an appearance in a gut study is an ecological association shaped by diet and community context, not evidence of infection.
Desulfovibrio's harms come from its metabolic output rather than classical toxins. The through-line is hydrogen sulfide, the same molecule produced by the sulfate-reduction pathway detailed under Metabolism.
| Virulence factor | Description and role |
|---|---|
| Hydrogen sulfide (H₂S) | The organism's respiratory end product. At colonic concentrations H₂S is genotoxic to epithelial cells and erodes the protective mucus barrier, linking it to ulcerative colitis and colorectal cancer.[4][1] |
| Dissimilatory sulfate reduction | The sulfate-to-sulfide respiratory pathway is the metabolic engine behind the sulfide load and its inflammatory effects.[3] |
| Lipopolysaccharide (LPS) | As Gram-negative bacteria, Desulfovibrio contributes endotoxin that can promote inflammation when the population expands and the gut barrier weakens.[2] |
Read through the diet-and-sulfur lens, Desulfovibrio's dependence on host-supplied sulfate is also its weakness: cut the substrate and the sulfide output falls.
| Weak point | Why it is exploitable |
|---|---|
| Dietary sulfate and sulfur amino acids | The bloom is fed by dietary sulfate and sulfur amino acids, which rise on Western, high-animal-protein diets; lowering that load reduces the substrate for sulfide production.[2] |
| Hydrogen sulfide as the target | Because the harm is mediated by hydrogen sulfide, limiting its production or buffering it protects the colonic epithelium.[4][1] |
| Loss of a fiber-fermenting community | A balanced, fiber-fermenting microbiota that favors butyrate over sulfidogenesis keeps sulfate reducers in check, a microbiome-level lever.[1] |
For a pathobiont, an intervention is anything that constrains its bloom or blunts its sulfide output. Everything below is research-stage or dietary and is not medical advice; each is classified by our validation method. The through-line is the sulfur supply line: starve Desulfovibrio of the sulfate it respires.
| Intervention | Class | Status |
|---|---|---|
| Lower dietary sulfate and animal protein | Diet | Validation In Progress |
| Fiber / butyrogenic dietary shift | Diet | Validation In Progress |
| Hydrogen-sulfide buffering | Concept | Validation In Progress |
| Intervention | Mechanism |
| Lower dietary sulfate and animal protein | Reduces the colonic sulfate and sulfur amino acids that Desulfovibrio respires, cutting hydrogen-sulfide output.[2] |
| Fiber / butyrogenic shift | Favors fiber-fermenting, butyrate-producing bacteria that compete with and constrain sulfate reducers.[1] |
| Hydrogen-sulfide buffering | Limiting or detoxifying colonic H₂S protects the epithelium from its genotoxic effects.[4] |
Chronically high intake of dietary sulfate and sulfur-rich animal protein, the exposures most consistently linked to the overgrowth of sulfidogenic bacteria and higher colonic sulfide.[2] The direct causal evidence is largely associative, so this is a mechanism to weigh, not a clinical prescription.
Where Desulfovibrio (NCBI:txid872) appears as a differentially abundant taxon across the Microbiome Medicine corpus. Each row aggregates every experiment in which the organism moved in a given condition; direction is its change in the case/exposure group, and grade is the strongest single study's methodology weight (A·D·S·C·R), the same engine that grades every signature on this site.
Across 120 conditions and 171 studies, the signal is genuinely mixed: enriched in 53, depleted in 38, and direction-conflicting in 29 (directional agreement 0.6). Because Desulfovibrio is a diet-responsive pathobiont, its direction in any one condition often reflects the cohort's dietary sulfur environment as much as the disease itself, so the aggregate evidence tier is Low.
How to read these. Desulfovibrio is a genuine, if low-abundance, member of the gut microbiota, so these signals are ecologically real rather than contamination artifacts. The caveat is interpretive: it is a diet-responsive pathobiont whose abundance and sulfide output track dietary sulfate and animal protein, so an enrichment in a given condition may reflect the cohort's diet as much as the disease. Genus-level 16S assignment also groups several Desulfovibrio species together. This is why the direction can conflict between cohorts and the aggregate tier stays Low.
Internal summaries of the 172 studies we reviewed in which Desulfovibrio was a differential taxon across this corpus.
This study investigated whether high-fat-diet (HFD) induced disruption of the gut microbiota contributes to erectile dysfunction (ED) in rats. Researchers compared erectile function and stool-based 16S rRNA sequencing profiles between rats fed a normal diet (ND) and rats fed an HFD for 24 weeks. To test whether the microbiota itself was responsible for this effect, they performed fecal microbiota transplantation (FMT), transplanting stool from ND-group and HFD-group rats into new groups of rats and again assessing erectile function, microbiota composition, and serum metabolomics after another 24 weeks.
The subjects were male Sprague-Dawley rats, aged 8 weeks at the start of the experiment. They were randomly divided into a normal diet group and a high-fat diet group for the initial phase, then two additional groups of rats received fecal microbiota transplants from those donor groups. No human subjects were studied; the findings come entirely from this rat model.
Erectile function and intestinal microbiota species diversity were both significantly lower in the HFD group compared to the ND group, and overall microbiota community structure differed markedly between the two groups. Critically, rats that received fecal microbiota transplants from HFD-diet donors (HFD-FMT group) also developed significantly lower erectile function than rats transplanted with normal-diet microbiota (ND-FMT group). The microbiota community characteristics in the FMT recipient groups mirrored those of their respective donor groups, and serum metabolomic differences were also detected between groups.
These findings suggest that HFD-induced gut microbiota dysbiosis is not merely associated with erectile dysfunction but can causally transmit impaired erectile function, since transplanting dysbiotic microbiota alone reproduced the deficit in previously unexposed rats. This supports a gut-microbiota-to-erectile-function axis, potentially mediated through microbial metabolites detectable in serum. The results point to the gut microbiome as a possible target for future diagnostic or therapeutic strategies in diet-related erectile dysfunction, though this remains to be tested in humans.
This study examined whether transferring gut bacteria from human donors with different Alzheimer's disease (AD) risk profiles could alter behavior and brain pathology in a mouse model of AD. Researchers used fecal microbiota transplantation (FMT) to introduce donor microbiota into female 3xTgAD mice over a two-month period with weekly dosing. They then measured cognitive and behavioral outcomes alongside brain amyloid, tau pathology, and neuroinflammation. The design compared microbiota from an AD patient, a cognitively healthy carrier of the protective APOEe2 allele, a young healthy donor, and untreated mice.
The human donors were an 80-year-old patient with AD, a 73-year-old cognitively healthy individual carrying the protective APOEe2 allele, and a 22-year-old healthy young donor. The animal subjects were female 3xTgAD mice, a transgenic model that develops AD-like amyloid and tau pathology, divided into four FMT groups (AD-FMT, APOEe2-FMT, Young-FMT, and untreated Mice-FMT). No human cognitive or clinical outcomes were assessed; the study population for outcome measures was entirely the mouse cohort.
Mice receiving APOEe2-FMT showed improved short-term recognition memory on the novel object recognition test compared to mice receiving AD-FMT, though no significant differences appeared on the Y-maze, open-field, or elevated plus maze tests. This cognitive improvement was accompanied by increased neuroinflammation in the hippocampus, detected via translocator protein autoradiography, with no corresponding change in brain amyloid or tau pathology. Specific bacterial genera, including Parabacteroides and Prevotellaceae_UGC001, were enriched in the APOEe2-FMT group and were associated with the neuroinflammatory changes.
The findings suggest that gut microbiota from a donor with AD-protective genetic factors can influence memory function in an AD mouse model, but the relationship between microbiota, cognition, and neuroinflammation is not straightforward. Improved memory occurred alongside increased neuroinflammation rather than reduced pathology, indicating that neuroinflammatory changes are not simply harmful or protective in this context. This highlights the need for caution when interpreting FMT as a uniformly beneficial intervention and points to specific bacterial genera as candidates for further mechanistic investigation.
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.
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 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 study tested whether flavonoids extracted from Amomum tsaoko (ATFs), a traditional Chinese medicinal food known mainly for regulating the gastrointestinal tract, could protect against Parkinson's disease (PD) using a rotenone-induced mouse model. The researchers measured motor function, constipation symptoms, and loss of nigrostriatal dopaminergic neurons, the neurons destroyed in PD. They also examined colonic expression of inflammation-related genes and gut barrier genes, and profiled the gut microbiota to see whether ATFs act partly through microbiome changes. No prior studies had tested Amomum tsaoko or its extracts in a PD context.
The subjects were mice in a rotenone-induced Parkinson's disease model, a standard experimental system that reproduces motor and constipation symptoms and nigrostriatal dopaminergic neuron loss seen in human PD. The abstract does not give specific group sizes, sex, age, or strain details, so those specifics cannot be reported here. This was an animal (mouse) study rather than a human clinical study.
ATFs ameliorated both motor symptoms and constipation in the rotenone-induced PD mice and reduced the loss of nigrostriatal dopaminergic neurons. ATFs also lowered expression of inflammatory genes (TNF-alpha, IL-1beta, IL-6, COX-2, and MCP-1) and increased expression of gut barrier genes (Muc-2, ZO-1, Occludin, Claudin3, and Claudin4) in the colon. Notably, ATFs reversed rotenone-induced gut dysbiosis, including a significant decrease in the abundance of conditionally pathogenic bacteria such as Desulfovibrio, a sulfate-reducing genus, along with Provotellaceae UCG-001 and the Lachnospiraceae_NK4A136_group.
These findings suggest that Amomum tsaoko flavonoids may offer a novel, food-derived approach to easing PD-related motor and gastrointestinal symptoms by acting on the gut-brain axis. The reduction in Desulfovibrio, a sulfate-reducing bacterium linked to gut inflammation and barrier disruption, points to gut dysbiosis and microbial sulfur metabolism as a mechanistic link between intestinal health and dopaminergic neuron protection. Restoring gut barrier integrity and reducing inflammation alongside dysbiosis correction suggests a multi-pronged mechanism worth further mechanistic and translational investigation.
This pilot study examined how Zhuyang Tongbian Decoction (ZTD), a Chinese herbal formula, works to treat functional constipation (FC). Researchers used 16S rRNA sequencing, metagenomics, and metabolomics to assess changes in gut microbiota composition and metabolic function. They also measured fecal short-chain fatty acid (SCFA) levels and serum markers of inflammation, including TLR4, NF-κB, TNF-α, and IL-6.
The study included 40 patients with functional constipation, randomly divided into two groups of 20: a control group given lactulose and a treatment group given ZTD. An additional 20 healthy volunteers were recruited during the same period for comparison. Gut microbiota, SCFA, and serum inflammatory markers were assessed before and after treatment in the patient groups.
In the ZTD treatment group, beneficial bacteria including Bifidobacterium, Lactobacillus, and Faecalibacterium prausnitzii significantly increased in relative abundance. At the same time, Desulfobacterota, a group associated with sulfate-reducing and sulfide-producing bacteria, along with Ruminococcus, were significantly reduced. Fecal acetic and propionic acid levels also changed with treatment, reflecting a shift in short-chain fatty acid production alongside these microbial changes.
The findings suggest ZTD may relieve functional constipation partly by reshaping the gut microbiota toward more beneficial, SCFA-producing bacteria while reducing sulfate-reducing organisms like those within Desulfobacterota. This points to a microbiota-metabolite mechanism, rather than a purely symptomatic laxative effect, as seen with lactulose. Further research with larger cohorts is needed to confirm these mechanistic links and their relevance to inflammatory signaling in constipation.
This case-control study examined whether a distinct blood microbiome exists in myocardial infarction (MI) and whether such microbes might translocate from the gut or oral cavity into the bloodstream. Researchers compared microbial composition and diversity across blood, fecal, and saliva samples using 16S rRNA sequencing. They performed differential analyses to identify key microbiota distinguishing MI patients from healthy controls, and used Spearman correlation to link microbiota to clinical indicators.
The study included twenty-four myocardial infarction patients and twenty-four healthy controls, for a total of 144 samples spanning blood, fecal, and saliva specimens. This design allowed the same individuals' three microbial compartments to be compared directly against matched controls. No further demographic details (age, sex, geographic recruitment site beyond "Chinese patients") are given in the abstract.
The study found striking microbial shifts across all three compartments, blood, gut, and oral, in MI patients relative to healthy controls. In blood specifically, the researchers observed significant enrichment of certain bacterial phyla, supporting the idea that microbial signals detectable in blood may originate from the gut or oral cavity rather than representing a native blood microbiome. The abstract's findings section is cut off before phylum-level or taxon-level names are given, so specific organisms cannot be reported here.
By profiling blood, gut, and oral microbiota together, this study supports the hypothesis that circulating microbial signatures in cardiovascular disease may reflect translocation from other body sites rather than a true resident blood microbiome. This has implications for how researchers interpret blood microbiome findings in MI and other cardiovascular conditions, pointing to the gut and oral cavity as possible sources to monitor or target. Correlating microbiota with clinical indicators also suggests a path toward using multi-site microbial profiles as biomarkers or intervention targets in MI, pending further mechanistic study.
This study asked whether gut microbiome features can reliably diagnose Parkinson's disease (PD) using machine learning. The researchers performed a large-scale meta-analysis pooling data from multiple existing PD microbiome studies to build and test classification models. They also analyzed shotgun metagenomic sequencing data to identify microbial functional pathways linked to PD, rather than relying only on which microbes are present.
The analysis drew on a very large pooled dataset of 4489 samples combined from multiple previously published PD gut microbiome studies. The abstract does not name individual cohorts, countries, or specific patient counts within each study, but the samples represent PD patients and comparison groups whose microbiome data had already been collected across separate research efforts. Models were also evaluated against microbiome data from people with other neurodegenerative diseases to test disease specificity.
Machine learning models trained within a single study classified PD patients accurately, with an average AUC of 71.9 percent, but performance dropped to an average AUC of 61 percent when models were applied to different studies, showing poor generalizability. Training models on multiple combined datasets improved generalizability, raising the leave-one-study-out AUC to 68 percent, and improved specificity against other neurodegenerative diseases. Meta-analysis of shotgun metagenomes also identified PD-associated microbial pathways that may contribute to gut health decline and to translocation of harmful molecules along the gut-brain axis. Notably, microbial pathways for breaking down solvents and pesticides were enriched in PD samples.
The findings suggest that single-study microbiome signatures for PD are not robust enough alone to serve as reliable diagnostic tools, and that multi-cohort training is needed to build models that generalize across populations. The enrichment of solvent and pesticide biotransformation pathways in PD-associated microbiomes aligns with epidemiological evidence linking these chemical exposures to PD risk. This raises the possibility that gut microbes actively modulate the toxicity of environmental chemicals, pointing to a mechanistic link between environmental exposures, the gut microbiome, and PD pathogenesis worth further investigation.
This observational study examined the association between the gut microbiota and malaria across three malaria-endemic provinces of Rwanda (West, South, and East). The researchers considered host nutritional habits, soil-transmitted helminth coinfections, and age alongside malaria status. Malaria and helminth infection were diagnosed by microscopy, and gut microbial composition was profiled using bacterial 16S rRNA gene amplicon sequencing of fecal samples. Demographic and questionnaire-derived data on geographic region, age, and nutrition were also collected.
The study included 169 participants from malaria-endemic regions of Rwanda, comprising 85 females and 84 males. Participants ranged in age from 2 to 78 years, spanning preschool children, school-age children, and adults. Blood and fecal samples were collected from this community-based cohort across the three provinces studied.
Preschool children had significantly lower gut microbiota diversity than both school-aged children (q = 0.027) and adults (q = 0.011). In contrast, infection status, whether uninfected, malaria alone, helminth alone, or coinfection, was not significantly associated with gut microbiota diversity. Using Bray-Curtis distances, the researchers also found a significant difference in gut microbial beta-diversity, with a convergent distribution pattern described across the sampled groups. Age and geographic location, rather than malaria or helminth infection, emerged as the factors most clearly linked to microbiota differences.
The findings suggest that age and geography are stronger drivers of gut microbiota composition in these Rwandan populations than malaria or soil-transmitted helminth infection status. This implies that host developmental stage and local environmental or dietary context may shape the gut microbiome more than acute parasitic infection alone. These results caution against attributing microbiome differences in malaria-endemic settings solely to infection status without accounting for age and regional variation. Future work on host-microbiota-malaria interactions should stratify or control for these demographic and geographic factors.
This cross-sectional study examined how chronic psychological stress relates to gut microbiota composition and microbiota-derived metabolites in adolescents. Researchers used validated stress instruments to stratify participants by stress level, then profiled fecal microbiota using 16S rRNA gene sequencing across the full sample. A subset also underwent deeper metagenomic sequencing and untargeted metabolomics to characterize functional and metabolic differences tied to stress. The aim was to clarify a multi-omics gut-stress relationship that remains understudied in adolescent populations.
The study population was 124 adolescents aged 12 to 16 years, assessed with the Adolescent Life Events Scale and the Study Stress Scale. Participants were divided into low stress (n=42), medium stress (n=41), and high stress (n=41) groups based on these measures. A smaller subset of 30 high-stress and 29 low-stress adolescents was selected for the additional metagenomic and metabolomic analyses. All participants provided fecal samples for microbiota testing.
Adolescents with high chronic stress showed lower gut microbial alpha diversity, distinct beta diversity, and a more complex microbial co-occurrence network compared to lower-stress peers. Statistical testing identified five bacterial genera reduced in abundance among high-stress adolescents, including Faecalibacterium, Bacteroides, Akkermansia, and an unclassified Lachnospiraceae genus. These genera are commonly associated with short-chain fatty acid production and gut barrier support, suggesting stress corresponds with a less favorable, lower-diversity microbial community. The abstract text was truncated before metabolomic results could be fully detailed.
The findings support a link between chronic psychological stress and a disrupted, less diverse gut microbiota in adolescents, a population where this multi-omics relationship has been little studied. Depletion of genera like Faecalibacterium, Bacteroides, and Akkermansia points toward reduced capacity for beneficial microbial functions under high stress. This raises the possibility that gut microbiota profiles could serve as biomarkers of chronic stress exposure or as targets for intervention in stressed youth. Further work integrating the metabolomic data would help clarify the mechanistic pathways connecting stress, microbiota, and adolescent health.
This study examined how dietary patterns shape the gut resistome, the collection of antimicrobial resistance genes (ARGs) carried by gut bacteria. Researchers compared the effects of a high-fat/low-fiber diet against a high-fiber/low-fat diet, using comparative metagenomic analysis. They tracked changes in ARG abundance, virulence genes (VGs), and mobile genetic elements (MGEs) as diets shifted away from a normal baseline diet. Network analysis was also used to identify which gut bacteria act as hosts for these resistance and virulence genes.
The core experiments were conducted in mice, whose diets were shifted from a normal diet to either a high-fat/low-fiber or a high-fiber/low-fat diet. The abstract also references a human comparison showing a similar trend, though it does not specify the human cohort size or characteristics. Based on the available text, the human data appear to come from a separate metagenomic dataset or cohort used to corroborate the mouse findings.
The high-fat/low-fiber diet significantly increased the relative abundance of the resistome (from 0.14 to 0.25), virulence genes (0.56 to 0.91), and mobile genetic elements (0.20 to 1.66), all with p < 0.001. In contrast, the high-fiber/low-fat diet decreased these same measures, including the resistome (0.14 to 0.09) and virulence genes (0.58 to 0.50), with p < 0.05. Bacteroides, Parabacteroides, and Alistipes were identified as key bacterial hosts of ARGs and VGs, with their abundance shifts closely tracking changes in resistance and virulence gene levels. Mobile genetic elements such as Tn916, ISBf10, IS91, and intl1 were linked to these changes, including genes conferring vancomycin resistance and capsule-related virulence genes. A similar pattern, higher resistome levels with high-fat diets and lower levels with high-fiber diets, was also observed in humans.
These findings suggest that diet, particularly fat and fiber content, is a modifiable driver of antimicrobial resistance gene burden in the gut microbiome. The consistency between mouse and human data strengthens the case that high-fiber, low-fat dietary patterns could help suppress the spread of resistance and virulence genes. Because specific gut bacteria and mobile genetic elements were identified as mediators of this effect, the results point to potential microbial and genetic targets for reducing the gut's role as a reservoir for antimicrobial resistance.
This study examined how obesity affects the gut microbiome and biomarkers of microbial translocation (MT) and inflammation during simian immunodeficiency virus (SIV) infection and subsequent antiretroviral therapy (ART). Researchers tracked changes in gut bacterial community composition alongside circulating markers of gut barrier breakdown and immune activation. The work was motivated by the rising rate of obesity among people living with HIV and the shared role of dysbiosis and impaired gut barrier integrity in driving chronic immune activation in both conditions.
The study used lean and obese rhesus macaques that were experimentally infected with SIV and then treated with ART. This is an animal model of HIV infection rather than a human cohort, allowing controlled comparison of body-weight status on gut and immune outcomes over the course of infection and treatment. The abstract does not give an exact number of animals per group.
Obese animals had higher MT and inflammation biomarkers from the start, and these levels stayed constant throughout the study, whereas lean animals showed significant increases in these same markers that eventually approached the levels seen in obese animals. At baseline, lean and obese animals had similar numbers of observed amplicon sequence variants (ASVs), but obese animals lost ASV diversity during acute SIV infection before rebounding after 39 weeks of ART. Beta diversity differed between the two groups and continued to shift over time in the obese animals, which also showed significant changes in about four times as many bacterial genera as the lean animals. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism specifically.
The findings suggest that obesity establishes a baseline state of elevated gut barrier disruption and inflammation that changes little with SIV infection or ART, while lean animals start healthier but converge toward similarly elevated inflammatory states as infection progresses. This implies that obesity may reshape how the gut microbiome and immune activation respond to HIV infection and treatment, with broader and more sustained microbial community disruption in obese hosts. These results support considering body weight status when evaluating gut health and inflammation in people living with HIV on ART.
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.
This study examined whether rifaximin, a gut-specific non-absorbable antibiotic, could reduce systemic inflammation and pancreatic injury in severe acute pancreatitis (SAP). The researchers combined murine models, including antibiotic-treated and germ-free mice, with a single-center, open-label randomized controlled trial. They assessed pancreatic injury, systemic inflammatory markers, gut microbiota composition, and clinical outcomes including infection rates and adverse events.
The animal component used mouse models of SAP, including conventional mice as well as antibiotic-treated and germ-free mice, to test whether rifaximin's effects depended on the gut microbiota. The clinical component enrolled 60 patients with predicted severe acute pancreatitis in a randomized controlled trial registered with the Chinese Clinical Trial Registry (ChiCTR2100049794). Patients were randomized to receive rifaximin or standard care as controls.
In mice, rifaximin reduced pancreatic injury and systemic inflammation and altered gut microbiota composition, notably decreasing mucin-degrading genera such as Akkermansia. These protective effects persisted even in antibiotic-treated and germ-free mice, indicating that rifaximin's benefits are not solely explained by its modulation of gut microbiota. In the clinical trial, rifaximin significantly lowered white blood cell counts (median from 11.50 to 8.49 x10^9/L) and TNF-alpha levels (median from 15.05 to 11.00 pg/mL) compared with controls. However, culture-confirmed infection rates were identical between groups (13.3% vs 13.3%), and adverse events were comparable.
The findings suggest rifaximin could serve as an adjunct therapy to blunt the systemic inflammatory response in severe acute pancreatitis, a condition driven partly by gut barrier dysfunction and dysbiosis. Because protective effects persisted in germ-free mice, rifaximin may act through microbiota-independent mechanisms, warranting further mechanistic investigation beyond simple microbial modulation. The lack of difference in infection incidence indicates that reducing inflammation with rifaximin does not appear to compromise, or improve, infection control in this setting.
This study investigated whether gut microbiota composition differs by severity of metabolic dysfunction-associated steatotic liver disease (MASLD) in people with HIV (PWH). Stool samples underwent 16S rRNA gene sequencing to characterize bacterial genera, and PICRUSt was used to generate functional predictions from the microbiota data. Severe MASLD was defined by the presence of metabolic dysfunction-associated steatohepatitis (MASH), based on cytokeratin-18 levels, and/or significant liver fibrosis, based on liver stiffness measurement. Differential abundance of taxa and predicted functions was analyzed using a generalized linear model with a negative binomial distribution.
The study prospectively recruited people with HIV who had MASLD, defined by a controlled attenuation parameter (CAP) of 238 dB/m or greater. People with viral hepatitis coinfection or alcohol abuse were excluded from the cohort. Among 34 PWH with MASLD, 18 (53%) met criteria for severe MASLD, while the remainder did not, allowing comparison between these two groups within the same population.
Gut microbiota profiling revealed significant differences in bacterial genera between PWH with severe MASLD and those without severe disease. Notably, enrichment of the Ruminococcus gnavus group was observed in association with severe disease status. These findings indicate that distinct microbial signatures track with the presence of MASH and/or significant fibrosis rather than MASLD alone. The abstract as provided does not specify additional taxa or the full set of predicted functional pathways beyond this enrichment.
These findings suggest that gut microbiota alterations, particularly enrichment of the Ruminococcus gnavus group, may be linked to more severe liver disease in people with HIV who have MASLD. This raises the possibility that gut microbiota profiling could eventually help identify PWH at higher risk of MASH or significant fibrosis. Because PWH are already a high-risk group for MASLD, understanding microbiome contributions to severity could inform future risk-stratification or microbiome-targeted approaches in this population. Further research is needed to determine whether these microbial signatures are causal or consequential to disease severity.
This study examined how common lifestyle factors relate to the risk of colorectal high-risk adenomas (HRAs), precursor lesions to colorectal cancer. It focused on whether gut microbiota composition helps explain, or mediates, the connection between lifestyle habits and HRA risk. Researchers combined lifestyle questionnaires with 16S rRNA sequencing of fecal samples, then used multivariate models and causal mediation analysis to link lifestyle exposures, microbial taxa, and HRA outcomes.
A total of 3,827 participants were enrolled from a multicenter colorectal cancer screening cohort. Within this group, 272 participants had high-risk adenomas and 1,253 served as controls. Lifestyle information covering the 12 months before enrollment was collected via questionnaires, and fecal samples were taken at enrollment for microbiome analysis.
High body mass index, smoking more than 30 pack-years, and drinking more than 4 alcoholic units per week were each identified as independent risk factors for high-risk adenoma. Using MaAsLin2, the researchers found associations between these lifestyle risk factors and specific gut microbial taxa. The abstract does not specify Desulfovibrio, sulfate-reducing bacteria, or hydrogen sulfide among the implicated taxa or pathways.
The findings suggest that gut microbiota do not merely correlate with colorectal adenoma risk but may actively mediate how obesity, smoking, and heavy alcohol use translate into higher risk of high-risk adenomas. This positions the microbiome as a potential intermediary target for reducing lifestyle-driven colorectal cancer precursor risk. Identifying the specific mediating taxa could inform future screening or prevention strategies aimed at modifying gut microbial composition in high-risk individuals.
This study examined how chronic intermittent hypoxia (CIH), the hallmark feature of obstructive sleep apnoea syndrome (OSAS), affects the gut microbiota. Researchers used a mouse model of OSAS to test whether repeated cycles of low oxygen exposure alter gut microbial community structure over time. They assessed both microbiota composition, via 16S rRNA gene sequencing, and predicted functional pathways using PICRUSt2. The goal was to fill a gap in understanding how CIH-driven metabolic and gastrointestinal complications might be mediated by the gut microbiome.
The subjects were male C57BL/6 mice, not human patients, exposed either to normoxia (NM) or chronic intermittent hypoxia (CIH) conditions for six weeks. Faecal samples were collected via stress defecation at baseline (NM0 and CIH0 groups) and again after six weeks (NM6 and CIH6 groups). In total, 40 faecal samples were analyzed, with 10 mice per group across the four conditions.
The abstract provided does not include the specific results section detailing which taxa changed or which functional pathways were predicted to shift. It confirms only that a full dataset of 40 faecal samples across four groups was generated and analyzed using 16S rRNA sequencing and PICRUSt2 functional prediction. No mention of Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism appears in the abstract text supplied. Without the omitted results, specific compositional or functional outcomes cannot be reported here.
By establishing a controlled mouse model comparing gut microbiota before and after chronic intermittent hypoxia exposure, this work lays groundwork for identifying microbiota-mediated mechanisms behind OSAS-associated metabolic and gastrointestinal complications. Such a model could help pinpoint specific microbial or functional changes that contribute to systemic disease in sleep apnoea. This approach may eventually support the identification of therapeutic targets aimed at the gut microbiome for patients with OSAS. Further reporting of the study's actual results would be needed to draw more specific conclusions.
This study examined how geographical origin, diet, and Blastocystis presence and subtypes relate to gut microbiota composition. Researchers sequenced the V3-V4 hypervariable regions of the 16S rDNA gene to profile bacterial taxa across groups following West African and Mediterranean dietary patterns. They used DESeq2 to link taxa abundance to specific foods and weighted correlation network analysis (WGCNA) to identify co-abundant bacterial genera. Blastocystis subtypes were also determined and correlated with the microbial composition found in each group.
Three cohorts of healthy subjects were compared: Italians residing in Rome, Africans residing in Cote d'Ivoire, and Africans living in Italy. This design allowed the researchers to separate the effects of geographic origin and long-term residence from current dietary intake. The abstract does not give exact participant counts for each cohort.
Distinct microbial taxa were associated with specific foods, including palm oil, Cube Maggi, sunflower oil, and olive oil, linking diet composition directly to gut bacterial profiles. Notably, following a Mediterranean diet for over two years did not change the abundance of Faecalibacterium and Dorea among Africans living in Italy. This suggests that some microbiota features tied to geographic origin can persist despite a sustained shift in diet. Blastocystis subtypes were also found to correlate with microbial composition across the three groups, tying eukaryotic gut residents to bacterial community structure.
The findings suggest that gut microbiota profiles reflect a combination of long-standing geographic and cultural dietary patterns, not just current food intake, since some taxa resisted change even after years on a new diet. This has implications for how researchers interpret microbiome studies in migrant or multi-ethnic populations, where origin-linked microbial signatures may persist. The study also reinforces the importance of considering eukaryotic components like Blastocystis alongside bacterial taxa when characterizing gut ecosystems. Together, this points to a need for more nuanced, origin-aware approaches when studying diet-microbiome relationships.
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 cross-sectional study examined how vitamin K status relates to gut microbiota composition and inflammation in patients undergoing hemodialysis. Vitamin K status was determined using plasma dephosphorylated-uncarboxylated matrix gla-protein (dp-ucMGP) levels, with adequate status defined as 500 pmol/L or below and inadequate status as above 500 pmol/L. Plasma cytokines were measured with a multiplex assay and uremic toxins by reverse-phase HPLC, while gut microbiota was profiled in a subgroup using fecal DNA extraction and 16S rRNA gene sequencing on the Illumina NovaSeq PE250 platform. The premise was that vitamin K insufficiency in chronic kidney disease may stem from gut dysbiosis that reduces vitamin K-producing bacteria, in turn worsening inflammation, vascular calcification, and oxidative stress.
The cohort consisted of 107 hemodialysis patients who completed the study, with a median age of 53 years and a median of 36 months on hemodialysis. Of these, 70 patients had inadequate vitamin K status (median age 53 years, BMI 24.2 kg/m2), and 37 patients had adequate vitamin K status (median age 52.5 years, BMI 25.6 kg/m2). Gut microbiota composition was assessed in a subgroup of these patients rather than the full cohort.
The majority of hemodialysis patients in this cohort, 70 of 107, had inadequate vitamin K status based on elevated dp-ucMGP levels. This grouping allowed comparison of plasma cytokines, uremic toxins, and gut microbiota composition between patients with adequate and inadequate vitamin K status. The abstract text provided is truncated before the specific comparative results are given, so the precise microbiota or cytokine differences between groups cannot be stated here. No mention of Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism appears in the portion of the abstract provided.
The findings support the premise that vitamin K insufficiency is common among hemodialysis patients and may be intertwined with gut microbiota changes and systemic inflammation in chronic kidney disease. This suggests that monitoring vitamin K status, for example via dp-ucMGP, could help identify hemodialysis patients at greater risk of inflammation-related complications such as vascular calcification. It also points to gut microbiota composition as a potential factor connecting vitamin K metabolism to inflammatory processes in this population, warranting further investigation into microbiota-targeted or vitamin K-directed interventions.
This randomized, placebo-controlled trial examined whether resistant starch (RS), a prebiotic, has therapeutic effects in metabolic dysfunction-associated steatotic liver disease (MASLD). The researchers focused on why RS efficacy was heterogeneous, since about 30% of participants showed limited benefit. Using multi-omics analysis, fecal microbiota transplantation, population stratification, network analysis, and in vitro and in vivo experiments, they sought the microbial basis of this variable response. They then built a predictive model combining baseline microbial and clinical features to forecast who would respond.
Participants were drawn from the original randomized, placebo-controlled trial of resistant starch in MASLD, with the finding of heterogeneous response replicated in a separate multi-center trial (ChiCTR2300074588). The abstract does not give exact participant numbers or demographic details for either trial. A strain, Bifidobacterium pseudocatenulatum RRP01, was isolated from the study cohort for further experimentation.
Baseline gut microbiota composition was the dominant contributor to whether a participant responded to resistant starch. Prevotella was identified as a key cause of low response because it inhibits RS-degrading bacteria, impairing RS utilization. In contrast, the cohort-derived strain Bifidobacterium pseudocatenulatum RRP01 restored RS degradation and improved the RS response that Prevotella had attenuated. A predictive model integrating baseline microbial and clinical features achieved an area under the curve of 0.74 to 0.87 for stratifying likely responders.
The findings show that pre-existing gut microbiota composition, not just the intervention itself, determines whether resistant starch benefits patients with MASLD. This supports moving toward microbiota-oriented precision therapeutics, where baseline microbial and clinical features are used to predict who will respond before treatment begins. It also points to specific microbiota-targeted strategies, such as supplementing Bifidobacterium pseudocatenulatum RRP01, to overcome Prevotella-driven non-response and expand the benefit of prebiotic therapy to more patients.
This study examined how the intestinal microbiota relates to abdominal fat deposition in meat ducks. Researchers compared ducks with high versus low abdominal fat rates using a combined multi-omics approach, including 16S rRNA gene sequencing, metagenomics, and whole transcriptomics. They first surveyed microbial communities across the duodenum, jejunum, ileum, rectum, and cecum before focusing further analysis on the cecum.
The subjects were ducks from an F2 population derived from crossing Cherry Valley Ducks (male) with Runzhou Crested White Ducks (female), evaluated at 42 days of age. Ducks were sorted into a low abdominal fat (LF) group, with fat rates of 0 to 0.75%, and a high abdominal fat (HF) group, with fat rates of 1.5 to 2.25%. The abstract does not specify the exact number of ducks sampled in each group.
The cecum showed the highest microbial diversity of all intestinal segments examined and was significantly enriched in carbohydrate metabolism pathways, underscoring its central role in nutrient utilization and growth. Because of this, the cecum was selected for deeper multi-omics analysis. Metagenomic analysis of cecal contents revealed significantly different microbial beta diversity between the high and low abdominal fat rate groups. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism in relation to this study.
The findings support a functional link between cecal microbial composition and abdominal fat deposition in meat ducks, an economically important trait affecting feed efficiency and carcass yield. Identifying microbial and metabolic differences tied to fat accumulation could inform strategies to reduce excess abdominal fat through microbiome-targeted approaches. Because the cecum stood out for its diversity and carbohydrate metabolism activity, it may represent a key target for future interventions in poultry production. Multi-omics integration offers a more complete picture than single-method approaches for understanding host-microbe interactions in fat deposition.
This study examined the composition of gut microbiota in men with asthenozoospermia (AS), a condition marked by reduced sperm progressive motility below 32 percent. The researchers explored whether gut microbiota dysbiosis could be linked to impaired testicular function through disruption of the blood-testis barrier. They considered how the gut microbiota may influence testicular spermatogenesis by affecting nutrient transport, immune regulation, and inflammatory signaling reaching the testes.
The study was described as a Chinese pilot study focused on men diagnosed with asthenozoospermia. The abstract provided does not give a specific sample size, age range, or recruitment setting for the cohort. Based on the available text, the population can only be described as a small, exploratory Chinese cohort of infertile men with asthenozoospermia.
The abstract describes asthenozoospermia as arising from complex and varied causes, including inflammation, immune defects, irregular lifestyles, and genetic factors. It proposes that gut microbiota dysbiosis may compromise the integrity of the blood-testis barrier, disrupting normal spermatogenic processes. The abstract also notes that the testes depend on nutrients such as vitamins and minerals transported from the digestive system, some of which are synthesized or metabolized by gut microbiota, though the abstract text provided does not include the study's specific measured outcomes or statistical results.
The findings support the concept of a gut-testis axis, in which gut microbiota dysbiosis contributes to male infertility through immune and nutrient-related pathways rather than through the reproductive tract alone. This framing suggests that restoring gut microbial balance could be a plausible avenue for addressing some cases of asthenozoospermia. Because the provided abstract is incomplete and cohort details are not specified, these implications should be treated as preliminary until confirmed by larger, fully described studies.
This study examined whether orally administered neohesperidin, a natural flavonoid found in citrus fruits, could protect against neurodegeneration in a mouse model of Parkinson's disease. The model was induced using the neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). Researchers assessed motor function, neural damage, colonic inflammation, and gut microbial composition, along with molecular signaling pathways underlying neuroinflammation.
The subjects were mice injected with MPTP to induce Parkinson's disease-like pathology. The abstract does not specify the exact number of animals, strain, sex, or age used in the experiments. This was an animal model study rather than a human cohort.
Neohesperidin administration improved motor impairment and reduced neural damage caused by MPTP injection. It also reduced colonic inflammation and tissue damage while regulating gut microbial imbalance in these mice. Mechanistically, neohesperidin suppressed the MPTP-induced inflammatory response by inhibiting excessive activation of the NF-kB and MAPK signaling pathways.
These findings suggest that neohesperidin may attenuate Parkinson's disease-related neurodegeneration by simultaneously targeting neuroinflammation and gut microbial composition. This supports the broader concept that gut microbial regulation and anti-inflammatory pathways are linked in Parkinson's disease pathogenesis. The authors propose this provides a scientific basis for exploring neohesperidin as a potential treatment for Parkinson's disease and related conditions.
This study examined the oral and gut microbiota of rats to explore a possible microbiological basis for major depressive disorder. Researchers induced depression-like symptoms using chronic unpredictable mild stress (CUMS), a validated animal model of stress-triggered depression. They then used 16S rRNA sequencing to characterize the diversity and composition of bacterial communities at both body sites. The goal was to identify microbial features that distinguish depressed rats from unstressed controls.
The subjects were laboratory rats divided into a CUMS-exposed group and a control group. Depression-like status was confirmed through body weight measurements and behavioral testing after the stress protocol was applied. The abstract does not specify the exact number of animals, strain, or sex used. This was an animal model study rather than a human cohort.
Rats in the CUMS group showed significant differences from controls in both alpha and beta diversity of the oral microbiota. In the oral cavity, Rothia, Psychrobacter, and Streptococcus were the most abundant genera, with Rothia significantly decreased and Psychrobacter-related taxa significantly increased in the CUMS group. In the gut, Lactobacillus, Ruminococcus, and Oscillospira predominated, with Ruminococcus significantly decreased in CUMS rats. Spearman correlation analysis linked these differentially abundant taxa to depression-like behavioral measures, though the abstract does not report Desulfovibrio, sulfate-reducing bacteria, or hydrogen sulfide findings.
The findings suggest that chronic stress and depression-like states are accompanied by measurable, site-specific shifts in both oral and gut bacterial communities, not just gut microbiota alone. The consistent decrease of Rothia orally and Ruminococcus in the gut points to candidate microbial markers worth investigating further in depression research. Because oral samples are easier to collect than gut samples, this raises the possibility of oral microbiota as a less invasive proxy for studying depression-related microbial changes. These are preclinical rat findings, so translation to human MDD etiology or diagnostics would require further validation.
This prospective study examined the nasopharyngeal and oropharyngeal microbiota in children with obstructive sleep apnea (OSA) compared to children without OSA. The researchers used 16S rRNA V3-V4 gene sequencing to characterize microbial communities at different anatomical sites of the upper airway. They also assessed how surgical treatment, adeno-tonsillectomy, altered the oropharyngeal microbiome one month after surgery. Correlation analysis linked microbial composition to clinical measures of disease severity.
The study included 30 children with OSA and 10 children without OSA (non-OSA controls) who were undergoing adeno-tonsillectomy. Throat swab samples were collected from different parts of the oropharynx and nasopharynx in both groups before surgery. A follow-up oropharyngeal sample was collected from the same patients one month after their adeno-tonsillectomy.
Alpha diversity differed significantly across upper airway sites in children with OSA, but this site-to-site difference was not observed in non-OSA children. Beta diversity also differed significantly between the OSA and non-OSA groups, and genus-level composition varied by anatomical site differently in each group. Notably, the relative abundance of Neisseria was significantly correlated with the obstructive apnea hypopnea index, a measure of OSA severity. Functional prediction analysis suggested that microbial pathways related to cell proliferation and material metabolism were implicated, though the abstract text is truncated at this point.
These findings suggest that pediatric OSA is associated with distinct, site-specific shifts in upper airway microbial communities rather than a uniform, whole-airway change. The correlation between Neisseria abundance and apnea severity raises the possibility that specific airway taxa could serve as biomarkers or contributors to OSA pathophysiology in children. Tracking oropharyngeal microbiota after adeno-tonsillectomy may help clarify whether surgical correction of anatomical obstruction also normalizes microbial imbalances. This abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, sulfide, or sulfur metabolism, so no such angle applies here.
This study examined the microbial composition and temporal dynamics of the human microbiome at four body sites: stool, oral, skin, and nasal. The researchers tracked how these microbial communities changed over time and how they related to host multi-omics data, immune markers, and clinical features. The goal was to understand how the microbiome behaves dynamically during both health and disease.
The study followed 86 participants over a period of 6 years, sampling microbiomes from four body sites in each person. The abstract does not specify additional demographic details such as age range or sex distribution. Some participants in the cohort were insulin-resistant, allowing comparison between metabolically healthy and metabolically disrupted individuals.
Microbiome stability and individuality were found to be body-site specific and strongly shaped by the host, with the stool and oral microbiomes proving more stable than the skin and nasal microbiomes, likely due to differing levels of interaction with the host and external environment. The researchers identified both individual-specific and commonly shared bacterial taxa, and individualized taxa showed greater stability over time. Notably, microbiome dynamics were correlated across different body sites, pointing to systemic patterns driven by host-microbial-environment interactions. Insulin-resistant individuals showed altered microbial stability and disrupted associations among microbiome composition, molecular markers, and clinical features.
The findings suggest that microbiome stability is not uniform across the body and that host factors play a central role in shaping which microbial communities remain stable versus dynamic over time. The correlation of microbiome dynamics across separate body sites implies a systemic, whole-body relationship between host and microbiota rather than site-isolated behavior. The disrupted microbiome-host associations seen in insulin resistance suggest that metabolic disease may involve a breakdown in normal host-microbial coupling, offering a potential angle for understanding or monitoring metabolic disease through longitudinal microbiome tracking.
The study tested whether Parkinson's disease alters the oral microbiome associated with periodontitis. Researchers recorded clinical, periodontal, and neurological parameters, including severity of Parkinson's motor dysfunction. Unstimulated saliva and stool samples were collected and profiled using next-generation sequencing of the 16S ribosomal RNA gene (V1-V3 regions) to compare oral and gut microbial composition across groups.
Three groups were enrolled: patients with periodontitis and Parkinson's disease (PA+P), patients with periodontitis but without Parkinson's disease (P), and systemically and periodontally healthy controls (HC). The PA+P patients had mild-to-moderate motor dysfunction. Plaque scores were comparable between the PA+P and P groups, indicating that oral hygiene was similarly effective in both.
Salivary beta diversity differed significantly between HC and PA+P, between HC and P, and between P and PA+P, showing that periodontitis status and Parkinson's disease each shaped the oral microbial community. Saliva and fecal microbial profiles were distinct from one another. Mycoplasma faucium, Tannerella forsythia, Parvimonas micra, and Saccharibacteria (TM7) were increased in periodontitis patients without Parkinson's disease, whereas Prevotella pallens, Prevotella melaninogenica, and Neisseria multispecies were more abundant in the PA+P group. In the P group's fecal samples, Ruthenibacterium lactatiformans, Dialister succinatiphilus, Butyrivibrio crossotus, and Alloprevotella tannerae were detected.
The findings support the hypothesis that Parkinson's disease measurably shifts the periodontitis-associated oral microbiome, independent of oral hygiene quality. Because oral and gut microbial signatures diverged between groups, oral and fecal sampling may offer complementary, non-invasive windows into Parkinson's-related microbial changes. This distinct salivary and fecal profile in PA+P patients could inform future work on microbial biomarkers linking periodontal disease and neurodegeneration.
This study examined whether the gut microbiota plays a causal role in inflammatory depression, a treatment-resistant subtype of depression linked to low-grade inflammation. Researchers analyzed gut microbiota composition in stool, inflammatory factors and short-chain fatty acids (SCFAs) in plasma, and inflammatory and permeability markers in the intestinal mucosa. They then used fecal microbiota transplantation (FMT) and probiotic supplementation in animal experiments to test causality. The work combined observational human data with mechanistic animal modeling.
Human participants were patients with inflammatory depression enrolled in an observational trial (registered as ChiCTR1900025175). The abstract does not give a specific sample size for this cohort. The causal experiments were conducted in mice, using recipient animals that received fecal microbiota transplants from the human patient groups and a separate mouse model of inflammatory depression for probiotic testing.
Patients with inflammatory depression showed higher Bacteroides and lower Clostridium in their gut microbiota, along with an increase in SCFA-producing species exhibiting abnormal butanoate metabolism. After FMT, mice receiving microbiota from the inflammatory depression group developed increased peripheral and central inflammatory factors, greater intestinal mucosal permeability, and depressive and anxiety-like behaviors. Administration of Clostridium butyricum normalized the gut microbiota, reduced inflammatory factors, and produced antidepressant-like effects in the mouse model.
The findings support a causal, not merely correlational, role for the gut microbiota in driving low-grade inflammation and depressive behavior in inflammatory depression. Restoring a healthier microbiota, such as through Clostridium butyricum supplementation, may offer a targeted therapeutic strategy for this treatment-resistant subtype. This positions gut microbiota composition and butanoate metabolism as potential biomarkers and intervention targets for inflammatory depression.
The study examined whether gut microbial composition differs between colorectal cancer (CRC) patients who developed liver metastasis (LM) and those who did not (NLM). Researchers used high-throughput 16S rRNA sequencing to characterize microbial richness, diversity, and taxonomic composition in stool and tumor tissue samples. The goal was to identify microbial features associated with LM and poor prognosis in CRC, since liver metastasis is a major driver of mortality in advanced disease and gut microbiota has been linked to liver disease progression.
The study drew on colorectal cancer patients grouped by metastasis status across three cohorts. A supplementary discovery cohort (cohort 1) analyzed primary carcinoma tissue from 8 LM and 10 NLM patients. A discovery cohort (cohort 2) used fresh feces from 18 LM and 36 NLM patients, and a validation cohort (cohort 3) used fresh feces from 13 LM and 41 NLM patients.
Intestinal microbiota richness and diversity were higher in the LM group compared to the NLM group. Species composition differed significantly between the two groups. Across the two discovery cohorts, which used different sample types, the dominant bacterial phyla were consistent, though composition varied at lower taxonomic levels. The phylum Fusobacteria showed consistent alterations associated with liver metastasis across these analyses.
The consistent association between Fusobacteria alterations and liver metastasis across independent discovery and validation cohorts suggests gut and tumor-associated microbiota could serve as a biomarker for metastatic risk and prognosis in colorectal cancer. This raises the possibility of using microbial profiling to help identify CRC patients at higher risk of liver metastasis. It also points toward the gut microbiota, and Fusobacteria specifically, as a potential target for future diagnostic or therapeutic strategies in advanced CRC.
This pilot prospective cohort study examined whether gut microbiome dysbiosis in gestational diabetes mellitus (GDM) differs across Asian ethnic groups. It also investigated whether diet and lifestyle modifications after a GDM diagnosis could modulate the gut microbiome. Fecal samples were collected at two time points in pregnancy, at 24-28 weeks and 36-40 weeks' gestation, and analyzed using targeted 16S rRNA gene-based amplicon sequencing. Differences between groups were assessed using PERMANOVA, DeSeq2-based differential abundance analysis, and PICRUSt2 functional prediction.
The study included women with GDM (n = 53) and women without GDM (n = 16), all living in Singapore. Participants belonged to three Asian ethnic groups: Chinese, Malay, and Indian. This design allowed the researchers to compare gut microbiome dysbiosis patterns both between GDM status and across ethnicities within the same population.
Among women with GDM, the gut microbiome across the three different Asian ethnicities harbored common features, based on the abstract's description before it was truncated. The abstract does not provide further specific taxa, effect sizes, or functional pathway results beyond this shared pattern. No mention is made of Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism in the provided text.
The findings, as described, suggest that GDM-associated gut microbiome dysbiosis may not be strongly driven by ethnic background among Chinese, Malay, and Indian women. This implies that clinical or dietary strategies targeting the gut microbiome in GDM may not need to be heavily tailored by these specific ethnicities. As a pilot study, these conclusions are preliminary and would need confirmation in larger, more definitive cohorts.
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 investigated whether the oral microbiome, independent of the gut microbiome, contributes to depression through a proposed microbiota-oral-brain axis. The researchers combined clinical comparisons of oral microbial composition and metabolomics with an animal model using chronic restraint stress (CRS) and saliva transplantation into germ-free mice. The goal was to determine whether oral microbial dysbiosis could causally drive depression-like behavior and altered host metabolism.
The clinical portion compared 87 patients with depressive symptoms to 70 healthy controls, analyzing their oral microbial and metabolic profiles. The animal portion used germ-free mice that received saliva transplants from mice exposed to chronic restraint stress. This paired human cohort with a controlled mouse model allowed the researchers to move from association in people to causal testing in animals.
Oral microbial and metabolic signatures differed significantly between depressed patients and healthy controls. Germ-free mice given saliva from chronically stressed mice developed depression-like behaviors along with oral microbial dysbiosis, marked by enrichment of Pseudomonas, Pasteurellaceae, and Muribacter and depletion of Streptococcus. Metabolomic analysis also showed altered plasma metabolites accompanying these behavioral and microbial changes, though the abstract does not describe sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism as part of these findings.
The findings suggest the oral microbiome can influence depression-like behavior independent of the gut, supporting a microbiota-oral-brain axis alongside the gut-brain axis. Saliva-based microbial transfer inducing behavioral changes in germ-free mice points to a potentially causal, transmissible mechanism linking oral dysbiosis to mood-related metabolism. This raises the possibility that oral microbial and metabolic signatures could serve as biomarkers or intervention targets for depression.
This study examined gut microbial features associated with Parkinson's disease (PD) by meta-analyzing shotgun metagenomic sequencing data across six countries. The researchers established GC-MS and LC-MS/MS assays to quantify fecal short-chain fatty acids (SCFAs) and fecal polyamines, respectively, alongside taxonomic and functional pathway analyses. They assessed alpha-diversity, species-level taxonomic shifts, carbohydrate-active enzyme (CAZyme) categories, and vitamin biosynthesis pathways (riboflavin and biotin) in relation to PD.
The core dataset came from 94 PD patients and 73 controls in Japan, whose fecal samples were newly shotgun-sequenced and metabolomically profiled by the authors. This Japanese dataset was combined with five previously reported shotgun sequencing datasets from the USA, Germany, China (two separate cohorts, China1 and China2), and Taiwan. Altogether, six independent country-level datasets of PD patients and controls were meta-analyzed.
Alpha-diversity was increased in PD across all six datasets, and Akkermansia muciniphila was increased while Roseburia intestinalis and Faecalibacterium prausnitzii were decreased in PD. Genes involved in riboflavin and biotin biosynthesis were markedly decreased in PD after adjusting for confounders, and five of six CAZyme categories were reduced. Fecal SCFAs and polyamines were significantly decreased in PD, and these metabolite levels correlated positively with riboflavin and biotin biosynthesis genes. Notably, the specific bacteria responsible for decreased riboflavin biosynthesis differed between Japan, the USA, and Germany versus China1, China2, and Taiwan.
By pooling data across six countries, this meta-analysis identifies convergent, reproducible gut microbial and metabolic signatures of PD, including reduced vitamin biosynthesis capacity, depleted beneficial taxa, and lower SCFA and polyamine output. The correlation between riboflavin and biotin biosynthesis genes and fecal SCFA and polyamine concentrations suggests these microbial functional pathways may be mechanistically linked to metabolite depletion in PD. The finding that different bacterial taxa drive the same functional deficit (riboflavin biosynthesis) in different geographic regions implies that functional pathway analysis may be a more robust and generalizable biomarker strategy than taxonomic composition alone across diverse populations.
This study examined whether irisin, a myokine released during physical activity, could improve reproductive and endocrine abnormalities in a mouse model of polycystic ovary syndrome (PCOS). The researchers induced PCOS using dehydroepiandrosterone (DHEA) combined with a high-fat diet, then treated animals with intraperitoneal irisin every other day for 21 days. They assessed serum sex hormones, ovarian tissue histology and immunohistochemistry, and profiled the gut microbiota and fecal metabolome using 16S rRNA gene sequencing and LC-MS. The goal was to clarify the mechanism by which irisin, as a mediator of exercise's benefits, affects PCOS-related metabolic and reproductive disturbances.
The subjects were mice, not human patients, divided into three groups: an untreated control group, a PCOS group, and a PCOS-plus-irisin treatment group. PCOS was experimentally induced in the animals using DHEA and a high-fat diet rather than occurring naturally. The abstract does not specify the number of animals per group or their strain, sex, or age.
Irisin supplementation alleviated reproductive endocrine disorders in the PCOS mice, including abnormalities in the estrous cycle, alongside measurable changes in serum sex hormones and ovarian tissue features. These improvements were accompanied by shifts in the composition of the gut microbiota and in fecal metabolomic characteristics, as detected by 16S rRNA sequencing and LC-MS. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so this study should be summarized on its own terms without forcing that angle. The specific taxa and metabolites altered by irisin treatment are referenced but not enumerated in the abstract excerpt provided.
The findings suggest that irisin may mechanistically link the known benefits of physical activity to improvements in PCOS-related reproductive and endocrine dysfunction, partly through modulation of the gut microbiota and its metabolic output. This positions irisin as a candidate mediator worth investigating for PCOS management strategies that mimic or supplement exercise effects. Because the work was conducted in a chemically and dietarily induced mouse model, further research would be needed to determine whether similar irisin-microbiota-metabolome relationships hold in humans with PCOS.
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 used shotgun metagenomics to compare the microbial composition and function of normal rectal mucosa against matched fecal samples. The researchers analyzed both microbial taxonomic classification and KEGG Orthology (KO) functional annotations for each sample type. They then examined how the mucosal microbiota related to host factors including age, gender, BMI, and colonic polyp risk level.
The study included 20 patients with colonic polyps, each contributing a paired sample of normal rectal mucosa and feces. This matched within-person design let the researchers directly compare the two sample types from the same individuals. No further demographic breakdown is given in the abstract beyond age, gender, and BMI being used as variables of interest.
The mucosal and fecal microbiomes were clearly distinct from one another, with the mucosal microbiome containing fewer genera overall. Burkholderia was identified as the single most discriminating genus separating feces from mucosa, indicating a notably strong mucosal presence. The team also identified novel taxonomic biomarkers linked to host factors, such as Clostridium ramosum and Enterobacter cloacae in association with age. Functionally, the mucosal microbiota was enriched for KO pathways involved in sugar transport and short-chain fatty acid metabolism.
The findings show that fecal samples alone do not capture the distinct microbial community living at the rectal mucosal surface, a gap most gut microbiome research has overlooked. Because the mucosal niche appears compositionally and functionally distinct, with its own host-associated biomarkers and short-chain fatty acid-related activity, mucosal sampling may add diagnostic or mechanistic information that feces cannot provide. This supports incorporating mucosal microbiome analysis alongside fecal analysis in future studies of colonic polyps and related conditions.
This study investigated the role of MyD88, the core adaptor protein for Toll-like receptor signaling, in the development of intestinal inflammation. The researchers used MyD88 knockout mice and a pharmacological MyD88 inhibitor (TJ-M2010-5) to test whether blocking MyD88 would protect against acute dextran sodium sulfate (DSS)-induced colitis. They assessed colitis severity through disease activity index, colon length, histological scoring, and inflammatory cytokine levels. RNA transcriptome analysis and 16S rDNA sequencing were used to probe the underlying mechanism connecting MyD88 loss to gut microbiota and inflammatory pathways.
The study population consisted of laboratory mice, specifically MyD88 knockout (MyD88-/-) mice and wild-type control mice treated with either the MyD88 inhibitor TJ-M2010-5 or vehicle. All animals were subjected to an acute DSS-induced colitis model. The abstract does not provide specific numbers of animals per group or additional demographic details beyond the genetic and pharmacological manipulation of MyD88.
Contrary to expectation, loss of MyD88 function, whether through genetic knockout or pharmacological inhibition, did not alleviate the severity of DSS-induced colitis, even though NF-kB activation was significantly reduced in these mice compared to controls. Sequencing and transcriptomic analysis revealed that MyD88 disruption was associated with a higher abundance of intestinal Proteobacteria. This shift in gut microbiota composition coincided with up-regulation of the nucleotide oligomerization domain-like receptor (NLR) signaling pathway, suggesting a compensatory inflammatory mechanism activated in the absence of MyD88 signaling.
The findings indicate that suppressing MyD88 alone is not a viable therapeutic strategy for colitis, because reducing NF-kB activation through this pathway is offset by dysbiosis favoring Proteobacteria and compensatory activation of NLR signaling. This suggests MyD88 plays a protective, microbiota-regulating role rather than being purely pro-inflammatory in the gut. Therapeutic approaches targeting innate immune adaptors in inflammatory bowel disease may need to account for this microbiota-immune crosstalk and compensatory signaling rather than focusing on a single pathway in isolation.
This study examined the composition and function of the gut microbiota in people with schizophrenia. Researchers used both 16S rRNA gene sequencing and whole-genome shotgun metagenomic sequencing to characterize microbial diversity, taxonomic composition, and functional gene content. The aim was to explore how gut microbes, acting through the gut-brain axis, might relate to this severe and complex psychiatric disorder.
The study included 29 patients diagnosed with schizophrenia and 30 age-matched normal controls. This is a relatively small clinical cohort, and the abstract does not specify additional demographic details such as sex distribution, geographic location, or illness duration. Both 16S rRNA and metagenomic sequencing were performed on samples from these same participants.
Patients with schizophrenia had higher abundances of the bacterial genera Clostridium and Megasphaera compared to controls. Functional analysis linked schizophrenia to alterations in sphingolipid metabolism, phosphonate and phosphinate metabolism, and glutamine metabolism. These findings were consistent across both the 16S rRNA and metagenomic sequencing approaches. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings support the idea that the gut microbiota has a measurable effect on schizophrenia, reinforcing the relevance of the gut-brain axis to this disorder. Specific taxa such as Clostridium and Megasphaera, along with the identified metabolic pathways, may serve as leads for future mechanistic or biomarker research. These results provide a foundation for further investigation into microbiome-based understanding or management of schizophrenia.
This study investigated gut microbiota composition and systemic immune function in patients with schizophrenia comorbid with metabolic syndrome (SZ-MetS). Researchers used 16S rRNA gene sequencing (V3-V4 hypervariable regions) to profile fecal bacterial communities. They paired this with a 27-plex cytokine assay to characterize host immune responses. The goal was to clarify how gut dysbiosis and immune dysfunction relate to one another in this comorbid condition.
The study enrolled 114 Chinese patients with schizophrenia comorbid with metabolic syndrome and 111 age-matched healthy controls, all recruited from Zhejiang, China. Fecal samples from these participants were sequenced to assess gut bacterial diversity and composition. Blood-based cytokine profiling was performed using the same cohort to link microbial and immune findings.
Patients with SZ-MetS showed decreased bacterial alpha-diversity and significant shifts in beta-diversity compared to healthy controls. LEfSe analysis identified enrichment of acetate-producing genera, specifically Megamonas and Lactobacillus, alongside depletion of butyrate-producing bacteria, including Subdoligranulum and Faecalibacterium. These altered bacterial genera correlated with body mass index and with the severity of clinical measures, linking microbial shifts to metabolic and disease-related parameters. The abstract did not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings suggest that gut dysbiosis, marked by loss of butyrate producers and gain of acetate producers, may contribute to the pathogenesis of metabolic syndrome in people with schizophrenia. This supports a role for the gut microbiota as a potential mechanistic link between psychiatric illness and metabolic dysfunction. It also raises the possibility that microbiome-targeted approaches could be explored as adjunctive strategies for this high-risk comorbid population.
This study examined how chronic alcohol consumption affects the oral microbiota in rats that had periodontitis. The researchers used 16S rRNA gene amplicon sequencing to track dynamic changes in the oral microbial community over the course of alcohol exposure. They also assessed liver-related serum markers (alanine aminotransferase and aspartate aminotransferase) and alveolar bone status using histology and micro-computed tomography.
The study used twenty-four male Wistar rats, randomly divided into a periodontitis-only (P) group and a periodontitis-plus-alcohol (PA) group. The PA group had unrestricted access to alcohol for ten weeks, while the P group received only water. Both groups developed periodontitis by four weeks into the protocol, and oral swabs were collected from all animals after ten weeks for microbial analysis.
Rats in the alcohol-exposed PA group showed more severe periodontal tissue damage than the periodontitis-only P group. Serum liver enzyme levels and 16S rRNA sequencing of oral swabs were used to characterize the physiological and microbial differences between groups, though the abstract provided does not specify the exact taxa that shifted or their relative abundances. No mention is made in this abstract of Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings support a link between chronic alcohol consumption and worsened periodontal bone damage in the context of periodontitis, suggesting alcohol may accelerate disease progression. Because the study used an animal model, it points to oral microbial community shifts as a plausible mechanism connecting alcohol use to periodontal outcomes rather than confirming this in humans. Further work detailing which microbial taxa change and how they relate to bone loss would clarify the mechanism and its relevance to human oral health.
This study investigated how the dietary fiber beta-glucan (BG) helps improve colitis and examined the microbial and metabolic mechanisms behind that benefit. The researchers used multi-omics analysis along with validation experiments and loss-of-function studies to trace how BG intervention changes gut bacteria and their metabolites. They specifically focused on a cross-feeding interaction between two gut bacterial species and the downstream metabolite it produces.
The abstract describes work in colitic mice, indicating the core experiments were conducted in a mouse model of colitis. A proof-of-concept study was also performed to confirm the bacterial and metabolite findings. The abstract does not provide details on the number of animals, strains used, or any human cohort, so no further population specifics can be stated.
BG intervention ameliorated colitis and reversed the reduction in Lactobacillus seen in colitic mice, with Lactobacillus abundance negatively correlated with colitis severity. Lactobacillus johnsonii was identified as the most significantly enriched Lactobacillus species, and it produced abundant indole-3-lactic acid (ILA), which activated the aryl hydrocarbon receptor (AhR) to mitigate colitis. Notably, L. johnsonii could not use BG directly but instead relied on cross-feeding with Bacteroides uniformis, which degrades BG and generates nicotinamide (NAM) to support L. johnsonii growth. The proof-of-concept study confirmed that BG increased the abundance of both L. johnsonii and B. uniformis along with ILA levels.
The findings reveal a previously unrecognized bacterial cross-feeding pathway in which one species degrades dietary fiber to feed a beneficial partner species that produces a protective metabolite. This suggests that dietary beta-glucan could be explored as a way to reshape gut microbial interactions and boost protective indole metabolite production in inflammatory bowel disease. It also highlights indole-3-lactic acid and AhR activation as a potential mechanistic target for future colitis-related interventions.
This study examined how the gut microbiome and serum metabolome differ between people with lactose intolerance (LI) and those without it. Researchers combined a paired-sample analysis of American Gut Project (AGP) data with metagenomic and untargeted metabolomic analyses in a separate Chinese cohort. They also conducted fecal microbiota transplantation (FMT) experiments to test whether the LI-associated gut microbiome could itself drive inflammatory outcomes. The overall aim was to characterize the microbiome-metabolome interaction underlying lactose intolerance.
The study drew on two human data sources: paired samples from the American Gut Project, a large public metagenomic dataset, and a separately recruited Chinese cohort profiled with metagenomics and untargeted metabolomics. Exact sample sizes for either group are not stated in the abstract. In addition to the human cohorts, the researchers performed fecal microbiota transplantation experiments, implying an animal model was used to test causal effects of the LI-associated microbiome on inflammation.
Fourteen microbial genera differed significantly between the LI and control groups in the AGP data. In the Chinese cohort, a machine learning model separated LI from non-LI individuals using seven bacterial species and nine serum metabolites. Notably, Escherichia coli was elevated in the LI group and was negatively correlated with metabolites including PC (22:6/0:0), indole, and Lyso PC, while levels of Faecalibacterium prausnitzii and Eubacterium rectale were reduced in LI and positively associated with other metabolic changes.
The findings suggest that lactose intolerance is accompanied by a reproducible shift in gut microbial composition and circulating metabolites, not just a lactase-deficiency phenomenon. The FMT experiments indicate this altered microbiome may actively contribute to inflammatory outcomes rather than merely reflecting them. This points to specific taxa, such as E. coli, Faecalibacterium prausnitzii, and Eubacterium rectale, and their associated metabolites as potential targets for future microbiome-directed diagnostics or interventions in lactose intolerance.
This study examined how visceral adipose tissue (VAT) area relates to the gut bacterial microbiome and circulating markers of metabolic endotoxemia in aging women. Metabolic endotoxemia is chronic low-grade inflammation driven by elevated circulating lipopolysaccharide (LPS), a component of gram-negative bacterial cell walls. Researchers measured VAT by dual x-ray absorptiometry, assessed diet quality with a food frequency questionnaire, quantified plasma LPS, LPS-binding protein, and anti-LPS, anti-flagellin, and anti-lipoteichoic acid antibodies by ELISA, and performed metagenomic sequencing on fecal DNA. A parallel mouse experiment modeled metabolic endotoxemia by feeding female C57BL/6 mice diet-derived fecal LPS on high-fat or low-fat diets.
The human cohort consisted of fifty postmenopausal women with a mean age of 78.8 years who already had existing DXA-based adipose measurements. Participants were selected from the extremes of visceral adiposity: twenty-five women with low VAT area (about 45.6 cm2) and twenty-five with high VAT area (about 177.5 cm2). This extreme-groups design allowed comparison of gut microbiome and endotoxemia markers across a wide range of visceral fat. The companion animal experiment used female C57BL/6 mice on high-fat or low-fat diets to model the human findings.
The abstract indicates that high visceral adiposity in these postmenopausal women was linked to a gut bacterial microbiome shifted toward a pro-inflammatory profile compared to women with low VAT area. This shift accompanied signs of immunogenic metabolic endotoxemia, reflected in circulating LPS, LPS-binding protein, and antibody markers measured by ELISA. The provided abstract text is truncated before reporting the specific taxa, antibody levels, or mouse-model outcomes, so those detailed results cannot be stated here.
The findings support a model in which visceral fat accumulation after menopause is accompanied by microbiome-driven inflammatory signaling, not just local adipose tissue changes. Pairing human cohort data with a mouse model of diet-derived LPS exposure suggests the gut microbiome and endotoxemia pathway may be a mechanistic link between visceral obesity and chronic disease risk in older women. This points to the gut barrier and circulating bacterial products as potential targets for reducing inflammation associated with abdominal obesity in aging populations.
This study examined how laparoscopic sleeve gastrectomy (LSG), a form of bariatric surgery, affects cognitive function through the microbiota-gut-brain axis (MGBA). Researchers integrated fecal 16S microbiota profiling, serum metabolomics, cognitive assessment scales, and resting-state functional connectivity MRI (rs-fMRI) to capture changes across the gut, blood, and brain simultaneously. Correlation-based statistical methods, including Spearman correlation and Co-inertia analysis, were used to link microbiota shifts and metabolite changes to changes in brain connectivity and cognitive scores.
The cohort consisted of 39 obese patients who underwent laparoscopic sleeve gastrectomy. Each patient was assessed at two time points, before surgery and six months after, using demographic data, serum samples, fecal samples, cognitive testing, and rs-fMRI scans. The abstract does not specify age, sex distribution, or geographic location of the cohort.
LSG produced substantial weight loss, with reductions of up to 28% of body weight at six months. The surgery was accompanied by measurable changes in gut microbiota composition, serum metabolite profiles, and brain functional connectivity networks identified through rs-fMRI. The abstract indicates that these multi-omics changes were statistically correlated with alterations in cognitive assessment scores, suggesting coordinated shifts across the gut-brain axis, though the specific taxa, metabolites, and brain regions most strongly implicated are not detailed in the available text.
The findings support the idea that bariatric surgery's cognitive benefits may be mediated in part by changes in gut microbiota and their downstream metabolic effects on the brain, rather than weight loss alone. This multi-omics approach, linking microbiota, serum metabolomics, and neuroimaging, offers a framework for identifying specific microbial and metabolic targets that could explain or potentially enhance post-surgical cognitive improvement. Further work identifying the exact bacterial taxa and metabolites involved could inform future non-surgical interventions aimed at the same gut-brain pathways.
This study examined how changes in social living conditions affect the composition of the gut microbiota (GM), independent of diet. The researchers designed a longitudinal experiment that sequentially manipulated housing arrangements (single versus paired) and diet (variable versus controlled) so that the effects of each factor on GM composition could be separated. This approach directly addressed a limitation of prior human and non-human primate research, in which social effects on the GM were often confounded by shared diet.
The study population was a captive cohort of 13 male cynomolgus macaques followed over 15 months. Animals began in single housing on a variable diet for the first three months, then were switched to a controlled diet, moved to paired housing for six months, and finally returned to single housing. The abstract does not report ages, weights, or other demographic details beyond sex, species, and group size.
The abstract text provided is truncated before the results are described in detail, so specific findings on how housing and diet shifts altered GM composition are not available here. What can be stated is that the structured sequencing of diet and housing changes was designed specifically to let the researchers distinguish diet-driven from social-environment-driven shifts in the gut microbiota. No mention of Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism appears in the provided text.
By experimentally separating diet from social housing, this design offers a clearer causal framework for understanding how social environment shapes the primate gut microbiota. Such findings could inform how captive animal management, and by extension human social and living arrangements, might be adjusted to support a healthier microbiome. The approach also provides a methodological template for future studies aiming to disentangle correlated environmental influences on host-associated microbial communities.
This study tested whether the anti-obesity effect of the AT1 receptor blocker telmisartan can be transferred through gut microbiota alone, independent of the drug itself. Researchers used a fecal microbiota transfer (FMT) approach in mice fed a high-fat diet to isolate the microbiome's contribution to body weight regulation. Donor stool came from mice either treated with telmisartan or given vehicle while remaining obese, and this stool was transplanted into separate acceptor mice. Microbiota composition in the recipient mice was then analyzed using 16S rRNA gene amplicon sequencing.
The study used C57BL/6N mice, a standard inbred laboratory mouse strain, rather than human subjects. Acceptor mice were placed on a high-fat diet for seven weeks before receiving fecal microbiota by oral gavage for eight weeks, continuing the high-fat diet throughout. Donor mice were themselves distinguished by prior treatment: one group received telmisartan (8 mg/kg/day) for twelve weeks and stayed lean despite the high-fat diet, while control donors were obese mice given vehicle. The abstract does not report a specific cohort size for either donors or acceptors.
Mice receiving microbiota from telmisartan-treated, lean donors gained less weight than mice receiving microbiota from obese, vehicle-treated donors, but this difference appeared only after three weeks and was no longer present by eight weeks. Energy homeostasis, insulin sensitivity, and body composition did not differ between the two groups at the endpoint measured. Overall bacterial community structure (beta-diversity) differed significantly between the groups, even though the Firmicutes to Bacteroides ratio was unchanged. Several taxa varied in abundance between groups, including Ruminococcaceae and members of the Desulfovibrionaceae family, a group of sulfate-reducing bacteria, along with unclassified Desulfovibrionia.
These findings suggest that telmisartan's anti-adipose effect can be partially and transiently transmitted through gut microbiota, supporting a diet-independent, microbiome-mediated mechanism for the drug's action. The shift in Desulfovibrionaceae and other sulfate-reducing or sulfur-metabolizing bacteria points to microbial sulfur handling as a potential contributor to host metabolic responses after FMT. However, the loss of the weight-gain difference by eight weeks, despite persistent compositional differences in beta-diversity, indicates that microbiota transfer alone is not sufficient to sustain the full metabolic benefit of telmisartan over time. This underscores the need for further work to identify which specific taxa or microbial functions might be therapeutically relevant and durable.
This study investigated whether the gut microbiome contributes to the progression of adult T-cell leukemia/lymphoma (ATLL), a refractory blood cancer caused by HTLV-1 retroviral infection. The researchers analyzed the taxonomic and functional profiles of gut microbiota to identify microbial pathways and metabolites associated with ATLL. They then tested whether a candidate microbial metabolite could directly affect the growth of ATLL cells in vitro.
The study analyzed gut microbiota from 28 patients with adult T-cell leukemia/lymphoma and 37 individuals infected with HTLV-1 who had not developed ATLL. High-risk HTLV-1-infected individuals were also examined as part of the comparison. ATLL cell lines were used for the functional proliferation experiments.
The succinic semialdehyde (SSA) synthesis pathway was significantly enriched in the gut microbiome of ATLL patients (P = 0.000682). Klebsiella was identified as the main bacterial contributor to this pathway and was significantly more abundant in both ATLL patients and high-risk HTLV-1-infected individuals (P = 0.0326). When ATLL cell lines were treated with SSA, the cells showed significant proliferation.
These findings suggest the gut microbiome can actively promote ATLL progression through a specific bacterial metabolite rather than merely reflecting disease state. Klebsiella-driven succinic semialdehyde production emerges as a potential mechanistic link between gut microbial function and malignant T-cell proliferation in HTLV-1-infected individuals. This raises the possibility that monitoring or targeting this microbial pathway could help identify high-risk individuals or inform future interventions to slow ATLL development.
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 examined how aflatoxin B1 (AFB1), a common mycotoxin contaminant of grains and animal feed, and the parasite Eimeria ovinoidalis (a cause of sheep coccidiosis) affect uterine function when sheep are exposed individually or in combination. The researchers focused on a proposed gut-blood-reproductive axis, looking at whether gut microbiota and metabolite changes triggered by these exposures translate into reproductive toxicity. They assessed uterine histopathology, hormone levels, inflammation, and intestinal (colon) structure and barrier function.
The study used sheep as an animal model, with individual and combined exposure groups to AFB1 and E. ovinoidalis. The abstract does not specify exact group sizes, ages, or breed, so no further cohort detail can be honestly reported beyond that sheep were the study population.
AFB1 and coccidia each adversely affected reproductive system defense in sheep, altering uterine histopathology and hormone levels and triggering inflammation. These changes were associated with shifts in gut microbiota and metabolites. Co-exposure to AFB1 and coccidia disrupted colon intestinal structure, reducing crypt depth and impairing intestinal barrier function, suggesting a compounded, more severe effect than either exposure alone.
The findings suggest that combined mycotoxin and parasitic exposure can amplify reproductive toxicity in livestock through a gut-blood-reproductive axis, with gut microbiota and barrier integrity as key intermediaries. This has practical implications for sheep breeding operations, where feed contamination and coccidiosis often co-occur, since combined exposure may pose a greater threat to reproductive health than either risk factor managed in isolation. It also points to gut microbiota and intestinal barrier function as potential targets for protecting reproductive health in livestock exposed to environmental and infectious stressors.
This study examined how gut microbiome composition and function differ across subtypes of irritable bowel syndrome (IBS), including IBS with diarrhea (IBS-D), IBS with constipation (IBS-C), and unclassified IBS (IBS-U). Researchers used 16S sequencing data to compare taxonomic and functional profiles of gut bacteria between these IBS subtypes and matched non-IBS controls. They also examined how clinical characteristics, dietary factors, and depression status related to microbial composition within IBS.
The study drew on deeply phenotyped individuals enrolled in the American Gut Project, a large public microbiome dataset with associated clinical and dietary information. A total of 942 subjects with IBS (spanning IBS-D, IBS-C, and IBS-U) were included and matched by age, gender, body mass index, geography, and dietary patterns with 942 non-IBS controls. This design allowed comparison of microbiome features across IBS subtypes while controlling for major demographic and lifestyle confounders.
Subjects with IBS-D or IBS-U, but not IBS-C, showed significantly reduced bacterial diversity compared to controls. Each IBS subtype was associated with a distinct bacterial signature and corresponding functional shifts tied to disease pathogenesis. Notably, IBS-D was linked to an increased hydrogen sulfide production pathway, while IBS-C was linked to increased palmitoleate biosynthesis. Among IBS subjects, those with depression showed lower Bifidobacterium, Sutterella, and Butyricimonas and higher Proteus than those without depression, and short-chain fatty acid production pathways were reduced in affected patients.
These findings support treating IBS as a heterogeneous condition with subtype-specific microbial and metabolic signatures rather than a single uniform disorder. The elevated hydrogen sulfide production pathway identified in IBS-D points to sulfur metabolism, potentially involving sulfate-reducing bacterial activity, as a mechanistic feature worth further investigation in diarrhea-predominant disease. The link between depression and specific bacterial taxa also suggests that mental health status should be considered when characterizing IBS microbiome profiles. Together, these results could inform more precise, subtype-tailored approaches to diagnosing and managing IBS.
This study evaluated whether taking probiotics after surgery could reduce gastrointestinal complications and correct gut microbiota disturbances caused by chemotherapy in colorectal cancer (CRC) patients. Researchers compared a probiotic combination against a placebo, given from the post-operative period through the end of the first chemotherapy course. Gastrointestinal symptoms including nausea, acid reflux, abdominal pain, abdominal distention, constipation, and diarrhea were tracked throughout treatment. Fecal samples were analyzed using 16S rRNA high-throughput sequencing and short-chain fatty acid (SCFA) measurement to assess microbiota changes.
One hundred eligible CRC patients who underwent radical surgery and required subsequent chemotherapy were recruited for this study. Participants were randomly assigned to two equal groups of fifty: a Probio group receiving the probiotic combination, and a Placebo group receiving placebo instead. Fecal samples were collected from these patients at two time points, preoperatively and after the first postoperative chemotherapy cycle.
Probiotic administration effectively reduced chemotherapy-induced gastrointestinal complications, with a particularly strong effect on diarrhea (p < 0.01). Chemotherapy alone reduced the bacterial diversity of the gut microbiota in these CRC patients. This chemotherapy-induced loss of microbial diversity was significantly reversed by probiotic supplementation, indicating a protective effect on the gut ecosystem during treatment.
These findings suggest that postoperative probiotic supplementation could be a practical, low-risk strategy to improve chemotherapy tolerability in colorectal cancer patients. By reducing diarrhea and preserving gut microbial diversity, probiotics may help patients complete chemotherapy regimens with fewer disruptive side effects. This supports considering probiotic co-administration as part of standard supportive care during postoperative chemotherapy for CRC.
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 leptin-deficient obesity is linked to periodontal disease. Researchers analyzed periodontal status, alveolar bone phenotype, and the oral microbiome in obese mice lacking leptin. Alveolar bone and periodontal tissue were assessed with micro-CT, histology, TRAP staining for osteoclasts, and immunohistochemistry/RT-qPCR for inflammatory and osteoclastogenic markers. The oral microbiome was profiled using 16S rDNA sequencing.
The study used 12-week-old male mice, comparing wild-type animals to leptin-deficient ob/ob mice. This is an animal model of genetically induced obesity rather than a human cohort. No human subjects or additional demographic details were reported in the abstract.
Ob/ob mice showed a significantly greater CEJ-ABC distance in their maxillary molars compared to wild-type mice, indicating greater alveolar bone loss. Bone volume fraction (BV/TV) was reduced, and higher numbers of osteoclasts were found in the alveolar bone near the molar roots. The mice also showed gingival epithelial hyperplasia and disordered periodontal ligaments, along with altered RANKL/OPG expression and an altered oral microbiome, though the abstract does not report specific taxa.
The findings suggest leptin deficiency and its associated obesity phenotype can drive periodontitis-like bone loss and inflammation through altered bone remodeling signals and shifts in the oral microbiome. This supports a biological link between metabolic/obesity status and periodontal disease risk. It points to leptin signaling and RANKL/OPG balance as potential mechanistic targets for understanding or managing obesity-associated periodontitis.
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.
This study examined the faecal microbiota profiles of young children affected by acute gastroenteritis (AGE), a major cause of childhood illness marked by diarrhoea, abdominal pain, fever, and vomiting. Researchers focused on the composition and structure of the gut microbial community, comparing children with AGE to healthy children. The work aimed to characterize disease-associated microbial changes in an African setting, where such data have been limited.
The study population was Ghanaian children aged five years and below. It included children diagnosed with acute gastroenteritis as well as healthy controls for comparison. The abstract does not specify an exact sample size or recruitment sites beyond this age-defined, Ghana-based pediatric cohort.
Children with AGE showed altered faecal microbiota composition and structure compared with healthy controls. Consistent with prior evidence linking AGE to gut microbial disruption, the pattern described involves increased presence of pathogenic or opportunistic microbes alongside reduced beneficial taxa. The abstract does not report specific taxa, effect sizes, or statistical values for the Ghanaian cohort itself, so these findings should be read as a confirmed shift in overall community composition and structure rather than itemized taxon-level results.
The findings extend understanding of AGE-associated gut microbiota disruption to an African pediatric population, an area where evidence was previously limited. Documenting these microbial alterations in Ghanaian children supports the broader view that early-life microbiome disruption may increase susceptibility to infectious diarrhoeal disease. This regional data can inform future research into microbiota-targeted approaches for preventing or managing childhood gastroenteritis in developing-country settings.
This study examined how the chemotherapy drug Irinotecan affects gut microbiota composition, given that gut microbial enzymes convert Irinotecan into the toxic metabolite SN-38 during intestinal excretion. The researchers used 16S rRNA gene sequencing to characterize microbiota composition across different patient groups. They also tested whether specific probiotic Lactobacillus species, alone or combined, could suppress bacterial beta-glucuronidase enzyme activity, the enzymatic step implicated in Irinotecan-associated toxicity. In-vitro gene expression assays and an in-vivo mouse model of Irinotecan administration were used to evaluate the protective potential of these probiotics.
Stool samples were collected from three human groups: healthy individuals, colon cancer patients, and Irinotecan-treated patients, with five samples per group. In parallel, in-vitro experiments used Escherichia coli to assess beta-glucuronidase gene expression in response to three Lactobacillus species (L. plantarum, L. acidophilus, and L. rhamnosus). The in-vivo protective effects of these probiotics were assessed in mice administered Irinotecan, either with single probiotic strains or in mixed combinations.
Irinotecan treatment was associated with changes in gut microbiota composition compared to healthy individuals and colon cancer patients, based on 16S rRNA sequencing. The three Lactobacillus species tested, in both single and mixed forms, influenced expression of the E. coli beta-glucuronidase gene, the enzyme responsible for reactivating toxic SN-38 in the gut. In mice, administration of these probiotics before Irinotecan was evaluated for effects on reactive oxidative species (ROS) levels and intestinal outcomes, indicating a potential protective role against Irinotecan-induced toxicity.
These findings suggest that gut microbiota composition shifts during Irinotecan chemotherapy and that this altered microbial environment contributes to drug-related intestinal toxicity through beta-glucuronidase activity. Targeting this bacterial enzyme with specific Lactobacillus probiotics may offer a strategy to reduce Irinotecan-associated diarrhea and oxidative stress in the gut. This supports further investigation of probiotic co-administration as an adjunct to chemotherapy to improve tolerability in colorectal cancer treatment.
This study examined the relationship between the gut microbiome and disease severity in Parkinson's disease (PD), an area with limited prior research despite growing evidence linking PD to gut microbiota. Researchers used 16S rRNA amplicon sequencing and shotgun metagenomic sequencing on fecal samples to characterize microbial composition and function. They further used metagenome-assembled genome (MAG) analysis to identify specific bacterial genomes and their metabolic pathways associated with disease severity.
The study included 90 fecal samples collected from newly diagnosed, untreated patients with PD (n = 47) and matched healthy control subjects (n = 43). Because patients were newly diagnosed and untreated, the findings reflect microbiome changes not confounded by PD medications.
Desulfovibrio, a genus of sulfate-reducing bacteria, was significantly increased in PD patients compared to healthy controls and was positively correlated with disease severity. This increase was mainly driven by enhanced homogeneous selection and weakened ecological drift in the gut community. A specific Desulfovibrio metagenome-assembled genome (MAG58), also positively correlated with severity, possessed a complete assimilatory sulfate reduction pathway and a near-complete dissimilatory sulfate reduction pathway capable of producing hydrogen sulfide.
The findings suggest a potential pathogenic pathway in which expansion of sulfate-reducing Desulfovibrio and its hydrogen sulfide production may influence PD development and worsen disease severity. This positions Desulfovibrio and its sulfur metabolism as a candidate microbial driver and possible biomarker of PD progression. The results support further investigation into targeting sulfate-reducing bacteria or hydrogen sulfide production as a therapeutic or diagnostic strategy in PD.
This study examined how orlistat affects the gut microbiota and metabolite profiles in a rat model of polycystic ovary syndrome (PCOS). Researchers used 16S rRNA gene sequencing and untargeted metabolomics on fecal samples to characterize these changes. They also measured serum sex hormones and lipid levels to assess the physiological effects of orlistat treatment. The goal was to better understand the mechanism by which orlistat improves PCOS-related outcomes through gut microbiota changes.
The subjects were rats with PCOS induced by letrozole combined with a high-fat diet, not human patients. Ten rats served as an untreated PCOS control group, while three additional groups of ten rats each received low, medium, or high doses of orlistat. Fecal and blood samples were collected from these PCOS and orlistat-treated (ORL-PCOS) groups for analysis.
Orlistat treatment reduced body weight gain and lowered testosterone, LH, the LH/FSH ratio, total cholesterol, triglycerides, and LDL-C, while increasing estradiol and improving estrous cycle disorder. Gut microbiota richness and diversity were higher in the ORL-PCOS group than in the PCOS group, and the Firmicutes-to-Bacteroidetes ratio decreased with orlistat treatment. Orlistat also significantly decreased the relative abundance of Ruminococcaceae. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism in this excerpt.
The findings suggest orlistat's benefits in PCOS extend beyond weight loss and may involve reshaping the gut microbiota and its metabolite output. Restoring microbial diversity and shifting the Firmicutes-to-Bacteroidetes ratio could be a contributing mechanism behind improved hormonal and lipid profiles. This supports further investigation into gut microbiota as a therapeutic target in PCOS management. Because the model is rodent-based, translation to human PCOS treatment requires additional clinical study.
This study examined whether the gut microbiota is associated with the development of Graves' disease (GD), an autoimmune thyroid condition. Researchers profiled gut microbiota composition using 16S rRNA sequencing, comparing samples taken before and after treatment in GD patients. They also measured interleukin-17 levels to explore a possible immune link, and used a random forest model to see whether specific bacterial genera could distinguish GD patients from healthy individuals.
The study included 65 patients newly diagnosed with Graves' disease, sampled both before and after treatment. A comparison group of 33 physical examination personnel (presumed healthy individuals) was also profiled. All participants underwent gut microbiota analysis via 16S rRNA sequencing.
Gut microbiota composition differed significantly between GD patients and the comparison group, with differences spanning 1 class, 1 order, 5 families, and 14 genera. After treatment, bacterial taxa that had been enriched in GD patients decreased, while taxa that had been depleted increased, alongside a significant decrease in interleukin-17 levels. A random forest analysis identified 12 genera capable of distinguishing GD patients from healthy controls. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, sulfide, or sulfur metabolism.
The findings suggest that gut microbiota alterations in Graves' disease are linked to immune imbalance, given the parallel changes in microbiota composition and interleukin-17 levels after treatment. The identification of 12 discriminating genera raises the possibility that gut microbiota profiling could help distinguish GD patients from healthy individuals. The partial normalization of microbiota after treatment suggests gut microbiota may be a dynamic marker worth monitoring alongside thyroid disease activity.
This study examined whether the timing of offspring exposure to maternal glucocorticoids (GCs), stress-related hormones, during early gestation, late gestation, or lactation was associated with differences in the gut bacterial community of a wild primate. The researchers looked at bacterial diversity, composition, and function, and tracked whether any associations changed or persisted as offspring aged. The work addresses a gap in understanding how maternal hormonal exposure during development shapes long-term gut microbiome outcomes in long-lived species living in their natural habitat.
The study used a cross-sectional sample of wild Assamese macaques spanning infant, juvenile, and adult age classes. Naturally varying maternal glucocorticoid levels during early gestation, late gestation, and lactation were assessed in relation to each offspring's gut bacterial community. The abstract does not give an exact sample size, but the design draws on a natural, free-ranging primate population rather than a laboratory cohort.
Naturally elevated maternal glucocorticoids during early gestation, but not during late gestation or lactation, were associated with reduced gut bacterial richness in offspring. The association between early gestational maternal glucocorticoids and offspring gut bacterial composition and function grew stronger, not weaker, as the offspring aged. This early-gestation effect was about 10 times stronger than the effect linked to glucocorticoid exposure during the late prenatal or postnatal period, which showed a comparatively smaller association with the gut bacterial community. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings suggest that the timing of prenatal maternal hormonal exposure can programmatically shape offspring gut bacterial communities for the long term, rather than producing only transient effects. Because the early-gestation effect intensified with age instead of fading, this points to a durable, developmentally timed maternal influence on the gut microbiome rather than a short-lived one. This work extends maternal-effects and developmental-programming research from morphology and behavior into the gut microbiome domain in a wild, long-lived primate model. It also underscores that studying only late pregnancy or postnatal exposures could miss the most consequential window for maternal glucocorticoid effects on offspring gut bacteria.
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 examined the surface (external) microbiome of purple sea urchins affected by bald sea urchin disease (BSUD), a condition believed to be caused by bacterial infection that leads to loss of surface appendages and other symptoms. The researchers used 16S rRNA gene sequencing to characterize bacterial communities on the surface of urchins housed in aquaria. They compared microbiome composition across disease states, tracking urchins that contracted BSUD and later recovered, alongside healthy urchins in a separate aquarium. The aim was to fill a gap in prior BSUD research, which had focused on identifying causative agents rather than describing the broader surface microbiome.
The subjects were purple sea urchins housed in a closed marine aquarium system, rather than a human or animal clinical cohort. Some urchins had contracted BSUD and subsequently recovered, while others were healthy urchins maintained in a separate aquarium. The abstract does not give an exact number of urchins sampled, so the population is best described as a small, aquarium-based comparison of diseased/recovered versus healthy individuals across two distinct tank environments.
16S rRNA gene sequencing showed that different aquarium microhabitats harbored distinct microbial compositions. Diseased, recovered, and healthy sea urchins each had distinct surface microbial compositions rather than a single shared community. This pattern indicates a correlation between shifts in the surface microbiome and the process of recovering from BSUD. The findings suggest the microbiome changes in a stepwise or trackable way as urchins move from disease to recovery.
The results support monitoring the surface microbiome as a potential indicator of disease status and recovery in sea urchins affected by BSUD. Because aquarium microhabitat itself shaped microbial composition, environmental management may influence susceptibility to, or recovery from, this disease in captive settings. These findings lay groundwork for future studies to identify specific microbial shifts that could serve as recovery markers or inform husbandry practices in aquaria.
This study examined whether Zhishi Daozhi decoction (ZDD), a traditional formula, could relieve constipation caused by a high-fat and high-protein diet (HFHPD). The researchers looked at how ZDD affected the intestinal mucosal microbiota, oxidative stress markers, and gut-regulatory peptides in a diet-and-drug-induced constipation model. Mice were given loperamide hydrochloride alongside HFHPD to establish the constipation model before ZDD intervention.
The subjects were mice divided into five groups: a normal control (MN) group, a natural recovery (MR) group, and three ZDD-treated groups receiving low (MLD), medium (MMD), or high (MHD) doses. Constipation was induced in the relevant groups using a high-fat and high-protein diet combined with loperamide hydrochloride. This was an animal model study rather than a human cohort.
After ZDD treatment, serum cholecystokinin (CCK) content in the MR group decreased and calcitonin gene-related peptide (CGRP) content increased, though these changes were not significant. Superoxide dismutase (SOD) content, an antioxidant marker measured in the liver, was also affected by the intervention. The study used 16S rRNA amplicon sequencing of intestinal mucosal DNA to track changes in the mucosal microbiota alongside these biochemical shifts, though the abstract text describing the full microbiota and malondialdehyde (MDA) results was cut off.
The findings suggest ZDD may help correct constipation driven by high-fat, high-protein diets by acting on the intestinal mucosal microbiota and oxidative stress pathways, alongside gut peptides like CCK and CGRP. This points to a potential dietary-pattern-linked mechanism of constipation that could be addressed through microbiota-targeted or antioxidant-supporting interventions. Because this is a mouse model, further research is needed before these results can inform human clinical approaches to diet-related constipation.
This study examined whether multi-strain probiotic combinations of Bifidobacterium and Lactobacillus, mixed in four different ratios, could relieve constipation. Researchers built a mouse model of constipation using loperamide hydrochloride and then administered the probiotic blends for four weeks. They assessed changes in intestinal flora composition, short-chain fatty acid (SCFA) levels, gut motility-related hormones, and inflammatory markers. The goal was to compare how differently formulated probiotic blends might work through distinct mechanisms to relieve constipation.
The subjects were mice with loperamide hydrochloride-induced constipation, used as an experimental model rather than human patients. Four different multi-strain probiotic formulations, varying in their ratio of Bifidobacterium to Lactobacillus, were tested in this model. The abstract does not give a specific number of animals per group or additional demographic detail, so no further population specifics can be stated.
After four weeks, three formulations, BM1, BM2, and PB2, effectively relieved constipation, though through different pathways. The Bifidobacteria-dominated formulas BM1 and BM2 altered the composition and structure of the intestinal flora, decreasing Tyzzerella, Enterorhabdus, Faecalibaculum, Gordonibacter, and Mucispirillum while increasing Parabacteroides and stool SCFA content. These formulas also restored motilin (MTL) and vasoactive intestinal peptide (VIP) levels and downregulated serum IL-6 and IL-8, repairing the inflammatory response caused by constipation and promoting gastrointestinal peristalsis.
The findings suggest that the ratio of Bifidobacterium to Lactobacillus in a multi-strain probiotic blend meaningfully changes its mechanism of action against constipation, not just its effectiveness. Bifidobacteria-dominated formulations appear to work by reshaping the gut microbiota, raising SCFA production, and correcting motility hormone and inflammatory imbalances. This points to the potential for tailoring probiotic strain ratios to target specific physiological pathways involved in constipation relief.
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 how surgery-induced gut microbial dysbiosis contributes to perioperative neurocognitive disorders (PND), a common but poorly treated postoperative complication. The researchers investigated the mechanisms linking postoperative changes in the gut microbiota to disruptions in intestinal barrier function, serum metabolism, and cognitive outcomes. Behavioral testing, 16S rRNA gene sequencing, non-target metabolomics, intestinal permeability assays, protein analysis, and immunofluorescence staining were used to trace this gut-brain pathway. The metabolite palmitic amide was identified as a specific link between microbial changes and cognitive effects.
The study was conducted in mice, comparing aged and young animals subjected to surgery. Aged mice were the primary focus, since surgery-induced cognitive impairment occurred predominantly in this group. Interventions including fecal microbiota transplantation from young donors, dexamethasone, Lactobacillus supplementation, indole propionic acid, and palmitic amide administration were tested in these mouse models.
Surgery altered gut microbiota composition and worsened intestinal barrier disruption specifically in aged mice, which corresponded with the cognitive impairment seen mainly in this group. These adverse effects could be reduced by transferring microbiota from young donors or by strengthening intestinal barrier function with dexamethasone, Lactobacillus, or indole propionic acid. The abstract also points to microbiota-linked changes in metabolism, including the metabolite palmitic amide, as part of the mechanism connecting gut dysbiosis to cognitive outcomes.
The findings suggest that age-related vulnerability to postoperative cognitive decline may be driven in part by how surgery disrupts the gut microbiota and intestinal barrier. Because microbiota transfer, probiotic supplementation, and metabolite-targeted interventions each improved outcomes in this model, gut-directed strategies could represent a therapeutic avenue for PND. This supports viewing perioperative cognitive complications through a gut-brain axis lens rather than treating them as purely neurological events.
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 retrospective cohort study investigated whether intestinal obstruction caused by colorectal cancer (CRC) is associated with distinct changes in the gut microbiota. Researchers used 16S rRNA sequencing to compare microbiota composition in tumour and adjacent normal tissues between CRC patients with and without obstruction. Patients with and without obstruction were matched using 1:1 propensity score matching to reduce confounding. The study also examined whether obstruction status was linked to differences in survival outcomes.
A total of 313 patients with colorectal cancer were recruited for the study. Total DNA was extracted and amplified from tumour and adjacent normal tissues of 84 patients, along with 36 additional frozen tumour tissue samples. Patients were divided into obstruction and non-obstruction groups and compared after propensity score matching. The abstract does not specify additional demographic details such as age or sex distribution.
Patients with CRC-related intestinal obstruction had shorter overall survival and disease-free survival than those without obstruction. Microbial richness and diversity in tumour tissues were significantly higher in the obstruction group, with both alpha and beta diversity differing significantly between groups (P < 0.05). At the phylum and genus levels, Bacteroidetes were significantly enriched in the tumour tissues of patients with obstruction. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings suggest that intestinal obstruction in colorectal cancer is associated with a distinct, more diverse tumour-associated microbiota dominated by Bacteroidetes, and with worse clinical outcomes. This raises the possibility that microbiota alterations may be a marker of, or contributor to, the more aggressive clinical course seen in obstructed CRC. These associations could inform future research into microbiota-based prognostic markers or risk stratification for CRC patients presenting with obstruction. Further studies would be needed to clarify causality and underlying mechanisms.
This randomized clinical trial examined how mechanical debridement combined with an adjunctive mouthrinse affects the subgingival and submucosal plaque microbiome at sites with peri-implant mucositis and gingivitis. Patients received debridement plus one month of either delmopinol, chlorhexidine (CHX), or a placebo mouthrinse. Plaque samples from implants and teeth were collected at baseline and at 1 and 3 months, then profiled using 16S V4 rRNA gene amplicon sequencing.
Eighty-nine patients with peri-implant mucositis were enrolled in this double-blinded, randomized, placebo-controlled trial. Each patient contributed patient-matched samples from both peri-implant and dental sites, allowing direct within-person comparison of the two microbial niches. No further demographic details are given in the abstract.
Sites with peri-implant mucositis harbored a less diverse and less anaerobic microbiome than dental sites with gingivitis, despite eliciting an equal inflammatory response. Even at healthy sites, the microbiome around teeth was more diverse and more anaerobe-rich than the microbiome around implants. Adjunctive delmopinol or CHX, but not placebo, produced measurable microbial changes after one month, while mechanical debridement affected both dental and peri-implant biofilms.
The findings suggest that peri-implant and dental biofilms are ecologically distinct even under comparable inflammatory conditions, meaning peri-implant mucositis should not simply be treated as an implant-site analog of gingivitis. This ecological difference may help explain why peri-implant disease can behave differently from periodontal disease despite similar clinical inflammation. The results also support that antimicrobial mouthrinses, rather than debridement alone, contribute meaningfully to shifting the microbiome during peri-implant mucositis therapy.
This study examined whether Parkinson's disease (PD) medications themselves, rather than the disease process alone, alter gastrointestinal motility and microbiota composition in the small intestine. The small intestine is the primary site of drug absorption, yet it had not previously been studied in this context. Researchers treated healthy, non-PD rats with dopamine, pramipexole (combined with levodopa-carbidopa), or ropinirole (combined with levodopa-carbidopa) for 14 sequential days. The aim was to determine whether the medications alone could reproduce microbiota changes resembling those reported in human PD patients.
The subjects were healthy, non-PD, wild-type Groningen rats, not human patients or a public dataset. The rats were divided into treatment groups receiving dopamine, pramipexole with levodopa-carbidopa, or ropinirole with levodopa-carbidopa, alongside a vehicle (control) group. The abstract does not specify the exact number of animals per group. Using healthy animals allowed the researchers to isolate the effects of the medications from any confounding effects of PD itself.
Rats treated with dopamine agonists showed significantly reduced small intestinal motility and increased bacterial overgrowth in the distal small intestine. Treated animals also showed significant microbial taxa shifts compared to vehicle controls, including increases in Lactobacillus and Bifidobacterium and decreases in Lachnospiraceae and Prevotellaceae. These shifts closely resembled differences previously reported between human PD patients and healthy controls. Notably, certain Lactobacillus species correlated negatively with systemic levodopa levels, suggesting these bacteria may affect the drug's bioavailability.
The findings suggest that PD medications themselves, not just the underlying disease, can drive gastrointestinal motility changes and microbiota alterations previously attributed to PD pathology. This represents an important confounder that should be accounted for when interpreting microbiome studies in PD patients taking dopaminergic therapy. The negative correlation between certain Lactobacillus species and levodopa levels also raises the possibility that drug-induced microbiota shifts could feed back to affect medication bioavailability. Future PD microbiome research and drug-microbiome interaction studies should account for medication effects independent of disease status.
This study examined whether fecal microbiota composition and fecal amino acid levels change in the presence of colonic adenomas and after those adenomas are removed. Researchers longitudinally tracked stool samples collected before colonoscopy and again three months after polypectomy. The goal was to determine whether microbial and amino acid signals could help detect adenomas and monitor patients after endoscopic removal, given that surveillance colonoscopy has low yield and interval colorectal cancers still occur.
The study included patients with advanced adenomas and nonadvanced adenomas (0.5 to 1.0 cm) who underwent polypectomy during colonoscopy, totaling 19 patients. These patients were strictly matched on age, body-mass index, and smoking habits to 19 control participants who had no endoscopic abnormalities. Fecal samples were collected from both groups before bowel preparation, and microbial taxa were profiled by 16S rRNA sequencing while amino acids were measured by high-performance liquid chromatography.
Adenoma patients could be distinguished from controls based on both their amino acid profiles and their microbial composition. Levels of proline, ornithine, and serine were significantly increased in adenoma patients compared to controls, and these three amino acids together formed a candidate adenoma-specific panel with an AUC of 0.79. After endoscopic removal of the adenomas, levels of these amino acids decreased and came to resemble those seen in controls, suggesting the changes were tied to the presence of the lesion itself rather than fixed host traits. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, or sulfur metabolism among the described findings.
These findings suggest that fecal amino acid panels, potentially combined with microbial composition data, could serve as a noninvasive tool to help detect adenomas and monitor patients after polypectomy. Because these markers normalized after adenoma removal, they may also help confirm successful resection or flag patients who need closer follow-up. This approach could complement or improve upon current endoscopic surveillance strategies, which have low yield despite the continued occurrence of interval colorectal cancers.
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.
This study examined whether gut microbiome characteristics relate to how well medical nutrition therapy (MNT) controls blood glucose in women newly diagnosed with gestational diabetes mellitus (GDM). Researchers compared fasting and 2-hour postprandial blood glucose alongside stool microbiome composition before and after one week of MNT. The design used a nested case-control approach to contrast women whose glycemic control responded to nutrition therapy against those whose control did not.
Seventy-four pregnant women newly diagnosed with GDM who received one week of medical nutrition therapy were included. Within this group, women who did not meet glycemic targets after MNT (the ineffective group) were matched 1:1 by age (within 5 years) and pre-pregnancy BMI to women who did meet glycemic targets (the effective group). Stool samples were collected from these matched pairs before and after treatment.
Before treatment, the ineffective group's gut microbiome was enriched in Desulfovibrio, a sulfate-reducing bacterial genus, along with Aeromonadales, Leuconostocaceae, Weissella, Prevotella, Bacillales_Incertae Sedis XI, Gemella, and Bacillales. In contrast, the effective group was enriched in Roseburia, Clostridium, Bifidobacterium, Bifidobacteriales, Bifidobacteriaceae, Holdemania, and Proteus. After treatment, the effective group showed further enrichment in Bifidobacterium and Actinomycete, indicating a distinct pretreatment microbiome signature separated women who would respond to nutrition therapy from those who would not.
The presence of Desulfovibrio and related sulfate-reducing bacteria before treatment may signal a gut microbiome less likely to respond to standard nutrition therapy in GDM, while enrichment in beneficial genera like Bifidobacterium and Roseburia may favor a good response. These findings suggest gut microbiome profiling could help identify, in advance, which pregnant women with GDM are likely to need additional or alternative glycemic management beyond nutrition therapy alone. Further research is needed to confirm whether modulating sulfate-reducing bacteria or promoting beneficial taxa can directly improve glycemic outcomes in this population.
This study investigated atherosclerosis co-occurring with depression through the lens of the microbiota-gut-brain axis. Researchers examined changes in lipid metabolites in the prefrontal cortex and hippocampus, alongside characteristics of the gut microbiota, in ApoE-/- mice. The animal model combined a high-fat diet with binding stimulation for 16 weeks to induce both atherosclerotic damage and depression-like behavior. Non-targeted lipidomics using LC-MS/MS profiled brain lipid metabolites, while 16S rDNA amplicon sequencing characterized the gut microbiota, with association analysis linking the two.
The subjects were male ApoE-/- mice, a genetic knockout strain prone to atherosclerosis, assigned to a hyperlipid feeding combined with binding (HFB) group of 14 animals. This group was compared against a normal control (NC) group of mice not subjected to the high-fat diet and binding stimulation. The study is therefore a controlled animal model investigation rather than a human cohort study.
Compared with the normal control group, the HFB group showed depression-like behaviors, assessed through body weight changes, the sucrose preference test, open field test, and tail suspension test. Oil-red O staining, HE staining, and biochemical parameters confirmed atherosclerotic damage in the HFB mice. The abstract indicates that differential lipid metabolites were identified in the prefrontal cortex and hippocampus, and that differential gut microbial taxa were identified via 16S rDNA sequencing and linked to these lipid changes through association analysis. The abstract text provided does not specify which particular bacterial taxa or lipid species were altered.
The findings support the microbiota-gut-brain axis as a plausible mechanistic link between atherosclerosis and co-occurring depression, connecting peripheral gut microbial changes to lipid alterations in brain regions governing mood and cognition. This suggests that gut microbiota and brain lipid metabolism could represent new targets for understanding and potentially treating atherosclerosis co-depression. Because diagnosis, treatment, and prevention of this comorbid condition are currently poor, identifying such targets addresses an urgent clinical need. Further work would be needed to translate these animal-model associations into human-relevant mechanisms or interventions.
This study examined whether intestinal barrier dysfunction, on its own and without accompanying systemic inflammation, is enough to worsen neuroinflammation and neurodegeneration in a genetic mouse model of Parkinson's disease. Researchers used low dose (1%) dextran sodium sulfate (DSS) administered in cycles over 52 days to disrupt the intestinal barrier while trying to isolate this effect from broader inflammatory responses. They assessed intestinal barrier integrity, intestinal inflammation, stool microbiome community composition, systemic inflammation, motor function, microglial activation, and dopaminergic pathology. The goal was to clarify which gut-related factor, microbiota dysbiosis, barrier dysfunction, or colonic inflammation, primarily drives the disrupted gut-brain axis seen in Parkinson's disease.
The study used alpha-synuclein overexpressing (ASO) mice, a genetic rodent model of Parkinson's disease, compared against control mice. No human patients were involved. The abstract does not provide specific animal numbers, ages, or sex distribution for the cohort.
Low dose DSS was used specifically to induce intestinal barrier dysfunction while avoiding the systemic inflammation that typically accompanies higher-dose colitis models. The abstract's title states the central result directly: intestinal barrier dysfunction in the absence of systemic inflammation failed to exacerbate motor dysfunction and brain pathology in the ASO mice. This suggests that barrier disruption alone, without concurrent systemic inflammatory signaling, was not sufficient to worsen neurodegenerative outcomes in this model. The abstract does not report specific findings on Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings imply that intestinal barrier dysfunction by itself may not be the primary driver of gut-to-brain neuroinflammation in Parkinson's disease, and that systemic inflammation may be a necessary co-factor for gut-derived signals to worsen brain pathology. This challenges a simplified model in which leaky gut alone explains disease progression, pointing instead toward inflammatory signaling as a more critical mediator. These results could help refine which gut-brain axis components are prioritized as therapeutic targets in Parkinson's disease research.
This study performed a meta-analysis of gastric mucosal microbiome data across multiple published studies to determine whether microbial associations with gastric cancer are consistent across different patient populations. The researchers examined compositional and ecological shifts in gastric microbial communities across the stages of gastric carcinogenesis. They also assessed how bacterial co-occurrence patterns and microbial diversity change as the disease progresses from a healthy state toward cancer.
The abstract does not specify a single original cohort, since this was a meta-analysis pooling gastric mucosal microbiome data from multiple prior studies. The comparisons were made between samples representing gastric cancer (GC) and samples representing superficial gastritis (SG), spanning different stages of gastric carcinogenesis. Helicobacter pylori infection status was also used to stratify samples within this pooled dataset.
Opportunistic pathobionts including Fusobacterium, Parvimonas, Veillonella, Prevotella, and Peptostreptococcus were enriched in gastric cancer, while commensals such as Bifidobacterium, Bacillus, and Blautia were depleted compared to superficial gastritis. Co-occurrence correlation strength among GC-enriched bacteria increased with disease progression, while correlations among GC-depleted bacteria weakened. The study newly identified eight bacterial taxa, Veillonella, Dialister, Granulicatella, Herbaspirillum, Comamonas, Chryseobacterium, Shewanella, and Helicobacter, as universal biomarkers that discriminated gastric cancer from superficial gastritis with an area under the curve of 0.85. H. pylori-positive samples showed reduced microbial diversity, altered community composition, and weaker interactions among gastric microbes.
By pooling data across multiple independent studies, this meta-analysis establishes a set of universal, reproducible microbial signatures associated with gastric carcinogenesis rather than findings specific to one cohort. The eight-taxa biomarker panel, with an AUC of 0.85, suggests potential value as a non-invasive or biopsy-based tool for distinguishing gastric cancer from superficial gastritis. The finding that H. pylori infection reshapes microbial diversity and community interactions reinforces its role as a driver of dysbiosis during gastric cancer development, highlighting the broader gastric microbiome as a target for risk stratification.
This study examined how a high-fat diet (HFD) influences colorectal cancer (CRC) tumorigenesis and liver metastasis through changes in gut microbiota. The researchers assessed gut barrier function and inflammation in the colorectum and liver following HFD exposure. They used 16S rRNA sequencing to characterize microbiota shifts and tested whether a specific bacterial genus could reproduce the observed barrier and inflammatory effects.
The study drew on faecal samples from HFD-fed rats as well as from CRC patients with liver metastasis. Beyond this, the abstract does not provide details on sample size, age, or sex of the subjects. The rat model was used alongside human patient samples to compare microbiota changes across species.
A high-fat diet promoted gut barrier dysfunction and inflammation in both the colorectum and liver. 16S rRNA sequencing revealed an abundance of Desulfovibrio (DSV) in both HFD-fed rats and CRC patients with hepatic metastasis. DSV itself was shown to induce colorectal barrier dysfunction and inflammation in the colorectum and liver, indicating it can independently generate a tumor-permissive microenvironment.
These findings suggest that Desulfovibrio abundance driven by high-fat diet consumption may be a mechanistic contributor to CRC initiation and progression to liver metastasis. This positions gut microbiota composition, and DSV specifically, as a potential target for reducing metastatic risk in CRC. The results also support diet as a modifiable factor influencing the gut microenvironment relevant to cancer spread.
This observational study examined the gut microbiota and host immune response in elderly patients with schizophrenia compared to healthy controls. Researchers used 16S rRNA gene sequencing targeting the V3-V4 region to profile fecal bacterial communities. They then correlated these microbial profiles with measures of host immune function, including circulating cytokine levels.
The study included 161 fecal samples total, comprising 90 samples from elderly patients with schizophrenia and 71 samples from healthy controls. The abstract identifies the population as Chinese elderly individuals, consistent with the study title. No further demographic details are provided in the abstract.
Beta-diversity analysis separated schizophrenia patients and healthy controls into two distinct bacterial community clusters. Linear discriminant analysis effect size (LEfSe) identified compositional shifts in several genera associated with schizophrenia, including Faecalibacterium, Roseburia, Actinomyces, Butyricicoccus, and Prevotella. Alongside these microbial changes, pro-inflammatory cytokines such as IL-1β were markedly elevated in patients, while anti-inflammatory cytokines such as IFN-γ were markedly reduced. Correlation analysis linked these specific bacterial taxa to the observed immune disturbances.
The findings support a link between gut dysbiosis and immune dysfunction in elderly patients with schizophrenia. The identified bacteria correlated with inflammatory markers could serve as non-invasive biomarkers for this population. This suggests the gut microbiome and host immune signaling may be relevant targets for understanding or monitoring schizophrenia in older adults.
This study examined the composition of the gut microbiota in patients with colorectal cancer, comparing right-sided (RCC) and sigmoid, left-sided (SCC) tumor locations. It also assessed how microbiota composition changes after partial colectomy performed to remove these tumors. Stool samples were analyzed using terminal restriction fragment length polymorphism (T-RFLP) and 16S rRNA gene amplicon sequencing, with PICRUSt2 used to predict the metabolic function of the microbial community.
Forty-one subjects provided stool samples across five groups: 10 healthy controls, 10 patients with right-sided colon cancer (RCC), 6 patients with sigmoid colon cancer (SCC), 9 patients after right colon resection (RCR), and 6 patients after sigmoid colon resection (SCR). This design allowed comparison of microbiota both by tumor location and by surgical status.
T-RFLP analysis showed a reduced ratio of clostridial cluster XIVa in patients with sigmoid colon cancer and a reduced ratio of clostridial cluster IX in patients with right-sided colon cancer. These reductions were not evident in the corresponding post-colectomy groups (RCR or SCR), suggesting a difference between the pre-resection cancer state and the post-resection state. The abstract text was truncated before the 16S rRNA sequencing results and PICRUSt2 functional predictions were fully described.
The findings suggest that right-sided and left-sided (sigmoid) colorectal cancers are associated with distinct patterns of gut microbial dysbiosis, specifically involving different clostridial clusters. Because these dysbiosis patterns were not observed after curative colectomy, tumor location-specific microbiota alterations may be tied to the presence of the tumor itself rather than persisting as a fixed feature of the gut environment. This supports the idea that gut microbiota assessment could be a useful, location-aware tool in understanding colorectal cancer biology.
This cross-sectional study examined the association between gut microbiota composition and prediabetes in people living with HIV (PLWH). All participants were receiving antiretroviral therapy and had an undetectable plasma viral load. Fecal samples were collected and gut microbiome profiles were analyzed using 16S rRNA sequencing to compare bacterial diversity and taxa abundance between prediabetic and normoglycemic participants.
The study enrolled 40 people living with HIV, all on antiretroviral therapy with undetectable viral loads. Of these, 20 participants had prediabetes and 20 were normoglycemic, allowing a direct comparison between the two metabolic states within an HIV-positive population. No further demographic details are given in the abstract.
Alpha-diversity of gut microbiota was significantly lower in PLWH with prediabetes compared to those with normoglycemia, and beta-diversity also differed significantly between the two groups. Two Firmicutes genera, Streptococcus and Anaerostignum, were significantly more abundant in the prediabetes group. In contrast, 13 genera, including Akkermansia and Christensenellaceae R7 group, were significantly more abundant in the normoglycemic group. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings suggest that reduced gut microbiota diversity and a distinct compositional shift, marked by higher Streptococcus and Anaerostignum and lower Akkermansia and Christensenellaceae, may accompany prediabetes in people living with HIV. This points to gut dysbiosis as a potential feature of glucose dysregulation even when HIV is well controlled with undetectable viral load. These 15 bacterial taxa could serve as candidate markers for further investigation into microbiome-related metabolic risk in this population.
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.
This study examined the relationship between the gut microbiome and metabolomic profiles in ischemic stroke by comparing three different body-fluid sample types: stool, urine, and plasma. The researchers used metagenomic sequencing of feces alongside untargeted metabolomics of feces, plasma, and urine to determine which sample type most closely tracks with gut microbial composition and disease status. Differential analyses identified key microbes and metabolites distinguishing stroke from health, and Spearman's rank correlation plus linear regression were used to link microbiota to metabolites across the three sample types.
The abstract describes ischemic stroke patients and healthy volunteers, but it does not give the exact number of participants, age range, or other demographic details. Based on the methods described (metagenomic sequencing of feces plus paired feces, plasma, and urine metabolomics), the cohort appears to be a case-control clinical study directly recruiting stroke patients and matched or unmatched healthy controls, rather than a purely public or archival dataset.
Untargeted metabolomics showed that fecal samples contained the most abundant and most numerous identified metabolic features compared with urine and plasma. Feces also yielded the highest number of metabolites that differed significantly between ischemic stroke patients and healthy subjects, ranking above urine and plasma in this respect. This indicates that stool is the metabolic sample type most informative for capturing metabolomic differences associated with ischemic stroke.
The findings suggest that fecal metabolomics, rather than urine or plasma, may be the preferred biological sample for studying gut-microbiome-linked metabolic signatures of ischemic stroke. This has practical implications for designing future microbiome-disease studies, since sample choice affects the ability to detect meaningful microbiota-metabolite associations. By pairing fecal metagenomics with fecal metabolomics, researchers may be better positioned to uncover functional gut-microbiome signatures relevant to cerebrovascular disease.
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 how maternal dietary deficiencies affect reproduction, body growth, and gut microbiota in greater long-tailed hamsters (Tscherskia triton). Researchers compared low-protein diets and niacin-deficient diets under controlled laboratory conditions. They measured maternal reproductive performance, body weight of mothers and their offspring, and the composition and function of the offspring gut microbial community.
The subjects were female greater long-tailed hamsters (Tscherskia triton) and their offspring, studied under laboratory conditions. The abstract does not give an exact sample size or number of litters, so no specific cohort figure can be stated. The comparison groups were animals fed low-protein diets versus niacin-deficient diets relative to normal controls.
A maternal low-protein diet, but not niacin deficiency, significantly harmed reproduction, producing longer mating latency and smaller litter sizes, and reduced body weight in both mothers and offspring. Both protein- and niacin-deficient diets produced significant maternal effects on the offspring gut microbial community. The low-protein diet specifically reduced the abundance of major short-chain-fatty-acid-producing bacterial taxa, increased probiotic taxa abundance, and altered microbial function in offspring. Negative effects on gut microbiota were more pronounced in the protein-deficient group than the niacin-deficient group.
The findings suggest that maternal protein intake, more than niacin intake, is a critical driver of offspring reproductive fitness, growth, and gut microbial health in this rodent species. Because low-protein diets depleted short-chain-fatty-acid producers while favoring probiotic taxa, maternal nutrition appears to reshape the functional capacity of the offspring microbiome, not just its composition. This supports the broader concept that maternal diet can programmatically transfer microbiota-mediated metabolic consequences to offspring across generations.
This study examined how Parkinson disease (PD) medications, oral levodopa (LD) and levodopa-carbidopa intestinal gel (LCIG), relate to the composition of the gut microbiota (GM) and the fecal metabolome. Researchers analyzed fecal DNA using next-generation sequencing of the V3 and V4 regions of the 16S rRNA gene to characterize bacterial composition. Fecal metabolic extracts were also evaluated using gas chromatography mass spectrometry to assess metabolome differences. The goal was to determine whether these two treatment routes for levodopa are associated with distinct microbiota and metabolic signatures in PD.
The study included 107 patients with a clinical diagnosis of Parkinson disease, divided into three groups based on medication status. The LCIG group comprised 38 patients receiving levodopa-carbidopa intestinal gel, and the LD group comprised 46 patients on oral levodopa. A Naive group of 23 patients not taking any antiparkinsonian medications served as a comparison group.
Multivariate analysis found significantly higher abundance of Enterobacteriaceae, Escherichia, and Serratia in the LCIG group compared to the LD group. Compared to the Naive group, the LD group showed a reduction in Blautia and Lachnospirae. The LCIG group also showed an increase in Proteobacteria and Enterobacteriaceae alongside a reduction in Firmicutes, Lachnospiraceae, and Blautia relative to the Naive group. These findings indicate that the route and formulation of levodopa treatment are associated with distinct shifts in gut bacterial composition.
The results suggest that LCIG delivery is associated with a more pronounced shift toward Proteobacteria and Enterobacteriaceae than oral levodopa, which may have implications for gut health and treatment tolerability in PD patients. Because these bacterial groups can include opportunistic or pro-inflammatory taxa, their expansion during LCIG therapy may warrant monitoring in clinical practice. The findings also underscore that the route of drug delivery, not just the drug itself, can shape the gut microbiota in ways relevant to disease management. Further research is needed to determine whether these microbiota and metabolome changes influence PD progression or symptom control.
This study examined whether gut bacterial microbiome dysbiosis, already reported in type 2 diabetes mellitus (T2DM), also links to diabetic retinopathy (DR). Fecal samples were analyzed using 16S rRNA gene sequencing, with community composition assessed using QIIME and R software. The researchers compared gut bacterial diversity and abundance at the phyla and genera level across groups.
The study compared healthy controls (HC) with people who had T2DM without DR and people who had T2DM with DR. Exact sample sizes are not given in the abstract, but the design involved three human fecal-sample groups defined by diabetes and retinopathy status. This is described as the first report of its kind comparing gut microbiome dysbiosis specifically in people with DR against healthy controls.
Gut microbiome dysbiosis at the phyla and genera level was observed in both T2DM and T2DM-with-DR groups compared to healthy controls. People with DR showed greater discrimination from healthy controls than people with T2DM alone, and the microbiomes of the T2DM and DR groups were also significantly different from each other. Both diabetes and DR were associated with a decrease in anti-inflammatory, probiotic, and other beneficial bacteria relative to healthy controls, alongside an increase in potentially pathogenic bacteria, with this shift being more pronounced in people with DR.
This is the first report demonstrating gut microbiome dysbiosis specifically associated with diabetic retinopathy, distinct from T2DM alone. The findings suggest the gut microbiome could serve as a marker to distinguish DR from T2DM without retinal complications. The authors note this work could help inform the development of novel, targeted therapies aimed at improving treatment of diabetic retinopathy.
This study used 16S rRNA gene sequencing on rectal swabs to characterize the gut microbiota composition of patients with COVID-19 pneumonia. It compared microbial community structure between patients hospitalized in an intensive care unit (ICU), patients in infectious disease wards, and controls. The goal was to determine whether gut microbiota composition differs by COVID-19 disease severity.
The study included patients with COVID-19 pneumonia, divided into those admitted to the ICU (i-COVID19) and those admitted to infectious disease wards (w-COVID19). These groups were compared against a control (CTRL) group without COVID-19. The abstract does not report specific sample sizes, ages, or other demographic details for these groups.
ICU patients showed a decreased Chao1 index compared to controls and ward patients, indicating lower microbial richness in more severe disease, while Shannon index diversity did not differ. At the phylum level, Proteobacteria increased in ward patients compared to controls. Fusobacteria and Spirochetes decreased overall, with the Spirochetes decrease most pronounced in ICU patients compared to controls.
The findings show that gut microbial communities shift in COVID-19 pneumonia and that these shifts track with disease severity, with ICU patients showing the greatest loss of richness. The authors suggest these microbiota changes could serve as biomarkers for diagnosis and severity stratification. They note this is preliminary data that would need validation in larger cohorts before clinical application.
This study examined gut and oral (salivary) microbial profiles in relation to childhood obesity using 16S rDNA sequencing. Researchers compared microbial diversity and composition between African American (AA) and European American (EA) children. They also correlated microbiome data with salivary amylase and socioeconomic factors such as education and family income. The goal was to identify microbial clades that could serve as indicators of obesity in each ethnic group.
The study population consisted of African American and European American children, divided by obesity status (obese versus non-obese) within each ethnic group. Both gut and saliva samples were collected from these children for microbial profiling. The abstract does not give an exact total sample size, so the precise cohort count cannot be stated.
Gut and oral microbial diversity differed significantly between AA and EA children at the alpha-, beta-, and taxa-diversity levels. In AA children, greater abundance of gut Klebsiella and Megasphaera was associated with obesity, whereas gut microbial diversity did not distinguish obese from non-obese EA children. In EA children, obesity was instead associated with greater abundance of oral Aggregatibacter and Eikenella. Socioeconomic factors also influenced the microbiota in an ethnicity-dependent manner.
The findings suggest that microbial signatures of obesity are not universal but are ethnicity-specific, differing between gut and oral sites depending on population. This implies that a single microbial biomarker panel for childhood obesity may not generalize across ethnic groups. Socioeconomic context appears to shape these microbial associations, meaning interventions to address childhood obesity may need to be tailored separately for different populations rather than applying one universal approach.
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 investigated gut dysbiosis and abnormal bile acid metabolism in colitis-associated cancer (CAC), a form of colorectal cancer that can arise from prolonged inflammatory bowel disease. Researchers used an azoxymethane/dextran sodium sulfate (AOM/DSS) model to induce CAC and examined intestinal inflammation, mucosal barrier integrity, and bile acid receptor expression. They profiled the fecal microbiome with 16S rRNA sequencing and measured bile acids using liquid chromatography-mass spectrometry. The goal was to characterize how microbial and bile acid changes relate to inflammation and tumor development.
The study used C57BL/6 mice, randomly allocated into an AOM/DSS group and a control group. The AOM/DSS group received an azoxymethane injection followed by dextran sodium sulfate in their drinking water to induce colitis-associated cancer. The abstract does not report a human cohort; this was an animal model study.
The AOM/DSS group developed severe mucosal barrier impairment, an inflammatory response, and tumor formation in the colon. Gut microbiota richness and biodiversity decreased, with a significant shift in overall community composition. Pathogen abundance increased while short-chain fatty acid producing bacteria declined. Clostridium XlV and Lactobacillus, bacteria potentially involved in bile acid deconjugation, transformation, and desulfation, were significantly reduced in the CAC model.
The findings support a link between gut dysbiosis, disrupted bile acid metabolism, and the inflammatory processes that drive progression from colitis to cancer. Loss of bacteria capable of transforming and desulfating bile acids may allow abnormal bile acid profiles to accumulate and worsen mucosal injury. This suggests that restoring specific bile acid-metabolizing bacteria or correcting bile acid imbalance could be explored as strategies to reduce cancer risk in chronic IBD. The results also highlight the fecal microbiome and bile acid profile as potential markers to monitor colitis-associated cancer progression.
This study examined the relationship between the intestinal microbiota and SARS-CoV-2 infection in a United States hospital cohort. Researchers collected fecal samples and used 16S rRNA sequencing plus qPCR analysis to compare microbial composition across infection states. They compared actively infected patients, recovered patients, and uninfected controls seen for unrelated respiratory conditions, and also tested for fecal viral shedding.
The cohort included 50 patients actively infected with SARS-CoV-2, 9 patients who had recovered from SARS-CoV-2 infection, and 34 uninfected control subjects seen at the hospital for unrelated respiratory medical conditions. The study is described as a United States, majority African American and minority-dominated cohort. Fecal DNA and RNA were collected prospectively from all three groups for microbiota analysis.
Fecal microbial composition differed significantly between SARS-CoV-2 patients and controls, independent of antibiotic exposure, with Peptoniphilus, Corynebacterium, and Campylobacter enriched in COVID-19 patients. Actively infected patients also had a distinct gut microbiota compared to recovered patients, with Campylobacter most enriched during active infection and Agathobacter and Faecalibacterium enriched after recovery. Notably, recovered patients showed no difference in microbial community structure or alpha diversity compared to uninfected controls. Nearly half of the COVID-19 patients (24 of 50, 48%) tested positive by RT-qPCR for fecal viral material.
The findings suggest that SARS-CoV-2 infection is associated with a transient disruption of gut microbial composition that resolves as patients recover, rather than causing lasting dysbiosis. This return to an uninfected-like microbiome state in recovered patients supports the gut as a site of active but reversible interaction with the virus. The high rate of fecal viral detection also reinforces concern about potential fecal-oral transmission during active infection.
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 characterized the skin and gut bacterial communities of the invasive Asian common toad, Duttaphrynus melanostictus, in Toamasina, Eastern Madagascar. The researchers compared these microbial communities to those of a co-occurring native frog species, Ptychadena mascareniensis. Sampling took place at three sites where the toad had established at different times, allowing the study to assess whether its microbiome changes across the expansion range.
The subjects were skin and gut bacterial communities sampled from the invasive Asian common toad and the native frog Ptychadena mascareniensis, both collected at three sites in Toamasina, Eastern Madagascar. These sites represented different time points in the toad's invasion history. The abstract does not report a specific number of individual animals sampled.
Microbial composition in the invasive toad did not vary among the three sites, indicating that Duttaphrynus melanostictus maintains a stable skin and gut bacterial community as it expands across Madagascar. However, significant differences were observed between the invasive toad and the native frog. The toad harbored richer and more diverse bacterial communities and carried a high percentage of unique taxa not shared with the native species, 80 percent on the skin and 52 percent in the gut.
The stability of the toad's microbiome across its expansion range suggests it travels with a resilient, portable microbial community that may support its colonization success in new habitats. The high proportion of unique taxa carried by the toad raises the possibility that it introduces novel microbes into Malagasy ecosystems, with unknown consequences for native amphibians and the broader environment. These findings underscore the importance of tracking invader-associated microbiomes when assessing threats posed by biological invasions.
This study used a two-stage metagenome-wide association strategy to analyze fecal DNA samples and identify gut bacteria and microbiota-associated epitopes (MEs) linked to Parkinson's disease (PD). Researchers compared candidate bacterial biomarkers and epitope peptides between PD patients and control groups. They also examined how these microbial features related to host inflammatory blood markers and metabolic pathways.
The analysis included fecal samples from 69 PD patients and 244 controls. The controls were divided into three groups: 66 spouses, 97 age-matched individuals, and 81 normal samples. This design allowed comparisons across different types of control populations rather than a single reference group.
Researchers identified 27 candidate bacterial biomarkers and 28 candidate epitope peptides that differed significantly between PD patients and controls. Several enriched microbiota-associated epitopes in PD were positively associated with abnormal inflammatory indicators, including neutrophil percentage, monocyte count and percentage, and white blood cell count. These enriched epitopes were also positively associated with five bacterial biomarkers from the Actinobacteria phylum (including Bifidobacterium and Bifidobacteriaceae) and with histidine degradation and proline biosynthesis pathways.
The findings suggest a link between altered Actinobacteria-associated gut microbiota, microbiota-derived epitopes, and systemic inflammatory activity in Parkinson's disease. This supports the idea that gut microbial antigens may contribute to the inflammatory processes implicated in PD pathogenesis. The identified bacterial and epitope biomarkers could serve as candidates for further research into PD-related host-microbiome interactions and potential diagnostic or mechanistic markers.
This prospective observational study evaluated whether gut microbiome composition is associated with stroke-associated pneumonia (SAP) in patients with acute ischemic stroke. Researchers collected fecal and serum samples at admission and used 16S rRNA V4 tag sequencing, analyzed with QIIME and LEfSe, to characterize gut microbiota. They also measured fecal short-chain fatty acids and serum markers of gut barrier integrity, including D-lactate, intestinal fatty acid-binding protein, and lipopolysaccharide binding protein.
The training cohort included 188 patients with acute ischemic stroke, of whom 52 (27.7%) developed stroke-associated pneumonia. Findings were validated in an independent cohort of 144 patients, 28 of whom (19.4%) developed SAP. Disease severity scores were recorded by specialized physicians alongside the microbiome and biomarker data.
Gut microbiome composition differed significantly between patients who developed SAP and those who did not. Patients with SAP showed depletion of Roseburia along with enrichment of opportunistic pathogens, a pattern confirmed in the independent validation cohort. Multivariate analysis identified Roseburia as a protective factor against SAP in both the training and validation cohorts, supporting gut dysbiosis as an independent risk factor for this complication.
These findings suggest gut microbiota, particularly Roseburia abundance, could serve as an early biomarker to identify stroke patients at higher risk of pneumonia. Because Roseburia acted as a protective factor across two independent cohorts, restoring or supporting this taxon may represent a potential avenue for reducing SAP risk. The results also point toward gut-lung axis mechanisms as a relevant target for future preventive strategies in acute ischemic stroke care.
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 case-control study characterized the cervical microbiota of women undergoing in vitro fertilization (IVF) with embryo transfer (ET). Researchers collected cervical swabs on the day of embryo transfer and sequenced the V3-V4 regions of the 16S rRNA gene using Illumina MiSeq. The goal was to determine whether cervical microbial composition was associated with subsequent pregnancy outcomes, and to explore factors that might underlie any such association.
The study enrolled 100 subfertile patients undergoing IVF who received two fresh or frozen-thawed cleavage-stage embryos per cycle. Patients were divided into four groups based on clinical pregnancy outcome after embryo transfer. In the fresh IVF-ET cycles, the clinical pregnancy group comprised 25 women (FP) and the non-pregnancy group comprised 26 women (FN); in frozen-thawed cycles, the clinical pregnancy group comprised 27 women (TP).
In fresh IVF-ET cycles, women who achieved clinical pregnancy (FP group) showed significantly higher cervical microbiota alpha diversity than those who did not (FN group). Beta diversity analysis (ANOSIM) confirmed a significant difference in overall community composition between the pregnant and non-pregnant groups. In frozen-thawed ET cycles, a similar trend toward higher alpha diversity in the pregnant group (TP) was observed, though this difference did not reach statistical significance. The abstract as provided does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
These findings suggest that the composition and diversity of the cervical microbiota at the time of embryo transfer may influence the likelihood of achieving clinical pregnancy in IVF. Higher microbial diversity in the cervix could serve as a biomarker for reproductive outcome or reflect a favorable local environment for implantation. This raises the possibility that cervical microbiota profiling could eventually help individualize IVF protocols or identify patients who might benefit from microbiome-targeted interventions before embryo transfer.
This study examined the composition of the gut microbiome in patients with Parkinson's disease (PD) using shotgun metagenomic sequencing. Researchers compared the fecal microbial profiles of PD patients against those of healthy control subjects. The analysis included taxonomic composition as well as functional gene-category profiling using the Cluster of Orthologous Groups, KEGG Orthology, and carbohydrate-active enzyme databases. A random forest model was also built to test whether microbiome features could distinguish PD patients from controls.
The cohort consisted of 39 patients with Parkinson's disease (the PD group) recruited in central China. The comparison group was made up of the corresponding 39 healthy spouses of these patients (the SP group), who served as controls. Using spouses as controls is notable because it helps account for shared household diet and environment.
Gut microbial composition was significantly altered in PD patients compared to healthy spouses. A key novel finding was enrichment of Bilophila wadsworthia in the gut microbiome of PD patients, which had not been reported in prior studies. The random forest model reliably discriminated PD patients from controls, achieving an area under the receiver operating characteristic curve of 0.803. Klebsiella and Parasutterella abundances were positively correlated with PD duration and severity, while hydrogen-generating Prevotella was negatively correlated with disease severity, and functional analyses pointed to altered branched-chain amino acid-related proteins.
The enrichment of Bilophila wadsworthia, a sulfate-reducing, hydrogen sulfide-producing organism, suggests that sulfur metabolism in the gut may play a previously unrecognized role in PD pathophysiology. The strong discriminative performance of the microbiome-based model suggests gut microbial signatures could eventually support non-invasive screening or monitoring of PD. Correlations between specific taxa and disease duration or severity suggest the microbiome may track with clinical progression rather than being a static marker. These findings support further investigation into gut bacteria, including hydrogen and sulfide-related metabolism, as contributors to PD development or severity.
This study examined the gut microbiota of breast cancer patients across different menopausal statuses, comparing premenopausal and postmenopausal cases. The researchers aimed to characterize comprehensive microbial profiles, assess their diagnostic value, and explore associated functional pathways. The work was motivated by the fact that most prior gut microbiota research on breast cancer had focused on postmenopausal patients, leaving premenopausal disease understudied despite its rising prevalence in Asian countries.
The study analyzed 267 breast cancer patients with different menopausal statuses (premenopausal and postmenopausal) alongside age-matched female controls. The abstract does not specify additional demographic details such as country, recruitment setting, or exact group breakdowns. This appears to be a clinical cohort rather than a public dataset, given the direct comparison to matched controls.
Alpha-diversity was significantly reduced in premenopausal breast cancer patients, and beta-diversity differed significantly between breast cancer patients and controls overall. Through multiple analyses and classification approaches, the researchers identified 14 microbial markers that distinguished breast cancer by menopausal status. Bacteroides fragilis was specifically associated with premenopausal breast cancer in younger women, while Klebsiella pneumoniae was associated with postmenopausal breast cancer in older women.
The findings suggest that gut microbial signatures differ meaningfully by menopausal status in breast cancer, indicating that a one-size-fits-all microbiome model may miss important disease-stage-specific patterns. The identification of menopausal-specific markers, such as Bacteroides fragilis in premenopausal cases, points toward potential diagnostic tools tailored to age and menopausal status. This underscores the need for more research specifically into premenopausal breast cancer, a population that has been comparatively neglected in gut microbiota studies.
This study examined how fecal and oral sample collection methods, along with room temperature storage, affect measurements of the human microbiota. Researchers compared fecal preservation using RNAlater and fecal occult blood test (FOBT) cards over four days at room temperature. They also compared oral sampling using OMNIgene ORAL kits versus Scope mouthwash. Comparability and stability were assessed using interclass correlation coefficients (ICCs) across alpha and beta diversity metrics and phylum-level relative abundance.
Participants were drawn from two Iranian cohorts: a rural population in Yazd (n = 46) and an urban population in Gonbad (n = 38). Both fecal and oral samples were collected from these participants for the method-comparison analyses. The abstract does not provide further demographic detail such as age or sex distribution.
Fecal samples remained stable at room temperature for four days, with generally high ICCs across microbial metrics for both RNAlater and FOBT cards. Comparability between RNAlater and FOBT cards was also high, with ICCs ranging from 0.63 for relative abundance of Firmicutes to 0.93 for unweighted UniFrac. Scope mouthwash likewise showed generally high ICCs for stability. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so this study is summarized on its own terms.
The findings support the feasibility of using RNAlater, FOBT cards, and Scope mouthwash for microbiota collection in field settings where cold storage may not be available for several days. This has practical value for prospective cohort studies conducted in resource-limited or geographically dispersed settings, including the rural and urban Iranian sites studied here. Reliable room temperature stability could reduce logistical burden and cost for large-scale microbiome research.
This study examined the oral microbiome of dogs, comparing microbial composition and predicted microbiome functions between healthy dogs and dogs with periodontal disease. The researchers looked beyond the typically dominant Porphyromonas and Tannerella species to characterize how sub-dominant microbial populations shift with disease. They also assessed how microbiome functional pathways change in periodontal disease, an aspect the abstract notes had not previously been studied.
The abstract does not give specific sample sizes, ages, or breeds. Based on the description, the study compared the oral cavity microbiome of a group of healthy dogs against a group of dogs diagnosed with periodontal disease. The comparison was based on sampling and analysis of the oral microbial community in these two dog groups.
The microbiomes of healthy and periodontal-disease dogs clustered separately, indicating meaningful compositional differences between the groups. Periodontal disease was marked by a significant increase in Bacteroidetes and reductions in Actinobacteria and Proteobacteria, with Porphyromonas abundance rising 2.7 times alongside increases in Bacteroides and Fusobacterium. Functionally, aerobic respiratory processes were predicted to decrease, while fermentative processes, anaerobic glycolysis, and lipopolysaccharide biosynthesis were enriched, suggesting a shift toward an anaerobic oral environment. The abstract does not report on Desulfovibrio, sulfate-reducing bacteria, or hydrogen sulfide specifically.
The findings suggest periodontal disease in dogs involves not just an increase in known pathogens but a broader ecological shift toward an anaerobic, fermentation-favoring oral environment with higher endotoxin (lipopolysaccharide) biosynthesis potential. This functional reframing implies that assessing sub-dominant taxa and predicted metabolic activity, not only dominant pathogens, may better characterize disease state. Such functional profiling could inform future diagnostic or therapeutic approaches targeting the anaerobic, fermentative shift rather than single organisms alone.
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.
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 examined the gut microbiota of children using 16S rRNA gene sequencing to determine whether obesity is associated with altered microbial diversity and composition. Researchers extracted genomic DNA from fecal samples and amplified the V4 region of the bacterial 16S rDNA. Sequencing was performed on the Illumina HiSeq 2500 platform to compare community structure between normal weight and obese children.
The study included twenty-three normal weight children and twenty-eight obese children recruited from Nanjing, China. Participants were selected according to defined inclusion and exclusion criteria. The abstract does not provide additional demographic details such as age range or sex distribution.
The number of operational taxonomic units decreased as body weight increased, indicating reduced gut microbiota diversity in heavier children. Alpha diversity indices, including Chao1, observed species, PD whole tree, and the Shannon index, were all significantly higher in the normal weight group than in the obese group. These results show a consistent pattern of diminished microbial richness and diversity accompanying childhood obesity. Principal coordinate analysis was also used to assess community structure, though the abstract is cut off before reporting those specific results.
The findings reinforce that gut microbiota dysbiosis, marked by lower diversity, is linked to childhood obesity and may play a role in its development. Because the microbiota continues to mature throughout childhood, this period may represent a key window for interventions aimed at promoting healthy weight or preventing obesity-related disease. Understanding pediatric gut microbiota structure and function could inform future microbiome-targeted strategies for obesity prevention in children.
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.
This study examined whether the gut microbiome influences the effectiveness of PD-1 antibody immunotherapy in microsatellite-stable (MSS)-type colorectal cancer, which is typically resistant to checkpoint blockade. Researchers manipulated the gut microbiome using different antibiotics in tumor-bearing mice and then evaluated the impact on PD-1 antibody treatment response. They also profiled which bacterial taxa and metabolites were enriched under each antibiotic condition.
The subjects were CT26 tumor-bearing mice, a mouse model of MSS-type colorectal cancer. Mice were divided into groups receiving sterile drinking water (Control), colistin (Coli group), or vancomycin (Vanc group), then treated with PD-1 antibody immunotherapy. This was an animal model study rather than a human clinical cohort.
Antibiotic treatment counteracted the tumor-inhibiting efficacy of PD-1 antibody compared with the Control group, confirming that the gut microbiome plays a key role in immunotherapy response. Distinct bacterial taxa were enriched depending on antibiotic exposure: Bacteroides_sp._CAG:927 and Bacteroidales_S24-7 in Control, Bacteroides_sp._CAG:927, Prevotella_sp._CAG:1031, and Bacteroides in the colistin group, and Prevotella_sp._CAG:485 and Akkermansia_muciniphila in the vancomycin group. Metabolite profiles also differed across these microbiome states, pointing to a metabolic pathway linking microbiome composition to immunotherapy outcomes.
The findings suggest that gut microbiome composition, and the metabolites it produces, can determine whether PD-1 antibody immunotherapy succeeds or fails in MSS-type colorectal cancer. Because antibiotic-induced disruption of specific bacteria such as Bacteroides and Akkermansia muciniphila altered treatment efficacy, microbiome-targeted strategies could potentially be used to improve checkpoint inhibitor responses in this traditionally treatment-resistant cancer subtype. This supports further investigation of microbiome and metabolite modulation as an adjunct to immunotherapy in pMMR/MSS colorectal cancer.
This pilot study examined whether the gut microbiome is associated with breast tumor characteristics, including receptor status, stage, and grade, as well as established breast cancer risk factors such as parity and body mass index. Fecal samples were analyzed using a 16S ribosomal RNA gene-based sequencing protocol. Researchers compared alpha diversity and specific bacterial taxa across these clinical and risk-factor groupings using statistical tests adjusted for total counts, age, and race/ethnicity.
The cohort consisted of 37 incident breast cancer patients whose fecal samples were collected prior to chemotherapy in a cross-sectional pilot design. Within this group, comparisons were made between 12 women with HER2-positive tumors and 25 women with HER2-negative tumors. A separate comparison examined 11 women with early menarche (age 11 or younger) against 26 women with later menarche (age 12 or older).
There were no significant differences in alpha diversity or phylum-level composition by estrogen or progesterone receptor status, tumor grade, tumor stage, parity, or body mass index. However, women with HER2-positive breast cancer showed 12 to 23 percent lower alpha diversity than those with HER2-negative disease, along with lower abundance of Firmicutes and higher abundance of Bacteroidetes. Early menarche was also associated with lower measures of microbial richness compared with later menarche. This study did not report findings related to Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
These pilot findings suggest that gut microbiome composition, particularly diversity and Firmicutes to Bacteroidetes balance, may differ by HER2 receptor status and by age at menarche, two factors with distinct biological and hormonal underpinnings. Because tumor grade, stage, and hormone receptor status showed no clear microbial associations, the gut microbiome's relevance to breast cancer may be more tied to specific molecular subtypes like HER2 status than to general disease severity. Given the small sample size, these associations warrant confirmation in larger cohorts before any causal or clinical significance can be drawn.
This study examined whether maternal exposure to fine particulate matter (PM2.5) during gestation and lactation affects serum lipoprotein levels and gut microbiota composition in offspring. Pregnant mice received PM2.5 by intratracheal instillation, and offspring were assessed at multiple postnatal timepoints. Serum lipoproteins were measured on postnatal day 35, while gut microbiota were profiled by 16S rDNA sequencing of colon contents on postnatal days 3, 10, 21, and 35. The design allowed comparison of sex-specific effects of maternal PM2.5 exposure on metabolic and microbial outcomes in offspring.
The subjects were male and female mouse pups born to dams exposed to PM2.5 during pregnancy and lactation, compared against pups from an unexposed control group. Offspring were evaluated at several postnatal ages (days 3, 10, 21, and 35) to track developmental changes in gut microbiota. The abstract does not specify the exact number of animals per group. This was an animal (mouse) model study rather than a human cohort.
Male offspring from PM2.5-exposed dams had significantly higher serum triglyceride concentrations than controls, while female offspring showed no significant lipoprotein differences. On postnatal day 35, PM2.5-exposed male offspring showed enrichment of Bacteroides, Desulfovibrio, and Anaerotruncus, whereas control males had more Streptococcus. Desulfovibrio, a sulfate-reducing bacterium associated with hydrogen sulfide production, was specifically enriched in the exposed male group. In female offspring, Clostridium XI was enriched in controls rather than the exposed group, and Bacteroides abundance correlated positively with serum triglyceride concentration.
The findings suggest that maternal PM2.5 exposure produces sex-specific, long-term effects on offspring metabolism and gut microbiota, with male offspring appearing more vulnerable to lipid disturbances. The enrichment of Desulfovibrio, a sulfate-reducing, hydrogen sulfide-producing genus, alongside Bacteroides in exposed males raises questions about links between air pollution exposure, sulfur-metabolizing gut bacteria, and triglyceride regulation. These results imply that prenatal air pollution exposure could programmatically shape gut microbial communities and metabolic risk in a sex-dependent manner. Further work would be needed to clarify the mechanistic role of these bacterial shifts in the observed lipid changes.
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 study examined the mucosal microbiome of oral squamous cell carcinoma (OSCC) using 16S rRNA gene sequencing. Researchers compared the microbial profile and composition of cancerous lesions with matched paracancerous tissue from the same patients. A random forest (RF) machine learning model was applied to identify a microbial signature capable of distinguishing tumor tissue from adjacent normal-appearing tissue. Functional analyses were also performed to assess metabolic pathways associated with the tumor-associated microbiome.
The study enrolled 24 patients diagnosed with oral squamous cell carcinoma. For each patient, paired samples were collected from the cancerous lesion and the matched paracancerous tissue, allowing within-patient comparison. No further demographic details are given in the abstract.
Significant differences in microbial profile and composition were found between OSCC lesions and paracancerous tissue. LEfSe analysis identified 15 bacterial genera enriched in cancerous lesions, including Fusobacterium, Treponema, Streptococcus, Peptostreptococcus, Carnobacterium, Tannerella, Parvimonas, and Filifactor. The RF classifier identified a 12-bacteria signature that distinguished cancerous from paracancerous tissue with an AUC of 0.82, and the microbial network in cancerous lesions appeared simplified and fragmented. Functional analyses showed altered amino acid metabolism and increased capacity for glucose utilization in OSCC tissue.
These findings suggest that a defined set of oral bacteria and their altered network structure are closely associated with the tumor microenvironment in OSCC. The RF-derived microbial signature, with an AUC of 0.82, points to the potential for microbiome-based classifiers to help distinguish cancerous from adjacent normal tissue. The shifts in amino acid and glucose metabolism suggest the tumor-associated microbiome may be functionally adapted to, or contribute to, the metabolic environment of the cancer, warranting further investigation into causal or diagnostic roles.
This study compared the gut microbiota of women with infertility to that of fertile women using 16S rRNA V3-V4 sequencing of fecal samples. It also examined a preliminary intervention with the prebiotic partially hydrolyzed guar gum, a water-soluble dietary fiber, to see whether it could correct gut dysbiosis. The researchers further looked at whether this fiber supplementation affected pregnancy outcomes in patients undergoing assisted reproductive technology. The rationale was that gut microbiota shapes local and systemic immunity, which in turn influences endometrial receptivity and hormonal adaptation needed for conception.
The study enrolled 18 fertile female subjects and 18 female patients with infertility, matched by age. Fecal samples were collected from all 36 participants for gut microbiome analysis. The abstract does not specify the geographic location, recruitment setting, or additional demographic details beyond age-matching.
Principal coordinate analyses, both unweighted and weighted, showed a trend toward separation between the fertile and infertile groups, suggesting differences in overall gut microbial community structure. The abstract text provided is truncated before specific taxa or statistical results are named, so the precise organisms or diversity metrics that differed cannot be reported here. No mention of Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism appears in the available abstract text.
The findings support the idea that gut microbiota composition differs between infertile and fertile women, reinforcing a potential gut-reproductive axis. Testing a prebiotic fiber intervention addresses a genuine gap, since clinical data on dietary fiber's effect on assisted reproductive technology success has been lacking. If confirmed in larger trials, this approach could offer a low-risk, low-cost adjunct to improve outcomes for patients undergoing fertility treatment.
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.
This pilot study examined the microbiota composition of breast tissue, comparing bilateral normal breast tissue within the same women to breast tumor tissue from a separate group of women. The researchers wanted to know whether microbiota composition differed by breast side (left versus right) within individuals, and whether it differed between normal and tumor tissue. DNA was extracted from tissue samples, amplified, and sequenced, then analyzed using QIIME and RStudio to characterize bacterial taxa and diversity.
Bilateral normal breast tissue samples (36 total) were collected from ten women undergoing routine mammoplasty procedures. Archived breast tumor samples (10 total) were obtained separately from a biorepository. The abstract does not provide additional demographic details such as age or health history for these women.
Bacteroidetes, Firmicutes, Proteobacteria, and Actinobacteria were the most abundant phyla in both tumor and normal breast tissue. There were statistically significant differences in the relative abundance of various bacterial taxa between the tumor and normal groups. Alpha diversity, measured by Simpson's index, was significantly higher in normal tissue than in tumor tissue (0.968 versus 0.957, p = 0.022). Breast tumor samples also clustered distinctly from normal samples based on unweighted UniFrac measures, indicating an overall difference in microbial community structure.
The findings support the idea that breast tissue harbors a distinct microbiome that differs between tumor and normal tissue, with tumors showing reduced bacterial diversity. This suggests specific bacterial taxa may be associated with, or influenced by, the tumor microenvironment and could warrant further investigation into a possible role in breast cancer etiology. Because this was a pilot study with a small sample, larger studies are needed to confirm which taxa are consistently associated with tumors and to clarify any causal relationship.
This study examined gut microbiota composition and fecal metabolite profiles in people with Parkinson's disease compared to controls. Researchers used next-generation sequencing to characterize bacterial taxa and gas chromatography-mass spectrometry to measure fecal metabolites. The goal was to identify microbiome and metabolome alterations associated with Parkinson's disease, a neurodegenerative disorder marked by misfolded alpha-synuclein aggregates along the cerebral axis. The abstract notes that a cause-effect relationship between intestinal dysbiosis and Parkinson's disease has not yet been established.
The study included 64 Italian patients with Parkinson's disease and 51 controls. Both groups underwent gut microbiota sequencing and fecal metabolite analysis. No further demographic details, such as age or sex distribution, are given in the abstract.
Parkinson's disease patients showed reduced levels of bacterial taxa linked to anti-inflammatory and neuroprotective effects, particularly within the Lachnospiraceae family, including Butyrivibrio, Pseudobutyrivibrio, Coprococcus, and Blautia. Fecal metabolite analysis revealed changes across several compound classes. These included lipids such as linoleic acid, oleic acid, succinic acid, and sebacic acid, vitamins such as pantothenic acid and nicotinic acid, amino acids such as isoleucine, leucine, phenylalanine, glutamic acid, and pyroglutamic acid, and other organic compounds such as cadaverine, ethanolamine, and hydroxy propionic acid. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, or hydrogen sulfide.
The findings reinforce that Parkinson's disease is accompanied by a distinct pattern of gut dysbiosis and metabolic disturbance, with depletion of beneficial, anti-inflammatory Lachnospiraceae members standing out as a key feature. The combined microbiota and metabolome approach suggests that fecal biomarkers could eventually help characterize or monitor the disease. Because the abstract states that causality remains unestablished, these results should be viewed as associative rather than proof that gut changes drive Parkinson's disease pathology.
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 characterized alterations in the gut microbiome associated with chronic kidney disease (CKD). The researchers analyzed fecal samples to compare microbial diversity, community composition, and predicted microbial functions between CKD patients and healthy controls. They also constructed and validated diagnostic classifiers for CKD based on microbial markers using a random forest model, and examined relationships between specific taxa, disease progression, and clinical indicators.
A total of 520 fecal samples were collected from different regions of China. The discovery and comparison cohort included 110 patients with CKD and 210 healthy controls (HC). The classifier was further tested in a validation cohort of 49 CKD cases versus 63 HC, and in an extra diagnosis cohort from Hangzhou.
Gut microbial diversity was significantly decreased in CKD patients compared with healthy controls, and the overall microbial community composition was distinctly different between groups. The genera Klebsiella and Enterobacteriaceae were enriched in CKD, while Blautia and Roseburia were reduced. Fifty predicted microbial functions, including tryptophan and phenylalanine metabolism, increased in CKD, while 36 functions, including arginine and proline metabolism, decreased. A five-marker microbial classifier achieved an area under the curve (AUC) of 0.9887 in the discovery cohort, 0.9512 in the validation cohort, and 0.8986 in the extra Hangzhou diagnosis cohort, and Thalassospira and Akkermansia increased with CKD progression.
These findings indicate that CKD is associated with a distinct, less diverse gut microbial community and altered amino acid metabolism pathways. The high diagnostic accuracy of the identified microbial markers across discovery, validation, and independent cohorts suggests gut microbiome signatures could serve as a non-invasive tool for CKD detection. The correlation between specific taxa and clinical indicators, along with taxa that shift with disease progression, points to the gut microbiome as a potential avenue for monitoring CKD severity.
This study examined how HIV infection and men who have sex with men (MSM) status are each associated with changes in the gut microbiome. The researchers conducted a meta-analysis of 16S rRNA gene amplicon sequencing data related to HIV/AIDS. They evaluated alpha diversity, beta diversity, differentially enriched bacterial genera and species, and KEGG functional pathways to identify consistent patterns across studies.
The meta-analysis screened 12 published studies from the NCBI and EBI databases, six of which contained data relevant to MSM status. The HIV analysis included 1,288 gut microbiome samples, comprising 744 HIV-positive individuals and 544 HIV-negative individuals. The MSM analysis included 632 samples, comprising 328 MSM and 304 non-MSM individuals.
HIV-positive status was associated with decreased alpha diversity of the gut microbiome compared to HIV-negative status. MSM status was identified as an important factor affecting the gut microbiome independent of HIV infection status. The abstract does not provide the specific differentially enriched genera, species, or KEGG pathway results before being cut off, so those details cannot be reported here.
By pooling multiple studies, this meta-analysis helps clarify a consistent pattern of gut microbiome change associated with HIV infection, namely reduced alpha diversity. Recognizing MSM status as an independent influencing factor suggests that future gut microbiome research on HIV must account for sexual orientation as a confounding variable rather than attributing all differences to HIV infection itself. This distinction could improve the design and interpretation of future microbiome studies in HIV populations.
This study investigated whether the R6/2 mouse model of Huntington's disease shows evidence of increased intestinal permeability and gut microbiota dysbiosis. The researchers examined tight junction protein levels (occludin and zonula occludens), colon length, gut permeability, and the relative abundance of the dominant intestinal bacterial phyla, Bacteroidetes and Firmicutes. The work builds on prior findings that reduced tight junction protein expression is linked to leaky gut in Parkinson's disease, testing whether a similar gut-barrier disruption occurs in Huntington's disease.
The subjects were R6/2 mice, a transgenic mouse model of Huntington's disease, compared against wild type littermates. The abstract does not specify exact group sizes, ages, or sex distribution. This was an animal model study rather than a human cohort.
R6/2 mice showed decreased body weight and body length alongside significantly shortened colon length and increased gut permeability compared to wild type littermates. Notably, these barrier changes occurred without any significant change in the protein levels of the tight junction proteins occludin and zonula occludens. The mice also displayed altered gut microbiota composition, with increased relative abundance of Bacteroidetes and decreased relative abundance of Firmicutes.
The findings suggest that increased intestinal permeability in Huntington's disease can arise independently of measurable tight junction protein loss, pointing to a barrier disruption mechanism distinct from the one described in Parkinson's disease. The co-occurrence of gut dysbiosis, a shifted Bacteroidetes to Firmicutes ratio, with leaky gut and colon shortening in this model supports the idea that gastrointestinal and microbial dysfunction may be intrinsic features of Huntington's disease rather than secondary consequences. This raises the possibility that the gut and its microbiota could be relevant targets for understanding or managing the disease's systemic and weight-related symptoms.
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.
This study examined how the composition of the human gut microbiota relates to age, sex, and stool consistency in healthy adults. Researchers analyzed fecal samples to characterize the gut microbiome and compared microbial community structure and diversity across demographic groups. They also assessed stool consistency using the Bristol stool scale (BSS) and tested its association with microbial composition. The investigation aimed to fill a gap, since sex-related and stool-consistency-related differences in gut microbiota had not been fully characterized previously.
The study enrolled 277 healthy Japanese subjects ranging in age from 20 to 89 years. Fecal samples were collected from this cohort to profile the gut microbiome. Both sexes were represented, allowing comparisons of microbial structure between males and females and across different age groups.
Overall microbial diversity (alpha-diversity) did not differ significantly by sex or by age group, but the underlying microbial community structure did differ significantly between males and females. Prevotella, Megamonas, Fusobacterium, and Megasphaera were significantly increased in males, while Bifidobacterium, Ruminococcus, and Akkermansia were significantly increased in females. Stool consistency also varied by sex: hard stools (BSS types 1 and 2) were more common in females, loose stools (BSS type 6) were more common in males, and no younger male had hard stool types 1 or 2. Fusobacterium levels in males were significantly higher among those with loose stool consistency.
These findings suggest that sex and stool consistency, rather than age or overall microbial diversity, are meaningfully linked to variation in gut microbial composition in healthy adults. The association between specific genera, such as Fusobacterium, and stool consistency indicates that bowel habit should be considered as a variable in microbiome research. This has implications for study design, since failing to account for sex and stool consistency could confound comparisons of gut microbiota across populations or in disease-association studies.
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. Abundance and diversity analyses were performed in QIIME, and compositional biomarkers distinguishing groups were identified using LEfSe.
The analysis included 180 patients 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 provide additional demographic details such as age or sex distribution.
IBD-A was associated with an increased abundance of microbial tyrosine degradation pathways compared with IBD-N. Both IBD-A and RA patients shared an increased abundance of Clostridiaceae relative to controls. A history of bowel surgery was a significant source of microbiome variability among IBD patients and was associated with decreased alpha diversity.
The shared increase in Clostridiaceae across IBD-associated arthropathy and rheumatoid arthritis suggests a common gut microbial signature may underlie joint inflammation across these conditions. The altered tyrosine degradation pathway in IBD-A points to a possible microbial metabolic contribution to extraintestinal arthritis specifically. These findings also highlight bowel surgery history as an important variable to account for when studying the gut microbiome in IBD patients.
This study used 16S rRNA gene sequencing to characterize the gut microbiota across the colorectal cancer disease course. It compared microbial diversity, overall community composition, and taxonomic abundance among colorectal adenoma patients, colorectal cancer (CRC) patients, and CRC patients after surgical treatment. The study also examined how postoperative gut microbiota related to colonoscopy findings and to CRC prognosis.
The comparison groups were colorectal adenoma patients, CRC patients, CRC postoperative (post-surgical) patients, and healthy controls. Postoperative patients were further divided into those with newly developed adenoma on colonoscopy versus those with a clean intestine. The abstract does not give specific sample sizes, so exact cohort numbers cannot be stated.
Gut microbiota composition shifted progressively along the adenoma-carcinoma sequence, with marked changes occurring before or during CRC development. The gut microbiota of postoperative patients differed significantly from that of CRC patients, showing that surgery does not restore a healthy-control-like microbial profile. Among postoperative patients, those who developed new adenomas had a microbiota more similar to carcinoma patients than to healthy controls, and differences between postoperative subgroups corresponded to CRC prognosis.
Persistent microbiota alterations after CRC surgery suggest the gut microbiome could serve as a monitoring tool for recurrence risk and prognosis in postoperative patients. A microbiota signature resembling carcinoma in patients with new adenomas points to the gut microbiome as a potential early warning marker distinct from clean-intestine recovery. This abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so no sulfide-related angle applies here.
The study examined how Zengye decoction (ZYD), a traditional Chinese medicinal formula, affects the gut microbiota and host metabolites in aged rats with constipation. Researchers used 16S rRNA gene sequencing to characterize the fecal microbiome and then predicted the metabolic function of the altered bacterial community. They paired this with 1H NMR profiling of urine and fecal samples to verify the metabolic changes suggested by the sequencing data. The overall goal was to clarify the mechanisms by which ZYD works, since these had remained unclear despite its clinical use for constipation and skin dryness syndrome.
The subjects were aged rats divided randomly into three groups of ten animals each: a control group, a recovery group, and a ZYD-treated group. An aged constipation model was established in both the recovery and ZYD groups before treatment began. Urinary and fecal samples were collected from each animal for microbiome and metabolite analysis, so no human cohort was involved; this was an animal model study.
ZYD reduced the abundance of harmful gut bacteria, including Desulfovibrio, Ruminococcus, and Prevotella, in the aged constipated rats. Desulfovibrio is a sulfate-reducing genus capable of generating hydrogen sulfide, so its reduction points to a shift in sulfur-related metabolic activity within the gut community. These bacterial changes were accompanied by alterations in metabolically active gut microbiota and were reflected in the host metabolite profiles measured by NMR in urine and feces. The convergence of sequencing-based predictions and NMR-based metabolite verification supports a genuine link between the microbiota shift and host metabolic changes.
The findings suggest that ZYD's therapeutic effect on constipation may work partly by remodeling the gut microbiota, including suppressing sulfate-reducing organisms like Desulfovibrio, rather than acting solely through direct host pathways. This supports a microbiota-mediated mechanism for a traditional medicinal formula that had previously lacked clear mechanistic explanation. It also suggests that gut bacteria capable of hydrogen sulfide production may be relevant targets when evaluating treatments for age-related constipation. Further work would be needed to confirm these mechanisms and their relevance to human patients.
This study examined how psyllium husk, a widely used fiber-based treatment for constipation, affects the composition of faecal microbiota. Psyllium works by trapping water in the intestine, which increases stool water content, eases defaecation, and alters the colonic environment. The researchers ran two randomised, placebo-controlled, double-blinded trials, comparing seven days of psyllium against a placebo (maltodextrin). Alongside microbiota composition, they measured gastrointestinal transit, faecal water content, and short-chain fatty acid (SCFA) levels.
The study included two separate cohorts: 8 healthy volunteers and 16 constipated patients. Both groups underwent the same seven-day psyllium versus placebo comparison in a randomised, double-blinded design. This dual-cohort setup allowed the researchers to compare psyllium's effects in people without bowel symptoms against those with constipation.
In healthy adults, psyllium had a small but significant effect on microbial composition, increasing Veillonella and decreasing Subdoligranulum. In constipated patients, the effects were greater, with increases in Lachnospira, Faecalibacterium, Phascolarctobacterium, Veillonella, and Sutterella, and decreases in uncultured Coriobacteria and Christensenella, alongside changes in acetate and propionate levels. Several taxa were associated with altered GI transit, SCFA levels, and faecal water content in the constipated patients. Notably, three genera known to produce butyrate, including Lachnospira and Roseburia, increased significantly.
The findings suggest that psyllium's benefit for constipation may work partly through reshaping the gut microbiota toward more butyrate-producing taxa, not just through its water-trapping mechanical effect. The stronger microbial response seen in constipated patients compared to healthy controls indicates that psyllium's impact may depend on the pre-existing gut environment or dysbiosis. These results support further research into fiber-driven microbiota changes and SCFA production as a mechanism underlying relief of constipation symptoms.
This study examined whether infection with Schistosoma haematobium, the parasite that causes urogenital schistosomiasis, is associated with changes in the composition of the gut microbiome. The researchers compared fecal microbiome profiles between infected and uninfected individuals to test the hypothesis that this helminthic infection disrupts immune system-microbiota homeostasis. They also assessed the functional potential of the microbial communities, looking at enrichment of specific bacterial gene orthologs.
The study population consisted of schoolchildren from the Argungu Local Government Area of Kebbi State, Nigeria. Participants were divided into two groups based on infection status: those infected with S. haematobium and those uninfected. Fecal samples from these schoolchildren were used to characterize and compare the two groups' gut microbiomes.
Infected schoolchildren showed significant differences in gut microbial community composition compared to uninfected children, most notably a decreased abundance of Firmicutes and an increased abundance of Proteobacteria, a shift previously associated with dysbiosis. At the lower taxonomic level, the infected group had decreases in Clostridiales along with increases in Moraxellaceae, Veillonellaceae, Pasteurellaceae, and Desulfovibrionaceae, the family that includes sulfate-reducing, hydrogen sulfide-producing bacteria. Functional analysis further revealed enrichment of urease orthologs in the infected group, a feature that has been linked to dysbiosis and inflammation.
These findings suggest that urogenital schistosomiasis may extend its impact beyond the urogenital vasculature to alter the gut microbiome, implicating a gut-parasite interaction with features of inflammation-associated dysbiosis. The rise in Desulfovibrionaceae points to a potential role for sulfate-reducing bacteria and hydrogen sulfide production in the dysbiotic shift seen with this infection. Because urogenital schistosomiasis is a neglected tropical disease affecting many children in endemic regions, these microbiome changes may represent an underappreciated dimension of disease burden worth further investigation.
This study examined whether the composition of the gut microbiome correlates with stroke risk in people who had never had a stroke. Researchers grouped participants by known stroke risk factors and chronic disease status into low-risk, medium-risk, and high-risk categories. They characterized gut bacterial composition using 16S rRNA gene amplicon sequencing analyzed with QIIME, and measured fecal short-chain fatty acid levels by gas chromatography.
The study included 141 participants aged 60 years or older who had no prior history of stroke. Participants were stratified into low-risk, medium-risk, and high-risk groups based on established stroke risk factors and the presence of chronic diseases. The abstract does not report additional demographic details such as sex distribution or geographic origin.
Opportunistic pathogens, including members of Enterobacteriaceae and Veillonellaceae, along with lactate-producing bacteria such as Bifidobacterium and Lactobacillus, were enriched in the high-risk group compared to the low-risk group. Butyrate-producing bacteria, including Lachnospiraceae and Ruminococcaceae, were depleted in the high-risk group. Fecal butyrate concentrations were correspondingly lower in the high-risk group than in the low-risk group.
These findings suggest that gut microbiome composition, and specifically the balance between opportunistic pathogens and butyrate-producing bacteria, may reflect or contribute to stroke risk even before a first stroke occurs. Reduced butyrate production could represent a modifiable feature linked to elevated risk in older adults. This supports the potential value of gut microbiota and fecal short-chain fatty acids as early risk indicators worth further prospective investigation.
This study investigated whether Gegen Qinlian decoction (GQD), a traditional Chinese medicine formula already used for ulcerative colitis and type 2 diabetes, could enhance the effectiveness of anti-PD-1 immunotherapy in microsatellite stable (MSS) colorectal cancer. MSS tumors make up most colorectal cancer cases and typically do not respond to PD-1 blockade alone. The researchers combined GQD with anti-mouse PD-1 antibody and evaluated tumor growth, gut microbiota composition, and metabolomic changes. Systemic pharmacology methods were also used to map the multiple targets and pathways through which GQD may act.
The study used a CT26 xenograft mouse model of colorectal cancer, meaning the findings come from an animal model rather than human patients. The abstract does not specify the number of mice used or additional cohort details. Gut microbiota and metabolomic analyses were performed on samples from these tumor-bearing mice.
Combination therapy with GQD and anti-PD-1 potently inhibited CT26 tumor growth compared to other conditions tested. Gut microbiota analysis showed the combination significantly enriched Bacteroides acidifaciens and an uncultured organism within the Bacteroidales S24-7 group. Metabolomic analysis revealed profoundly altered metabolites in the combination group, with glycerophospholipid metabolism and sphingolipid metabolism identified as key affected signaling pathways. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, or sulfur metabolism as part of these findings.
These results suggest that a classical herbal formula can convert an immunologically unresponsive tumor type into one that benefits from checkpoint blockade, by remodeling both the gut microbiota and the tumor microenvironment. The identification of specific bacterial taxa and lipid metabolic pathways offers potential mechanistic targets for future combination immunotherapy strategies. Because this work was conducted in a mouse xenograft model, further studies would be needed to determine whether GQD combined with PD-1 blockade produces similar benefits in human MSS colorectal cancer patients.
This study examined whether the composition of the gut microbiota can modulate the severity of malaria infection during pregnancy. Researchers used a mouse model of gestational malaria to test whether altering gut microbes changes infection progression and pregnancy outcomes. They manipulated the gut microbiota by first disrupting native gut microbes with broad-spectrum antibiotics and then performing faecal microbiota transplants using microbial communities previously linked to either susceptibility or resistance to malaria.
The subjects were pregnant outbred Swiss Webster mice, infected with Plasmodium chabaudi chabaudi AS in early gestation. Some dams were followed to term to evaluate foetal size and viability, while in other cases pups were delivered by caesarean section and fostered to assess neonatal survival and pre-weaning outcomes. No human cohort was involved; this was an experimental animal study using an outbred mouse strain rather than an inbred line.
The gut microbiota was able to influence the severity of malaria infection in pregnant mice beyond what host genetics alone would predict. Transplanting gut microbes previously associated with susceptibility or resistance shaped how infection progressed across gestation. The abstract does not report Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism as part of these findings.
The findings suggest that the gut microbiota is a modifiable factor that can affect maternal malaria severity and pregnancy outcomes, independent of fixed genetic determinants. This points to the gut microbiota as a potential target for interventions aimed at reducing malaria related harm during pregnancy. Because the model uses outbred mice, it may better reflect the genetic diversity seen in human populations, strengthening the relevance of these results for understanding gestational malaria risk.
This study examined whether gut microbiota alterations previously reported in Parkinson's disease are stable over time and whether they track with disease progression. Researchers collected clinical data and stool samples at two timepoints, roughly 2.25 years apart on average, and characterized the microbiota using 16S rRNA gene amplicon sequencing. Disease progression was assessed through changes in the Unified Parkinson's Disease Rating Scale and Levodopa Equivalent Dose. The design allowed comparison both between patients and controls and between patients with stable versus faster-progressing disease.
The cohort consisted of 64 Parkinson's disease patients and 64 control subjects, each sampled twice over the study period. This longitudinal repeated-sampling design distinguishes the study from most prior cross-sectional comparisons in this field. No further demographic details are given in the abstract.
Significant differences in gut microbial community composition between patients and controls persisted after correcting for confounders, and these differences were present at both timepoints rather than appearing only once. Specific taxa consistently differing between patients and controls included Roseburia, Prevotella, and Bifidobacterium, echoing several previously reported associations. In contrast, no significant differences in microbiota were found between the two timepoints within groups, and taxa associated with faster versus stable disease progression were inconsistent across comparisons. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings support that gut microbiota differences in Parkinson's disease, particularly involving Roseburia, Prevotella, and Bifidobacterium, are stable and reproducible features of the disease rather than transient or timepoint-specific artifacts. This temporal stability strengthens confidence that these taxa reflect a genuine disease-associated signature rather than noise. However, the lack of a consistent microbiota signal tied to progression rate suggests that gut microbiota composition alone may not serve as a reliable biomarker for tracking how quickly Parkinson's disease advances. Future work may need larger cohorts or additional markers to link microbiota changes to clinical trajectory.
This study examined whether alterations in the gut microbiota are linked to systemic inflammation in chronic kidney disease (CKD). The researchers used 16S ribosomal DNA pyrosequencing on fecal samples to characterize microbial composition. They also measured serum inflammatory factors to explore possible correlations between gut dysbiosis and inflammation in CKD.
The study included 50 patients with chronic kidney disease and 22 healthy control subjects. Fecal microbiota samples and serum inflammatory markers were collected from both groups for comparison. The abstract does not provide further demographic details such as age, sex distribution, or CKD stage.
Patients with CKD had significantly reduced richness and altered structure of their fecal microbiota compared to healthy controls. At the phylum level, CKD patients showed reduced Actinobacteria but increased Verrucomicrobia. At the genus level, Lactobacillus, Clostridium IV, Paraprevotella, Clostridium sensu stricto, Desulfovibrio, and Alloprevotella were enriched in CKD patients, while Akkermansia and Parasutterella were enriched in healthy controls, with Akkermansia notably lower in the CKD group.
These findings support the idea that gut dysbiosis, including enrichment of taxa such as Desulfovibrio, may be tied to the chronic systemic inflammation seen in CKD. The depletion of Akkermansia in CKD patients suggests a potential loss of a genus often associated with gut barrier health. This work points toward the gut microbiota as a possible target for understanding or addressing inflammatory processes that contribute to CKD progression.
This study examined whether alterations in gut microbiome composition are linked to host cytokine responses in Parkinson's disease (PD). Researchers sequenced the V3-V4 region of the 16S ribosomal RNA gene from fecal samples to characterize gut microbiota communities. They then measured plasma concentrations of nine inflammatory cytokines (IL-1β, IL-2, IL-4, IL-6, IL-13, IL-18, GM-CSF, IFNγ, and TNFα) and analyzed relationships between microbiota composition, clinical characteristics, and cytokine levels.
The primary analysis included 80 Taiwanese patients with Parkinson's disease and 77 age and gender-matched controls. Diet and comorbidities were controlled for in the analyses. Findings on cytokine changes were then examined in a second, independent cohort of 120 PD patients and 120 controls.
Gut microbiota in PD patients differed from controls, with Verrucomicrobia, Mucispirillum, Porphyromonas, Lactobacillus, and Parabacteroides more abundant, while Prevotella was more abundant in controls. Bacteroides abundance was higher in the non-tremor PD subtype than the tremor subtype and correlated with motor symptom severity (UPDRS part III scores). Altered microbiota correlated with plasma IFNγ and TNFα, and the independent cohort confirmed significantly elevated plasma TNFα and IFNγ in PD patients compared to controls.
The findings support a link between gut microbiome alterations and immune activation in Parkinson's disease, suggesting that dysbiosis may contribute to neuroinflammation in the condition's pathogenesis. The correlation between specific bacterial taxa, cytokine levels, and motor symptom severity suggests the gut microbiome could serve as a biomarker of disease phenotype. These results point toward the gut-brain-immune axis as a potential target for future PD research and intervention.
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 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 examined whether the adhesive properties of Bifidobacterium strains influence their ability to relieve constipation. Researchers compared a combination of multiple adhesive Bifidobacterium strains (CMB1) against a combination of multiple non-adhesive Bifidobacterium strains (CMB2). They assessed effects on stool water content, fecal short-chain fatty acids (propionate and butyrate), gastrointestinal transit time, and both fecal and cecal microbiota composition.
The subjects were mice with loperamide-induced constipation, a standard pharmacological model used to mimic constipation symptoms for research purposes. The abstract does not give an exact number of animals or further details on strain, sex, or age, so no additional cohort specifics can be stated. This was an animal model study rather than a human cohort.
CMB1, the adhesive Bifidobacterium combination, alleviated constipation more effectively than CMB2 by improving fecal water content, propionate and butyrate levels, and overall gastrointestinal transit time. In fecal microbiota, CMB1 increased relative abundances of Bifidobacterium, Lactobacillus, and Prevotella, genera associated with faster bowel movement. In cecal microbiota, CMB1 increased Lactobacillus, Bacteroides, unclassified S24-7, Dorea, Ruminococcus, Coprococcus, and Rikenella, while decreasing Oscillospira and other genera. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings suggest that adhesion capacity is an important functional trait that can determine how effectively a probiotic strain reshapes the gut microbiome and relieves constipation. This implies that probiotic selection for constipation management should prioritize adhesive strains rather than treating all Bifidobacterium as functionally equivalent. The work also supports a mechanistic link between short-chain fatty acid production, targeted shifts in cecal and fecal microbiota, and improved gastrointestinal motility.
This study examined how the gut microbiome of Hispanic adults living in the USA is shaped by birthplace, migration history, and lifestyle factors. Researchers used 16S rRNA gene V4 amplicon sequencing to profile bacteria and ITS1 fragment sequencing to profile fungi in self-collected stool samples. The analysis was cross-sectional, looking at sociodemographic and migration-related variables alongside obesity status to explain differences in microbiome composition.
The study drew on 1,674 participants from four centers of the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), aged 18 to 74 years old at recruitment. Participants included people born in the USA as well as those who relocated from Latin America at different points in life, including early childhood and adulthood over age 45. This design allowed comparison across USA-born individuals, childhood arrivals, and adult migrants.
Those who relocated to the USA early in life showed reduced Prevotella to Bacteroides ratios that persisted throughout their lives, along with low Shannon diversity for both bacteria and fungi. In contrast, adults who relocated after age 45 had high bacterial and fungal diversity and high Prevotella to Bacteroides ratios compared to USA-born individuals and childhood arrivals. Low bacterial diversity was associated with obesity, and unlike prior studies in other populations, this Latino cohort showed an increasing Prevotella to Bacteroides ratio with greater obesity. Several taxa, including Acidaminococcus, Megasphaera, Ruminococcaceae, Coriobacteriaceae, and Clostridiales, were also implicated in these patterns.
The findings suggest that age at migration is a durable determinant of gut microbiome composition, with effects that persist across the life course rather than fading with time in a new country. Because the Prevotella to Bacteroides and obesity relationship ran counter to patterns seen in other populations, the results caution against generalizing microbiome-obesity associations across ethnic and migration backgrounds. This points to a need for population-specific reference ranges when interpreting gut microbiome signatures tied to metabolic health.
This study examined whether psychological stress alters gut microbiota alongside the integrity of the intestinal barrier and blood-brain barrier. The researchers used an improved communication box to create a psychological stress model and compared tight junction protein expression across intestinal regions (duodenum, jejunum, ileum) and brain regions (amygdala, hippocampus) between stressed and control animals. They also measured stress hormone markers and performed fecal microbiota analysis using 16S rRNA gene sequencing to characterize microbial changes associated with stress.
The study used a rat model of psychological stress, comparing a model group exposed to the communication box paradigm against a control group of rats. Sample size and specific strain details are not given in the abstract. Fecal samples from these rats were used for the 16S rRNA sequencing analysis.
Stress-related indicators, including adrenocorticotropic hormone, NR3C1,2, and norepinephrine, were elevated in the model group compared to controls. Psychological stress reduced levels of tight junction proteins, including claudin5, occludin, alpha-actin, and ZO-1, in both brain and intestinal tissue, indicating barrier disruption. Fecal microbiota analysis showed increased microbial diversity and elevated proportions of Intestinimonas, Catenisphaera, and Globicatella in the model group, with further analysis suggesting a correlation between these microbial shifts and barrier changes. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so this study is summarized on its own terms.
These findings suggest that psychological stress can simultaneously compromise gut and blood-brain barrier integrity while reshaping the fecal microbiota. The parallel changes in tight junction proteins across intestinal and brain regions point to a possible gut-brain axis mechanism linking microbiota shifts to barrier dysfunction under stress. This supports further investigation into specific bacterial taxa, such as Intestinimonas, Catenisphaera, and Globicatella, as potential contributors to or markers of stress-related barrier impairment.
This cross-sectional study examined differences in gut microbiota composition between people with schizophrenia and healthy controls using 16S rRNA sequencing. The researchers compared microbial abundance at the phylum and genus levels and then tested whether the resulting microbiota profile could serve as a diagnostic biomarker. Functional potential of the microbiota was also explored using PICRUSt predictive analysis.
The study included 64 patients diagnosed with schizophrenia and 53 healthy controls. Inclusion criteria were applied strictly to limit confounding bias between the two groups. No further demographic details, such as age or sex distribution, are given in the abstract.
At the phylum level, Proteobacteria was significantly more abundant in schizophrenia patients than in healthy controls. At the genus level, Succinivibrio, Megasphaera, Collinsella, Clostridium, Klebsiella, and Methanobrevibacter were elevated, while Blautia, Coprococcus, and Roseburia were reduced compared with controls. A panel of 12 microbiota biomarkers distinguished the schizophrenia group from controls with an AUC of 0.837, indicating fairly strong discriminatory performance. Sulfate-reducing bacteria, Desulfovibrio, and hydrogen sulfide or sulfur metabolism are not mentioned in this abstract.
These findings support the idea that gut microbiota alterations are associated with schizophrenia and could potentially aid diagnosis alongside clinical assessment. The identified biomarker panel suggests a possible auxiliary, non-invasive tool for distinguishing schizophrenia patients from healthy individuals. Because this is a cross-sectional, single-population study, the findings describe association rather than causation and would need validation in independent and more diverse cohorts before clinical use.
This study examined how the human gut microbiome changes during infection with soil-transmitted helminths (STHs), intestinal parasites that infect roughly 1.5 billion people worldwide. Researchers used a cross-sectional analysis to compare microbial signatures across two countries, Liberia and Indonesia, and also analyzed longitudinal samples from a double-blind randomized deworming trial. The goal was to characterize cross-kingdom interactions between STHs and gut bacteria and to see how the microbiome responds to treatment.
The abstract describes cohorts from two countries, Liberia and Indonesia, that were compared in a cross-sectional design. A subset of participants was also followed longitudinally as part of a double-blind randomized trial of deworming treatment. Exact sample sizes are not given in the abstract, so no specific participant count can be stated.
Conserved microbial signatures were positively or negatively associated with STH infection across both Liberia and Indonesia, including 12 bacterial taxa significant in both countries and one taxon, Lachnospiraceae, negatively associated with infection in both settings. Olsenella, a taxon associated with reduced gut inflammation, was also significantly reduced in abundance after infection clearance. Individuals who self-cleared their infection had more similar microbiome assemblages to one another than those who remained infected, and deworming altered microbial community gene abundances, including functional categories such as arachidonic acid metabolism, without fully shifting the microbiome back to an uninfected-like state.
The findings suggest that STH infection leaves a reproducible, cross-population signature on the gut microbiome rather than a country-specific one, pointing to shared host-parasite-microbe biology. The persistence of an altered microbiome state even after deworming implies that treatment alone may not restore a pre-infection microbial community, which could have consequences for recovery and reinfection risk. Identifying taxa like Olsenella and functional pathways such as arachidonic acid metabolism offers potential leads for understanding inflammation and immune modulation during STH infection and clearance.
This case-control study examined the fecal microbiota composition of patients with Parkinson's disease (PD) in a Chinese cohort. Researchers used high-throughput Illumina Miseq sequencing targeting the V3-V4 region of the 16S ribosomal RNA gene to profile bacterial communities. The study aimed to characterize gut microbiota dysbiosis in Chinese PD patients, a population not previously examined for this question, and to relate microbiota features to clinical characteristics of the disease.
The study included 45 patients with Parkinson's disease and their healthy spouses, who served as controls. Using spouses as controls helps account for shared household diet and environment. Clinical characteristics analyzed alongside the microbiota data included age, gender, body mass index (BMI), constipation status, disease duration, levodopa equivalent dose (LED), and non-motor symptoms such as cognitive impairment.
The structure and richness of the fecal microbiota differed between PD patients and healthy controls. After adjusting for age, gender, BMI, and constipation, the genera Clostridium IV, Aquabacterium, Holdemania, Sphingomonas, Clostridium XVIII, Butyricicoccus, and Anaerotruncus were enriched in PD patients. Escherichia/Shigella were negatively associated with disease duration, Dorea and Phascolarctobacterium were negatively associated with levodopa equivalent dose, and Butyricicoccus and Clostridium XlVb were associated with cognitive impairment. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings confirm that gut microbiota dysbiosis occurs in Chinese patients with Parkinson's disease, extending prior evidence from other populations. The associations between specific genera and disease duration, medication dosing, and cognitive symptoms suggest the microbiome may track with clinical progression and treatment response rather than being a static feature. These patterns support further investigation of fecal microbiota as a potential biomarker or contributor to PD's motor and non-motor manifestations.
This study investigated whether rheumatoid arthritis (RA) itself alters the subgingival (below-the-gumline) oral microbiome, independent of periodontitis. Prior work linking RA to dysbiotic oral microbiomes had been confounded because those RA patients often also had extensive periodontal disease. Here, researchers isolated the effect of RA by studying only periodontally healthy individuals, comparing those with RA to those without. Subgingival plaque samples underwent 16S rRNA gene sequencing on an Illumina MiSeq platform, and community composition and co-occurrence patterns were analyzed with the QIIME and PhyloToAST bioinformatics pipelines.
The cohort consisted of 41 periodontally healthy individuals: 22 with rheumatoid arthritis and 19 without RA serving as controls. All participants were confirmed periodontally healthy, which removed periodontitis as a confounding variable. The abstract does not provide further demographic details such as age, sex distribution, or geographic origin.
Subgingival microbiomes differed significantly between RA patients and controls, with 41.9% of the community differing in relative abundance and 19% differing in membership (which taxa were present at all). Co-occurrence network analysis showed a striking structural difference: control networks were sparse and made up mostly of congeneric (same-genus) relationships, while RA patient networks formed a highly connected grid anchored by a large intergeneric hub built from known periodontal pathogens. Predictive metagenomic analysis (PICRUSt) suggested that arachidonic acid and ester lipid metabolism pathways may partly explain why this pathogen-anchored network was so tightly clustered in RA patients.
The findings indicate that RA is associated with a distinctly dysbiotic subgingival microbial community structure even in the complete absence of periodontitis, meaning RA itself, not just co-occurring gum disease, may reshape the oral microbiome. The emergence of a periodontal-pathogen-anchored co-occurrence hub in clinically healthy gums suggests these organisms could be functionally primed to promote inflammation before overt disease appears. This supports the oral microbiome, and its lipid-metabolism-linked pathogen networks, as a candidate factor in RA pathogenesis worth further mechanistic and longitudinal investigation.
This study examined whether sex influences the composition of gut microbiota in patients with major depressive disorder (MDD). Building on prior work suggesting gut microbiota disturbances may causally contribute to MDD onset, the researchers analyzed 16S rRNA gene sequences from fecal samples. They used principal-coordinate analysis, partial least squares-discriminant analysis, a random forest algorithm, and linear discriminant-analysis effect size to detect sex-specific microbial differences.
The study included first-episode, drug-naive MDD patients and healthy controls, with fecal samples analyzed separately for female and male subjects. The abstract does not provide exact sample sizes or demographic details beyond the first-episode, drug-naive status of the MDD group. The comparisons were structured to separate female MDD patients from female healthy controls, and male MDD patients from male healthy controls.
Analysis identified 57 differential operational taxonomic units separating female MDD patients from female healthy controls, and 74 separating male MDD patients from male healthy controls. Female MDD patients showed increased Actinobacteria compared with their healthy counterparts, while male MDD patients showed decreased Bacteroidetes compared with theirs. These results indicate that the specific bacterial taxa altered in MDD differ depending on sex, rather than following a single uniform pattern. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings suggest that sex is an important variable to account for when studying gut microbiota alterations in depression, since males and females may show distinct dysbiosis signatures. This has implications for future microbiome research design, since pooling male and female samples without stratification could obscure sex-specific patterns. It also raises the possibility that microbiome-targeted approaches to MDD may need to be tailored differently for men and women rather than applied uniformly.
This study analyzed alterations in the fecal microbiota of Chinese patients with inflammatory bowel disease (IBD). Researchers used 16S ribosomal DNA (rDNA) gene sequencing targeting the V4 hypervariable region to characterize bacterial communities in stool samples, sequenced on the Illumina MiSeq platform. Reads were processed through QIIME software for quality control and operational taxonomic unit classification, and alpha and beta diversity were compared across groups using R software.
The cohort included 15 patients with Crohn's disease (11 active, 4 inactive), 14 patients with active ulcerative colitis, and 13 healthy individuals, all of Chinese origin. Fecal samples were collected from each participant for sequencing and comparison across the three groups.
Community richness (chao index) and overall microbial structure differed significantly between both Crohn's disease and ulcerative colitis groups compared with normal controls. At the phylum level, Proteobacteria was significantly more abundant in IBD patients than in controls. At the genus level, 8 genera in Crohn's disease and 23 genera in ulcerative colitis, particularly Escherichia, showed significantly greater abundance than in controls. Additionally, Bacteroidetes abundance was markedly lower in active Crohn's disease than in inactive Crohn's disease.
The findings confirm that fecal dysbiosis, marked by expansion of Proteobacteria and Escherichia, is a consistent feature of IBD in a Chinese population, paralleling patterns reported in other populations. The differences observed between active and inactive Crohn's disease, particularly in Bacteroidetes abundance, suggest that microbiota composition may track with disease activity. These results support fecal microbial profiling as a potential tool for understanding IBD subtypes and disease state, and point to Proteobacteria and Escherichia as targets for further mechanistic or therapeutic investigation.
This study examined how gut microbiota respond to a short-term, self-directed personalized diet intervention. Researchers compared the effects of long-term dietary habits versus a brief two-week dietary change on gut community structure. Stool samples were analyzed using 16S rRNA sequencing before and after the intervention to detect shifts in microbial composition. The work aimed to clarify how the duration of a diet change relates to its impact on the gut microbiome.
The study involved 248 citizen-science volunteers who participated in a self-reported, uncontrolled two-week personalized diet intervention. Participants provided stool samples both before and after the intervention, and their long-term dietary habits and lifestyle information were also collected. This was a citizen-science cohort rather than a tightly controlled clinical trial population.
Long-term dietary habits correlated strongly with overall gut community structure, and higher vegetable and fruit intake was linked to more butyrate-producing Clostridiales and greater community richness. Even the brief, uncontrolled two-week intervention produced substantial changes in community structure, including decreased Bacteroidaceae, Porphyromonadaceae and Rikenellaceae and reduced alpha-diversity. This shift was accompanied by increases in Methanobrevibacter, Bifidobacterium, Clostridium and butyrate-producing Lachnospiraceae, along with a change in the prevalence of a permatype (a bootstrapping-based variant of enterotype). The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, sulfide, or sulfur metabolism.
The findings suggest that gut microbiota can shift meaningfully within just two weeks, even without tightly controlled dietary conditions. This implies that short, self-directed diet changes may be a practical lever for altering microbial composition, including beneficial shifts toward butyrate producers. The results also support the value of citizen-science approaches for studying personalized nutrition at scale. Both long-term dietary patterns and short-term interventions appear to matter for shaping the gut microbiome, suggesting they may act through different or complementary mechanisms.
This study examined whether gestational diabetes mellitus (GDM) is associated with changes in gut microbiota composition. Researchers profiled the gut microbiota using 16S rRNA gene amplicon sequencing of the V1-V2 region. Sampling occurred at two time points: the third trimester of pregnancy and about 8 months postpartum. Insulin and glucose homeostasis were assessed with a 75 g 2-hour oral glucose tolerance test during and after pregnancy.
The cohort included 50 pregnant women with gestational diabetes mellitus and 157 normoglycaemic pregnant women, all assessed in the third trimester and again roughly 8 months postpartum. This gives a total study population of 207 women followed longitudinally across the perinatal period. The abstract does not specify additional demographic details such as age range or geographic origin.
Gut microbiota composition differed between women with GDM and normoglycaemic women at multiple taxonomic levels, including phylum and genus. Actinobacteria at the phylum level and the genera Collinsella, Rothia, and Desulfovibrio were more abundant in the GDM cohort. Desulfovibrio is a sulfate-reducing bacterial genus capable of producing hydrogen sulfide, so its enrichment points to altered sulfur metabolism accompanying GDM. Seventeen species-level operational taxonomic units differed in abundance with GDM, and after adjusting for pre-pregnancy BMI, five of these remained differential, with enrichment of Faecalibacterium and Anaerotruncus species and depletion of others.
The findings suggest that GDM is associated with a distinct gut microbiota signature that is detectable in late pregnancy and that some features may persist or relate to metabolic status postpartum. The enrichment of Desulfovibrio, a sulfate-reducing, hydrogen-sulfide-producing genus, alongside Actinobacteria-level shifts, suggests altered sulfur metabolism could be part of the metabolic perturbations linked to GDM. Because some associations remained after adjusting for pre-pregnancy BMI, the gut microbiota changes appear connected to GDM independent of baseline body weight. These results support further investigation of the gut microbiota, and sulfur-metabolizing taxa in particular, as potential contributors to or markers of glucose dysregulation in pregnancy.
The study examined how the fatty acid profile of the maternal diet during gestation and lactation shapes the development of the offspring gut microbiota. It also tested whether these maternal fatty acid effects translate into later metabolic health outcomes in offspring fed a high-fat diet. The researchers used a transgenic mouse model capable of endogenously producing n-3 polyunsaturated fatty acids (PUFA), allowing them to compare offspring exposed to higher versus lower maternal n-3 PUFA levels.
The subjects were murine (mouse) offspring from dams with differing endogenous n-3 PUFA production during gestation or lactation. Both male and female offspring were assessed, and offspring were subsequently fed a high-fat diet to evaluate metabolic outcomes into adulthood. The abstract does not give specific animal numbers, so no precise cohort size can be stated.
Higher maternal n-3 PUFA production during gestation or lactation significantly reduced weight gain and markers of metabolic disruption in male offspring on a high-fat diet, but had no significant effect on weight gain in female offspring. Reduced maternal n-3 PUFA exposure was linked to significantly depleted Epsilonproteobacteria, Bacteroides, and Akkermansia, along with a higher relative abundance of Clostridia. The maternal fatty acid profile during lactation had a more profound influence on offspring microbiota and metabolism than exposure in utero, and this effect on microbiota composition and function persisted into adulthood after lifelong high-fat diet feeding.
The findings suggest that maternal n-3 PUFA status during lactation can durably reprogram the offspring gut microbiota in a sex-specific way, with lasting consequences for metabolic health. This points to the early postnatal period, particularly lactation, as a key window in which maternal diet could be targeted to influence lifelong obesity risk. The results also highlight a potential mechanistic link between modern Western dietary patterns low in n-3 PUFA, the intestinal microbiome, and metabolic disease susceptibility.
This study investigated whether the gut microbiota mediates the neuroprotective, anti-seizure effects of the ketogenic diet (KD). The researchers examined how the KD alters gut microbial composition and whether these changes are necessary for protection against seizures. They also traced downstream metabolic pathways, including gamma-glutamylation and shifts in amino acid and neurotransmitter levels, that could link the microbiota to seizure susceptibility.
The subjects were two mouse models of epilepsy, one using acute electrically induced seizures and one using spontaneous tonic-clonic seizures. Comparisons were made between conventionally raised mice, mice treated with antibiotics, and germ-free mice, all fed either the ketogenic diet or a control diet. Additional gnotobiotic mice were co-colonized with specific KD-associated bacteria, and other mice received microbiota transplants from KD-fed donors.
Mice that were antibiotic-treated or germ-free lost the seizure-protective benefit of the ketogenic diet, showing that an intact gut microbiota is required for this effect. Enrichment with, or co-colonization by, the KD-associated bacteria Akkermansia and Parabacteroides restored seizure protection, and transplanting the KD-shaped microbiota into control-diet mice conferred the same protection. Protection correlated with reduced systemic gamma-glutamylated amino acids and elevated hippocampal GABA to glutamate ratios, and bacterial cross-feeding lowered gamma-glutamyltranspeptidase activity. Directly inhibiting gamma-glutamylation reproduced seizure protection in vivo, tying the bacterial and metabolic findings together.
These findings establish the gut microbiota as a causal mediator of the ketogenic diet's anti-seizure effects rather than a passive bystander. They point to specific bacteria, Akkermansia and Parabacteroides, and a specific metabolic pathway, gamma-glutamylation of amino acids affecting hippocampal GABA and glutamate balance, as potential targets for treating epilepsy without requiring strict dietary compliance. This raises the possibility of microbiome-based or metabolite-targeted therapies as alternatives or adjuncts to the ketogenic diet for refractory epilepsy.
This study examined the gut and oral microbiome in Behcet's disease (BD), a recurring inflammatory disease that can cause irreversible blindness. Researchers used metagenomic sequencing of fecal samples and 16S rRNA gene sequencing of saliva samples to compare microbial composition and biological function between BD patients and healthy controls. They then transplanted pooled fecal samples from active BD patients into mice undergoing experimental autoimmune uveitis (EAU) to test whether the gut microbiome could causally influence disease development.
The human cohort consisted of 32 patients with active Behcet's disease and 74 healthy controls, who each provided fecal and saliva samples. The animal component of the study used B10RIII mice with induced experimental autoimmune uveitis, a model used to study the eye inflammation seen in BD. Together these groups allowed comparison of microbial signatures in humans alongside a causal test in an animal model.
Fecal samples from active BD patients were enriched in Bilophila species, a sulfate-reducing bacteria (SRB), along with several opportunistic pathogens including Parabacteroides and Paraprevotella species. This enrichment occurred alongside a lower level of butyrate-producing bacteria compared to healthy controls. These shifts point to a gut microbial imbalance involving sulfate-reducing organisms and reduced beneficial short-chain fatty acid producers in BD patients.
The findings suggest that gut microbiome composition, particularly the expansion of sulfate-reducing bacteria like Bilophila and the loss of butyrate producers, may contribute to the inflammatory processes underlying Behcet's disease. Using fecal transplantation into an autoimmune uveitis mouse model supports the idea that the gut microbiome may play a causal role rather than simply reflecting disease state. This work highlights the gut microbiome, and specifically sulfate-reducing and butyrate-producing bacteria, as a potential target for understanding or managing BD-related inflammation.
This study examined how the absence of dietary isoflavones affects constipation-related physiology and gut microbiota composition in rats. Researchers compared rats fed a normal chow diet containing isoflavones (ISO group) against rats fed a non-isoflavone diet (NISO group), building on earlier work that had found differences in isoflavone pharmacokinetics between these two diets. The isoflavones studied were derived from Semen sojae praeparatum. The team used 16S rRNA sequencing to characterize shifts in gut bacterial populations linked to these dietary differences.
The subjects were rats divided into two dietary groups: one fed a normal chow diet containing isoflavones (ISO) and one fed a non-isoflavones diet (NISO). The abstract does not specify the exact number of animals, their strain, sex, or age. Findings therefore reflect a controlled animal-model comparison rather than a human cohort.
Rats on the non-isoflavone diet showed significantly reduced fecal pellet numbers, lower fecal water content, and slower intestinal transit rate compared to the isoflavone-fed group, all indicating worsened constipation. Serum concentrations of substance P and vasoactive intestinal peptide, both involved in gut motility signaling, were also decreased in the NISO group. Sequencing revealed that 5 phyla and 21 genera changed significantly with diet, with Firmicutes, Bacteroidetes, Blautia, Prevotella, Lactobacillus, and Bifidobacterium most closely tied to constipation status. Lactobacillus, which produces beta-glucosidase needed to convert glycosides into bioactive aglycones, was decreased in the non-isoflavone group.
The findings suggest that dietary isoflavones help support gut motility and stool consistency partly by sustaining beneficial bacterial populations such as Lactobacillus and Bifidobacterium. Loss of these isoflavones appears to disrupt microbiota composition and motility-related signaling peptides, worsening constipation symptoms. This points to a diet-microbiota-motility axis in which isoflavone intake could be a modifiable factor in managing constipation. The abstract does not report on Desulfovibrio, sulfate-reducing bacteria, or hydrogen sulfide, so this study does not speak to sulfur metabolism pathways.
This study examined whether chronic early-life stress in rat pups alters basal corticosterone levels, intestinal permeability, and fecal microbiota composition at weaning. Wistar rat dams and litters were exposed to a limited nesting and bedding stress (LNS) paradigm from postnatal day 2 to postnatal day 10, then returned to normal housing until weaning at postnatal day 21. Researchers measured plasma corticosterone by enzyme immunoassay, in vivo intestinal to colonic permeability using fluorescein isothiocyanate-dextran, and fecal microbiota via 16S rRNA gene sequencing of the V4 region. The design specifically compared outcomes between male and female offspring to assess sex-dependent effects.
The subjects were Wistar rat dams and their litters, with pups randomized to either the limited nesting stress condition or a normal housing control condition. Both male and female pups from these litters were followed from the early postnatal period through weaning at postnatal day 21. The abstract does not report a specific total number of animals, so the exact sample size cannot be stated. This was a controlled animal model study rather than a human cohort.
At weaning, pups exposed to limited nesting stress showed elevated basal corticosterone (hypercorticosteronemia) and increased intestinal permeability compared to controls, with females showing a greater increase in permeability than males. Body weights were similar between stressed and control pups, indicating the effects were not simply due to growth differences. Limited nesting stress also decreased fecal microbial diversity and produced a distinct microbial community composition compared to controls. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism specifically.
These findings suggest that early-life stress can disrupt the hypothalamic-pituitary-adrenal axis, intestinal barrier integrity, and gut microbiota composition well before adulthood, with weaning representing a critical window of vulnerability. The sex-specific difference in permeability, with females affected more than males, points to biological sex as an important variable in how early adversity programs gut physiology. This model may help explain how early-life stress contributes to later-life gastrointestinal and stress-related disorders and underscores the need to consider sex as a factor in future mechanistic and therapeutic research.
This study examined whether melatonin's known ability to reduce body weight and improve energy balance is linked to changes in the gut microbiota. Mice were fed a high fat diet (HFD) to induce obesity, and melatonin was administered to test its effects on body weight, liver steatosis, low-grade inflammation, and insulin resistance. High-throughput pyrosequencing of the 16S rRNA gene was used to characterize shifts in gut microbiota composition following melatonin treatment. The study compared microbiota profiles across HFD, melatonin-treated HFD, and normal chow diet (NCD) groups.
The subjects were mice fed either a high fat diet or a normal chow diet, with a subset of high fat diet mice receiving melatonin supplementation. The abstract does not specify the number of animals, their strain, sex, or age. This was an animal model study rather than a human cohort, designed to isolate diet and melatonin effects on the gut microbiota.
Melatonin reduced body weight, liver steatosis, and low-grade inflammation, and improved insulin resistance in HFD-fed mice. High fat diet feeding altered 69 operational taxonomic units (OTUs) compared to the normal chow diet group, and melatonin supplementation reversed 14 of these OTUs back toward the NCD configuration. Melatonin decreased overall richness and diversity of the gut microbiota, lowered the Firmicutes-to-Bacteroidetes ratio, and increased the abundance of the mucin-degrading bacterium Akkermansia, which is associated with healthy mucosa. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.
The findings suggest that melatonin's protective effects against diet-induced obesity and metabolic dysfunction may be mediated in part through remodeling of the gut microbiota. The partial reversal of HFD-induced OTU changes and the boost in Akkermansia point to a plausible microbiota-mediated pathway supporting mucosal health and metabolic improvement. This positions melatonin as a candidate modulator of gut microbiota composition in the context of obesity, warranting further mechanistic and translational research.
This pilot study examined the short-term impact of the classical ketogenic diet, a high-fat, very low-carbohydrate normocaloric diet, on gut microbiota composition. The classical ketogenic diet is used to treat drug-resistant epilepsy and Glucose Transporter 1 Deficiency Syndrome (GLUT1 DS). Researchers compared fecal microbiota composition before starting the diet and after three months on it. The motivation stemmed from animal studies showing that high-fat diets can substantially alter gut microbiota in ways that harm gut health.
Six patients diagnosed with GLUT1 Deficiency Syndrome were enrolled and asked to provide fecal samples at two time points. Samples were collected once before starting the classical ketogenic diet and again after three months of adherence to the diet. The abstract does not report the ages, sex distribution, or other demographic details of these six patients. This was a small prospective observational pilot cohort rather than a large or randomized study population.
Using RT-PCR, researchers quantified several bacterial groups, including Firmicutes, Bacteroidetes, Bifidobacterium spp., Lactobacillus spp., Clostridium perfringens, Enterobacteriaceae, Clostridium cluster XIV, Desulfovibrio spp., and Faecalibacterium prausnitzii. Firmicutes and Bacteroidetes levels showed no statistically significant change between baseline and the three-month follow-up. However, Desulfovibrio spp., a sulfate-reducing bacterial group, increased significantly after three months on the diet (p = 0.025). Desulfovibrio spp. is thought to be involved in worsening gut mucosal inflammation when associated with high consumption of animal-derived fats, linking this finding to sulfate-reducing bacteria and their metabolic byproducts such as hydrogen sulfide.
The significant rise in Desulfovibrio spp. after a high-fat ketogenic diet raises concern that this dietary intervention could promote a bacterial group associated with gut mucosal inflammation, even over a short three-month period. Because the diet is normocaloric but very high in animal-derived fat, clinicians using it for GLUT1 DS or drug-resistant epilepsy should be aware of this potential shift in sulfate-reducing bacteria. The authors call for a future prospective study to further characterize changes in gut microbiota associated with the ketogenic diet. Given the small sample size of six patients, these findings should be viewed as preliminary signals warranting confirmation in larger cohorts.
This study examined how different combined antiretroviral therapy (cART) regimens affect bacterial translocation and gut microbiota composition in people living with HIV. HIV infection is known to increase bacterial translocation and disrupt gut microbiota, driving immune activation and inflammation that can persist even on cART. The researchers wanted to know whether the specific drug combination used, rather than cART in general, influences these outcomes. They measured soluble markers of bacterial translocation and inflammation alongside gut microbiota composition using 16S rDNA pyrosequencing.
The cross-sectional study included 45 HIV-infected patients on cART, split into three regimen groups: NRTIs plus protease inhibitors (n = 15), NRTIs plus non-nucleoside reverse transcriptase inhibitors (n = 22), and NRTIs plus integrase strand transfer inhibitors (n = 8). Five untreated HIV-infected patients and 21 non-infected volunteers were also included for comparison. Gut microbiota was assessed via faecal samples analysed by Illumina MiSeq sequencing.
Patients on the NRTIs plus integrase strand transfer inhibitors regimen showed systemic inflammation levels similar to those of uninfected controls, suggesting this combination may better limit HIV-associated inflammation. HIV infection was associated with a reduction in faecal bacterial diversity compared with uninfected controls. The abstract indicates that the effect of this diversity loss varied depending on which cART regimen was used, though the full comparative details were not provided in the excerpt.
The findings suggest that the choice of antiretroviral drug class, not just the presence of cART, can meaningfully influence gut microbiota health and systemic inflammation in HIV-infected patients. This raises the possibility that regimen selection could be optimized to reduce residual inflammation and bacterial translocation even after viral suppression. It underscores the need for clinicians to consider gut microbiota and inflammatory markers when tailoring long-term antiretroviral therapy.
This study investigated whether the probiotic Saccharomyces boulardii changes the composition of the gut microbiome in HIV-treated patients, and whether such changes explain the probiotic's previously observed benefits. The researchers used 16S rDNA gene amplification and parallel sequencing on faecal samples to characterize gut microbiome composition. This built on prior findings from the same double-blind, randomised, placebo-controlled trial showing that 12 weeks of Saccharomyces boulardii reduced markers of bacterial translocation and systemic inflammation compared to placebo.
The cohort consisted of 44 HIV virologically suppressed patients enrolled in a double-blind, randomised, placebo-controlled trial. Half of these patients (n = 22) were immunologic non-responders to antiretroviral therapy, defined as having fewer than 270 CD4+ T cells per microliter despite long-term suppressed viral load. All 44 patients had faecal samples analyzed after being randomized to receive either the probiotic or placebo.
The abstract text provided is truncated before the specific 16S rDNA microbiome results are described, so the direct compositional findings of this analysis cannot be reported here. What is established is the premise motivating the analysis: the same trial previously found that Saccharomyces boulardii significantly reduced plasma lipopolysaccharide-binding protein (a marker of bacterial translocation) and IL-6 (a marker of systemic inflammation) relative to placebo. The aim of the microbiome analysis was to determine whether a decrease in gut bacterial species linked to translocation and inflammation underlies this clinical benefit.
If confirmed, a link between probiotic-driven shifts in gut microbiome composition and reduced bacterial translocation would support Saccharomyces boulardii as an adjunct strategy for HIV patients who show poor immune reconstitution despite viral suppression. This approach targets the gut microbiota as a driver of chronic inflammation rather than the virus itself, offering a complementary avenue alongside HAART. Because immunologic non-response contributes to poor clinical outcomes despite effective antiretroviral therapy, microbiome-targeted interventions could address a persistent unmet need in this patient population.
This study examined how conventional anti-tuberculosis drug therapy affects the intestinal microbiome. Researchers used 16S rRNA sequencing to longitudinally track microbial diversity and community composition in Mycobacterium tuberculosis-infected mice treated with the standard isoniazid-rifampin-pyrazinamide (HRZ) regimen. They also tested each antibiotic individually and in various combinations to identify which drug or drugs drove any observed changes.
The study population was Mtb-infected mice, not human subjects. The abstract does not give an exact number of animals, but it describes longitudinal sampling across the treatment course and a post-treatment follow-up period of at least three months. Comparisons were made across mice receiving monotherapy, different combination therapies, and the full HRZ regimen.
HRZ treatment caused only a transient dip in microbial diversity, but it triggered an immediate, marked, and reproducible shift in gut community structure that persisted throughout therapy and for at least three months after stopping treatment. Members of the order Clostridiales decreased in relative frequency during treatment, while the family Porphyromonadaceae increased afterward. Experiments isolating individual drugs identified rifampin as the major driver of these compositional alterations.
Because this multi-drug regimen is administered to millions of people annually worldwide, a persistent, rifampin-driven dysbiosis lasting months beyond treatment could have broad public health relevance. The findings suggest that standard TB therapy leaves a durable signature on the gut microbiota rather than a transient one. This raises the question of whether such prolonged dysbiosis contributes to downstream health effects in treated patients, warranting further investigation in humans.
This pilot study examined the salivary microbiome as a possible indicator of carcinogenesis in oral and oropharyngeal squamous cell carcinoma. Researchers compared saliva samples from cancer patients against healthy controls using high-throughput sequencing of the 16S rRNA gene on the MiSeq platform. The goal was an initial, comparative look at whether microbial community composition differs between diseased and healthy states.
The study included 11 patients with oral and oropharyngeal squamous cell carcinoma (1 female, 10 male, mean age 61.6 years, SD 8.2) and 11 healthy controls (1 female, 10 male, mean age 46.7 years, SD 15.1). This was explicitly framed as a pilot study, meaning the sample size was small and intended to generate preliminary findings rather than definitive conclusions. Saliva was the biological sample analyzed for both groups.
Sequence data revealed microbial changes in saliva that may mirror disease progression in oral and oropharyngeal squamous cell carcinoma. These microbial shifts appeared to reflect clinical preconditions including patient age, alcohol consumption, tumour size, lymph node status, smoking habit, and tumour HPV positivity. The abstract does not report specific taxa, effect sizes, or statistical values, only that detectable compositional differences were observed.
Mapping microbial changes in the saliva of patients with these cancers could improve understanding of the disease's underlying pathobiology. Such mapping may also support development of novel diagnostic tools and treatment strategies tailored to oral and oropharyngeal squamous cell carcinoma. Because this was a small pilot study, these implications point toward directions for larger, confirmatory research rather than immediate clinical application.
This study examined the gut microbiota composition and metabolic functionality associated with functional constipation (FC), a common gastrointestinal disorder whose precise causes remain unclear. The researchers used 16S rRNA-based microbial profiling to characterize bacterial community composition, then applied shotgun metagenomics to assess the functional, metabolic capabilities of the gut microbiome. The goal was to clarify inconsistent prior findings and identify a clearer link between microbiota composition and constipation symptoms.
The 16S rRNA analysis included 147 stool samples collected from 68 individuals with functional constipation, compared against samples from 79 healthy subjects. A smaller subset, five FC individuals and five healthy subjects, underwent deeper shotgun metagenomic sequencing on a MiSeq platform to evaluate microbial metabolic pathways. No further demographic details are given in the abstract.
Individuals with functional constipation showed depletion of gut bacteria belonging to Bacteroides, Roseburia, and Coprococcus 3 compared to healthy subjects. Functionally, healthy subjects' microbiomes were enriched in pathways for carbohydrate, fatty acid, and lipid metabolism relative to those with constipation. In contrast, the microbiomes of constipated individuals showed high abundance of genes involved in hydrogen production, methanogenesis, and glycerol degradation. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, or hydrogen sulfide.
The findings suggest that functional constipation is associated with both compositional and functional shifts in the gut microbiome, not just changes in which taxa are present. The elevated hydrogen production and methanogenesis capacity in FC microbiomes point to altered gas metabolism as a potentially important factor in constipation. These composition and metabolic differences could offer candidate microbial targets or biomarkers for future research into functional constipation.
This study examined the enteric virome and bacterial microbiome in the context of HIV infection and its progression to immunodeficiency. The researchers investigated whether viral communities in the gut, not just bacterial ones, contribute to the intestinal microbial translocation and enteropathy known to accompany HIV disease. They compared viral and bacterial community composition across different stages of HIV infection and treatment status.
The cohort consisted of Ugandan patients, including individuals who were HIV-uninfected and individuals who were HIV-infected. Among the HIV-infected participants, some were being treated with anti-retroviral therapy (ART) and others were untreated. The abstract does not give an exact number of participants in each group.
Patients with low peripheral CD4 T cell counts showed an expansion of enteric adenovirus sequences, and this expansion occurred independently of ART treatment. These same low-CD4 patients also had a bacterial microbiome with reduced phylogenetic diversity and richness. Specific bacterial taxa showed differential abundance, most notably an increase in Enterobacteriaceae, a group previously linked to intestinal inflammation.
The findings suggest that immunodeficiency in progressive HIV infection is accompanied by coordinated shifts in both the enteric virome and the bacterial microbiome. These viral and bacterial alterations, including adenovirus expansion and Enterobacteriaceae enrichment, may actively contribute to AIDS-associated enteropathy and disease progression rather than merely reflecting it. This points to the enteric virome as a potentially overlooked factor alongside bacterial dysbiosis in HIV pathogenesis, worth further investigation as a target or biomarker.
This study examined gut bacterial community composition and predicted microbial function in children with early onset relapsing-remitting multiple sclerosis (MS) compared to control children. Fecal samples were analyzed by 16S ribosomal RNA sequencing, with predicted functional pathways estimated using PICRUSt analysis. The researchers assessed overall community diversity (beta diversity) and the relative abundance of specific taxa, and tested how these related to MS status and immunomodulatory drug (IMD) exposure. Statistical methods included non-parametric tests, permutational multivariate analysis of variance, and negative binomial regression.
The study included 18 children with relapsing-remitting MS and 17 control children, matched for age and sex, seen at a University of California, San Francisco pediatric clinic. Participants were 18 years old or younger, with a mean age of 13 years (range 4 to 18). MS cases were within two years of disease onset, had a short mean disease duration of 11 months (range 2 to 24), and about half had never been exposed to immunomodulatory drugs. Controls had no autoimmune disorders.
Overall gut bacterial beta diversity was not significantly associated with MS status itself. However, exposure to immunomodulatory drugs was significantly associated with beta diversity (Canberra distance, P < 0.02). Despite the lack of an overall diversity difference, MS cases showed significant enrichment in specific bacterial taxa relative to controls, indicating that particular organisms, rather than broad community shifts, distinguished cases from controls. The abstract as provided does not identify Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism among these findings.
The findings suggest that specific taxonomic enrichments, rather than global shifts in microbial diversity, may be more relevant to early pediatric MS pathophysiology. The significant link between immunomodulatory drug exposure and community diversity highlights the need to account for treatment status when studying the microbiome in MS. This case-control design in a young, early-disease population offers a window into microbiota alterations that may precede or accompany disease progression, supporting further research into specific bacterial taxa as potential contributors to pediatric MS.
This study examined whether the gut microbiome influences the development and severity of arthritis in a mouse model. The researchers used 16S rRNA sequencing to characterize gut bacterial communities in DBA1 mice before and after collagen-induced arthritis (CIA) induction. They compared mice that went on to develop arthritis with those that remained resistant, then tested whether transferring this microbiota into germ-free mice could transmit disease susceptibility.
The subjects were DBA1 mice, a strain commonly used to model collagen-induced arthritis, divided into groups that did or did not develop arthritis after collagen induction. A separate set of germ-free mice was also used as recipients in microbiota transfer (conventionalization) experiments. No human cohort was involved; this was an entirely animal-model study.
Gut microbiota composition diverged significantly between CIA-susceptible and CIA-resistant mice after induction. Lactobacillus was the dominant enriched genus in susceptible mice before arthritis onset, while Bacteroidaceae, Lachnospiraceae, and S24-7 increased significantly as disease developed. Germ-free mice conventionalized with microbiota from CIA-susceptible mice developed arthritis more frequently than those given microbiota from resistant mice, and they also showed higher serum interleukin-17, more CD8+ T cells, and more Th17 lymphocytes in the spleen.
The findings suggest that the gut microbiome is not just a bystander but can actively drive arthritis susceptibility through immune modulation, particularly by promoting Th17-skewed inflammatory responses. Because microbiota transfer alone was sufficient to raise arthritis incidence, the gut microbial community may represent a modifiable environmental factor in rheumatoid arthritis risk. This strengthens the case for investigating microbiome-targeted strategies, such as modulating specific bacterial taxa, as potential approaches to arthritis prevention or management.
This study examined the gut microbial community in obese versus lean individuals using 16S rRNA gene sequencing. Researchers sequenced the V3-V4 hypervariable regions of 16S rRNA from fecal samples using the Illumina MiSeq II system. The goal was to compare microbial diversity and taxonomic composition between the two body-weight groups within a Japanese population.
The study included 20 Japanese volunteers divided into two groups of 10 obese and 10 lean participants. The average body mass index was 38.1 kg/m2 in the obese group and 16.6 kg/m2 in the lean group, a statistically significant difference. Fecal samples from these volunteers were the basis for the 16S rRNA analysis.
The Shannon diversity index was significantly higher in the lean group than in the obese group, indicating greater microbial diversity in lean individuals. Firmicutes and Fusobacteria were significantly more abundant in obese people, while Bacteroidetes abundance and the Bacteroidetes/Firmicutes ratio did not differ between groups. At the genus level, Alistipes, Anaerococcus, Corpococcus, Fusobacterium and Parvimonas increased in obese people, whereas Bacteroides, Desulfovibrio, Faecalibacterium, Lachnoanaerobaculum and Olsenella increased in lean people. Notably, the anti-inflammatory species Faecalibacterium prausnitzii was significantly more abundant in lean individuals, while pro-inflammatory species trended higher in the obese group.
The findings support a link between reduced gut microbial diversity and obesity in a Japanese population. The enrichment of Desulfovibrio, a sulfate-reducing bacterial genus, and Faecalibacterium prausnitzii in lean individuals suggests these organisms may be associated with a healthier, less inflammatory gut ecosystem. The shift toward pro-inflammatory taxa in obese individuals points to a potential microbial contribution to the inflammatory processes underlying metabolic disease. These results reinforce the relevance of the Bacteroidetes/Firmicutes and diversity framework, while also indicating that genus-level shifts, rather than phylum ratios alone, may better distinguish obese from lean gut ecology.
This case-control study examined whether the composition of gut microbiota differs between infants with eczema and healthy infants. Researchers performed high-throughput sequencing of the V3-V4 hypervariable regions of the 16S rRNA gene from fecal samples. This approach allowed them to compare bacterial taxa abundance between the two groups at a fine level of resolution, identifying over 12,000 operational taxonomic units (OTUs) at 97% similarity.
The study included 50 infants with eczema (cases) and 51 healthy infants (controls). Fecal material was collected from each infant for gut microbiota profiling. The abstract does not provide additional demographic details such as age range, geographic location, or feeding method.
Overall taxonomic composition of the gut microbiota was similar between groups, but abundance of specific taxa differed significantly. Healthy infants had higher levels of Bifidobacterium, Megasphaera, Haemophilus, and Streptococcus. Infants with eczema had higher levels of Escherichia/Shigella, Veillonella, Faecalibacterium, Lachnospiraceae incertae sedis, and Clostridium XlVa, including species such as Faecalibacterium prausnitzii and Ruminococcus gnavus that have been linked to atopy or inflammation. A higher abundance of Akkermansia muciniphila was also noted in eczematous infants and was suggested to potentially reduce intestinal barrier integrity.
The findings support the idea that shifts in the abundance of specific gut bacterial taxa, rather than broad changes in overall community structure, are associated with eczema in infancy. Enrichment of taxa linked to inflammation and reduced levels of taxa such as Bifidobacterium point to potential mechanisms connecting gut microbiota to atopic skin disease. This suggests that specific bacterial genera and species could serve as targets for further research into eczema risk, barrier function, and possible microbiome-based interventions in infants.
This study examined whether human gut microbial enterotypes, defined by the ratio of Prevotella to Bacteroides abundance (P/B ratio), are a stable and biologically meaningful way to classify individuals. The researchers used quantitative PCR to measure the P/B ratio and 35 selected bacterial taxa. They then tested whether a 6-month controlled dietary intervention, comparing the new Nordic diet (NND) to the average Danish diet (ADD), could shift these microbial groupings or the underlying taxa.
The study included 62 subjects between 18 and 65 years old who had central obesity and components of metabolic syndrome. Participants were grouped into two discrete clusters based on their P/B ratio, then followed through the randomized 6-month dietary intervention comparing NND and ADD.
Subjects could be reliably divided into two discrete groups using only their P/B ratio, and this grouping remained stable across the 6-month diet intervention. Neither the P/B-based groups nor the broader cohort showed significant changes in the 35 quantified bacterial taxa when comparing the ADD and NND diets. Despite this microbial stability, the high-P/B group had higher total plasma cholesterol than the low-P/B group after the intervention.
The findings suggest that P/B-based enterotyping identifies a stable, diet-resistant trait of the gut microbiota rather than a state that shifts readily with short-term dietary change. Because the high-P/B group showed higher plasma cholesterol after intervention, stratifying individuals by P/B ratio could help identify subgroups with differing metabolic or cardiovascular risk responses to diet. This supports using P/B ratio as a simple stratification tool for future studies assessing individualized responses to dietary interventions.
This study examined whether fecal microbiota composition could serve as a non-invasive marker for detecting colorectal cancer (CRC). Researchers used metagenomic sequencing of stool samples to identify taxonomic markers distinguishing CRC patients from tumor-free controls. They then compared the accuracy of this metagenomic approach to the standard fecal occult blood test (FOBT), including a combined-test strategy. The study also explored whether fecal microbial changes reflected microbial community shifts at the tumor site itself, along with associated metabolic changes.
The initial study population comprised 156 participants whose fecal samples were profiled by metagenomic sequencing to build the taxonomic marker panel. The findings were then validated in independent patient and control populations totaling 335 individuals from different countries. Together, the cohorts spanned both early- and late-stage CRC cases alongside tumor-free controls, though the abstract does not specify age, sex, or other demographic details.
Metagenomic detection of CRC performed similarly to the standard FOBT, and combining the two approaches improved sensitivity by more than 45 percent relative to FOBT alone while maintaining its specificity. Detection accuracy did not differ significantly between early- and late-stage cancer, and the results were validated across independent populations from different countries. CRC-associated fecal microbiome changes partly mirrored microbial community composition at the tumor itself, suggesting tumor-related host-microbe interactions. The data also indicated a metabolic shift from fiber degradation in controls to utilization of host carbohydrates and amino acids in CRC patients, accompanied by increased lipopolysaccharide metabolism.
These findings suggest fecal metagenomic profiling could serve as a non-invasive, early-stage screening tool for colorectal cancer, particularly when combined with existing tests like FOBT to boost sensitivity without sacrificing specificity. The ability to detect early-stage cancer as reliably as late-stage disease points to potential use in earlier intervention and improved outcomes. The parallel between fecal and tumor-associated microbial shifts, along with a metabolic move toward host-carbohydrate and amino-acid utilization and elevated lipopolysaccharide metabolism, implicates the gut microbiome as an active participant in tumor-related host-microbe interactions rather than a passive bystander. This reinforces the rationale for further validation of microbiome-based screening across broader, more diverse populations.
This study examined the subgingival bacterial biodiversity of untreated chronic periodontitis patients using 16S rRNA gene sequencing. The primary goal was to compare the oral microbiome found in deep, diseased periodontal pockets against shallow, healthy sites. A secondary goal was to assess whether smoking, race, and dental caries influenced this deep-versus-shallow microbial relationship. A universal primer set targeting the V4-V6 region of the 16S rRNA gene was designed to amplify oral microbial sequences.
A total of 88 subjects were recruited from two clinics for this study. From each subject, paired subgingival plaque samples were collected, one from a deep site with probing depth greater than 5 mm and one from a shallow site with probing depth of 3 mm or less. This paired, within-subject design allowed direct comparison of diseased and healthy pocket microbiomes in the same individuals.
Statistical analysis using a two-part model with false discovery rate correction identified 51 of 170 genera and 200 of 746 species that differed significantly in abundance between deep and shallow sites. Beyond bacterial species already known to be associated with periodontal disease, additional species were found to be markedly changed in the diseased, deep sites. Cluster analysis further showed that the degree of microbiome difference between deep and shallow sites was shaped by patient-level factors, including clinic location, race, and smoking status. No sulfate-reducing bacteria, Desulfovibrio, or sulfur-related metabolism were reported in this abstract.
The findings reinforce that chronic periodontitis involves a broad, multi-species shift in subgingival bacterial communities, extending beyond previously recognized periodontal pathogens. Because patient-level factors such as smoking, race, and clinic location influenced the deep-versus-shallow microbiome difference, these variables may need to be accounted for in future periodontal microbiome research and clinical risk assessment. The paired deep-shallow sampling approach offers a model for identifying disease-associated bacterial signatures within the same patient, which could inform future diagnostic or monitoring strategies.
This study examined the composition and diversity of the gut microbiome in autistic children compared with neurotypical children. Researchers used pyrosequencing of the V2/V3 regions of bacterial 16S rDNA from fecal DNA samples to profile gut bacterial communities. The goal was to identify systemic changes in the gut microbiome associated with autism itself, rather than focusing only on pathogenic bacteria as prior studies had done, and to see how these changes relate to autism severity and gastrointestinal (GI) symptoms.
The study recruited 20 neurotypical children and 20 autistic children. Autistic severity and GI symptoms were assessed for participants through an accompanying survey. Fecal samples were compared between GI symptom free neurotypical children and autistic children, most of whom presented with GI symptoms.
Autistic children had less diverse gut microbiomes than neurotypical children, and this reduced diversity tracked with the presence of autistic symptoms rather than with the severity of GI symptoms. After rigorous statistical testing with multiple testing corrections, autistic samples showed significantly lower abundances of the genera Prevotella and Coprococcus and of unclassified Veillonellaceae. The abstract describes these depleted taxa as intriguingly versatile fermenters, though the excerpt provided ends before further detail on their functions is given.
The findings suggest that autism itself, not just co-occurring GI distress, is linked to a less diverse and altered gut microbiome. Because Prevotella, Coprococcus, and Veillonellaceae are fermentative organisms, their depletion points toward disrupted carbohydrate fermentation and short-chain fatty acid production as a possible feature of autism related gut dysfunction. This reframes autism microbiome research beyond a narrow focus on pathogenic bacteria toward broader losses of beneficial fermentative capacity, which could inform future work on microbiome-targeted approaches for autism related GI problems.
This study investigated the composition of the gut microbiota in preschool children with and without overweight or obesity. Researchers used quantitative PCR (qPCR) and terminal restriction fragment length polymorphism to profile specific bacterial groups in fecal samples. They also measured fecal calprotectin as a marker of intestinal inflammation and quantified liver enzymes in the overweight and obese children.
The cohort consisted of forty children aged four to five years recruited from the south of Sweden. Twenty of the children were classified as overweight or obese, and twenty had a body mass index within the normal range, serving as the comparison group.
The gram-negative family Enterobacteriaceae was present at significantly higher concentrations in the overweight/obese children. In contrast, levels of Desulfovibrio, a sulfate-reducing bacterial genus, and Akkermansia muciniphila-like bacteria were both significantly lower in the overweight/obese group. No significant differences were found for Lactobacillus, Bifidobacterium, or the Bacteroides fragilis group, and overall bacterial diversity tended to be lower in the overweight/obese children without reaching statistical significance. Bifidobacterium concentration was inversely correlated with alanine aminotransferase (ALT) levels in the overweight/obese children, while fecal calprotectin did not differ between groups.
The findings suggest that excess body weight in early childhood is already associated with distinct shifts in gut microbial composition, including reduced levels of Desulfovibrio and Akkermansia muciniphila-like bacteria alongside increased Enterobacteriaceae. The inverse relationship between Bifidobacterium and ALT hints at a possible link between specific gut bacteria and early liver enzyme changes in overweight children. These results point to the preschool years as a relevant window for studying how gut microbiota relates to weight status and metabolic health.
This study examined the structure of the gut microbiota in patients with colorectal cancer (CRC) compared with healthy controls, using pyrosequencing-based analysis of 16S rRNA genes. The researchers separately characterized microbiota from the intestinal lumen, cancerous tissue, and matched noncancerous normal tissue. They also examined mucosa-adherent microbial composition using rectal swab samples, since tissue-adherent bacterial communities can be altered by bowel cleansing prior to biopsy.
The study population consisted of patients diagnosed with colorectal cancer, whose intestinal lumen, tumor tissue, and adjacent noncancerous tissue samples were compared against matched microbiota from healthy individuals. Rectal swab samples were used specifically to capture mucosa-adherent bacteria in these patients. The abstract does not provide a specific sample size or demographic details for the cohort.
The microbial structure of the intestinal lumen differed significantly from that of cancerous tissue, with the lumen showing greater abundance of Firmicutes and lower abundance of Bacteroidetes and Proteobacteria, along with more phylotypes associated with energy harvest and host metabolic exchange. Cancerous and noncancerous tissue had broadly similar overall microbial structures, but tumor tissue showed lower microbial diversity. Both the intestinal lumen microbiota and the mucosa-adherent microbiota differed in CRC patients compared to matched microbiota in healthy individuals, and Lactobacillales was enriched in cancerous tissue.
By distinguishing luminal, tumor, and mucosa-adherent microbial communities, the findings suggest that CRC is associated with site-specific shifts in gut microbiota rather than a single uniform dysbiosis pattern. The reduced diversity in tumor tissue and altered mucosa-adherent communities point to a tumor microenvironment that selects for or is shaped by particular bacterial taxa. These distinctions underscore the importance of sampling method and anatomical site when investigating microbiota-CRC relationships in future research.
This study examined the fecal microbial flora of children with autism who had gastrointestinal symptoms, using bacterial tag encoded FLX amplicon pyrosequencing (bTEFAP). The researchers compared the composition and diversity of gut bacteria across groups differing in autism severity. Operational taxonomic unit counts and phylum-level bacterial composition were the primary measures analyzed.
The study included 33 children with varying severities of autism who also had gastrointestinal symptoms. Two control groups were used for comparison: 7 siblings of autistic children who did not show autistic symptoms, and 8 non-sibling control children. This design allowed comparison of gut microflora both within families and against unrelated children.
Statistically significant differences in bacterial diversity, based on maximum observed and maximum predicted operational taxonomic units, were found between autistic and control subjects, with p-values ranging from less than 0.001 to 0.009. At the phylum level, Bacteroidetes and Firmicutes showed the greatest differences across groups of varying autism severity. Bacteroidetes were found at high levels in the severely autistic group, while Firmicutes were more predominant in the control group. Smaller but still significant differences were also observed at other taxonomic levels, though the abstract does not specify which taxa beyond this point.
The findings support a distinct and identifiable gut microbial signature associated with autism severity in children with gastrointestinal symptoms. The strong association between Bacteroidetes and Firmicutes proportions and autism severity suggests the gut microbiome could serve as a marker linked to disease presentation. These results reinforce the idea that environmental factors, such as gut bacterial composition, may interact with genetic predisposition in autism. This work supports further investigation into the gut microbiome as a target for understanding or managing gastrointestinal and behavioral symptoms in autism.
This study used the curatedMetagenomicData Bioconductor package (version 3.2.1 or later) to calculate taxa prevalence across multiple human body sites. The body sites examined included the vagina, skin, feces, nasal cavity, milk, and oral cavity. Prevalence was calculated separately at the species level and the genus level. The result is a set of lists defining which taxa are typical, or characteristic, of each body site in healthy adults.
The analysis drew on healthy adult control samples compiled within the curatedMetagenomicData resource, a public repository of curated metagenomic sequencing data. The abstract does not report a specific participant count or describe the original cohorts from which these samples were drawn. A companion study using the same approach but restricted to children is referenced separately (Study 608), indicating the adult analysis here was limited to adult subjects only.
The study produced body site-typical microbiome signatures for adults, generated at both species and genus taxonomic levels. These signatures are reported under different thresholds of prevalence, meaning taxa can be classified as typical depending on how common they must be across samples to qualify. This provides a tiered reference of which microbial taxa reliably characterize each of the six body sites in healthy adults. No sulfate-reducing bacteria, Desulfovibrio, or sulfur-related metabolism were mentioned in the abstract.
These prevalence-based signatures offer a reference standard for what constitutes a normal, healthy adult microbiome at each body site. Such reference lists can support future studies in identifying deviations from typical colonization patterns that may be associated with disease states. Because thresholds are provided at multiple prevalence levels, researchers can select stringency criteria appropriate to their own analytic goals. The parallel pediatric dataset also enables future comparisons between adult and child body site microbiomes.
2026-07-04
Desulfovibrio majorTaxon page created: biology (morphology, dissimilatory sulfate reduction, pathogenicity), virulence factors, diet-and-sulfur vulnerabilities, research-stage interventions, the data-derived Conditions table across 120 conditions, and the full research feed.
Singh SB, Lin HC.
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Pimenta AI, Bernardino RM, Pereira IAC.
Role of sulfidogenic members of the gut microbiota in human disease.Adv Microb Physiol. 2024
Kushkevych I, Cejnar J, Treml J, Dordevic D, Kollar P, Vitezova M.
Recent advances in metabolic pathways of sulfate reduction in intestinal bacteria.Cells. 2020
Attene-Ramos MS, Nava GM, Muellner MG, Wagner ED, Plewa MJ, Gaskins HR.
DNA damage and toxicogenomic analyses of hydrogen sulfide in human intestinal epithelial FHs 74 Int cells.Environ Mol Mutagen. 2010
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