Parasutterella

What was studied?

Periodontitis is linked to dyslipidaemia, but the mechanism still requires further investigation. This study aimed to investigate the periodontitis-dyslipidaemia interplay, comparing the impact of periodontitis-associated versus healthy salivary microbiota on systemic lipid metabolism in mice via the oral-gut axis.

Who was studied?

NHANES analysis established epidemiological link. ApoE-/- mice received salivary microbiota from periodontally healthy (A-PH) or severe periodontitis (A-SP) donors. Serum lipids and gut microbiota were assessed; correlations between microbial shifts and lipid changes were evaluated.

What were the most important findings?

NHANES confirmed significant association between self-reported physician-diagnosed bone loss around teeth and hypercholesterolemia (OR=1.266). A-SP mice exhibited higher TC, LDL and non-HDL compared with A-PH group. Gut dysbiosis featured increased proinflammatory genera (Helicobacter and Prevotella) and reduced beneficial bacteria (Mucispirillum, Parasutterella, and Barnesiella). Prevotella positively correlated with TC, Helicobacter with LDL; beneficial genera negatively correlated with atherogenic lipids.

What are the greatest implications of this study?

Collectively, building upon the NHANES link, our findings demonstrate that the salivary microbiome from periodontitis patients, compared to that from healthy individuals, disrupts systemic lipid metabolism and induces gut dysbiosis in mice. The correlation between specific gut microbial shifts and atherogenic lipid profiles provides experimental support for the mediating role of the oral‒gut axis in linking periodontitis to hyperlipidaemia.

What was studied?

In this study, we aimed to explore the mechanisms by which melatonin targets gut microbes to alleviate HS-induced reproductive impairment.

Who was studied?

We firstly evaluated the alleviating effects of melatonin supplementation on HS-induced reproductive disorder in pregnant mice. Microbial elimination and fecal microbiota transplantation (FMT) experiments were then conducted to confirm the efficacy of melatonin through regulating gut microbiota. Finally, a lipopolysaccharide (LPS)-challenged experiment was performed to verify the mechanism by which melatonin alleviates HS-induced reproductive impairment.

What were the most important findings?

Melatonin supplementation reinstated gut microbiota in heat stressed pregnant mice, reducing LPS-producing bacteria (Aliivibrio) and increasing beneficial butyrate-producing microflora (Butyricimonas). This restoration corresponded to decreased LPS along the maternal gut-placenta-fetus axis, accompanied by enhanced intestinal and placental barrier integrity, safeguarding fetuses from oxidative stress and inflammation, and ultimately improving fetal weight. Further pseudo-sterile and fecal microbiota transplantation trials confirmed that the protective effect of melatonin on fetal intrauterine growth under HS was partially dependent on gut microbiota. In LPS-challenged pregnant mice, melatonin administration mitigated placental barrier injury and abnormal angiogenesis via the inactivation of the TLR4/MAPK/VEGF signaling pathway, ultimately leading to enhanced nutrient transportation in the placenta and thereby improving the fetal weight.

What are the greatest implications of this study?

Melatonin alleviates HS-induced low fetal weight during pregnancy via the gut-placenta-fetus axis, the first time highlighting the gut microbiota as a novel intervention target to mitigate the detrimental impact of global temperature rise on vulnerable populations.

What was studied?

The aim of the study was to explore the alteration of microbiota and SCFA in gut and inflammation in acute exacerbation chronic obstructive pulmonary disease (AECOPD) patients, and to test the hypothesis that a disorder of gut microbiota will lead to the alteration of SCFA, which will aggravate inflammation in AECOPD patients.

Who was studied?

24 patients with AECOPD and 18 healthy volunteers were included in the study. Gut microbiota were analyzed by 16S rDNA and serum was used to detect levels of inflammatory factors by ELISA. Fatty acid concentrations were determined in lumen via gas chromatography-mass spectrometry. The richness and diversity of gut microbiota were decreased in AECOPD patients. β-diversity analysis revealed differences between AECOPD patients and healthy controls. p_Bacteroidetes, g_Paraprevotella, g_Ruminococcus2, g_Parasutterella, o_Rhodospirillales, and g_Romboutsia in the healthy controls and p_Firmicutes, o_Actinomycetales, f_Actinomycetadeae, g_Actinomyces, g_Mogibacterium, f_Veillonellaceae, f_Enterococcaceae, and g_Enterococcus in AECOPD patients were the most abundant microbiota. SCFA levels were decreased in patients with AECOPD. In addition, the results demonstrated that except for a reduction in IL-6, there was no change in inflammatory markers in AECOPD patients.

What are the greatest implications of this study?

In AECOPD patients, the gut microbiota-SCFA-inflammation axis is augmented, with decreased diversity and abundance of gut microbiota, leading to a reduction in SCFA and an imbalance of inflammation.

What was studied?

Common variable immunodeficiency (CVID) is characterized by hypogammaglobulinemia and recurrent infections. Significant morbidity and mortality are caused by immune dysregulation complications (CVIDid), which affect around one-third of CVID patients and have a poorly understood etiology. Here, we investigate the hypothesis that gut microbial dysbiosis contributes to the inflammation underlying CVIDid.

What were the most important findings?

Bacterial invasion of colonic crypts was observed in CVID (3/15) and X-linked agammaglobulinemia (XLA, 1/3), but not in healthy control (HC, 0/9) biopsies. Fecal gut microbiota was characterized using 16S rRNA-targeted amplicon sequencing. Increased bacterial load, decreased alpha diversity and distinct beta diversity were observed in CVIDid (n = 42) compared to HC (n = 48), and similar results were seen in CVID with IgA deficiency (n = 40) compared to HC. CVIDid and CVID-IgA showed enrichment of the genus Enterococcus, and in vitro studies confirmed the inflammatory potential of Enterococcus gallinarum and Enterococcus hirae in patient monocytes.

What are the greatest implications of this study?

This study further supports the hypothesis that a dysregulated gut microbiota, with IgA deficiency as an important driving factor, contributes to systemic inflammation in primary antibody deficiency, and introduces enterococci as potential pathobionts in CVIDid. Video Abstract.

What was studied?

Functional constipation (FC) significantly impacts children's health. This study investigates the prevalence and microbiota characteristics of FC in children aged 0-4 years in Zunyi area.

Who was studied?

From October to December 2023, 2039 children aged 0-4 years in Zunyi were selected using stratified sampling and cross-sectional survey methods. A questionnaire based on Rome IV diagnostic criteria was used. Twenty-nine children with FC were randomly selected as the functional constipation group (FCG), and 26 healthy children, matched for age, sex, and area, were selected as the control group (CG).

What were the most important findings?

A total of 2051 questionnaires were collected, with 2039 valid responses. Among them, 151 children had FC, resulting in a prevalence rate of 7.4%. The prevalence rates in boys and girls were 6.6% and 8.5%, respectively, with no significant gender difference (P > 0.05). Alpha diversity analysis revealed higher richness and diversity of intestinal flora in the FCG compared to the CG. At the phylum level, Actinobacteria, Firmicutes, Proteobacteria, and Bacteroidetes were dominant in both groups. The FCG showed a higher relative abundance of Firmicutes, Actinobacteria, and Proteobacteria compared to the CG (P < 0.05).

What are the greatest implications of this study?

The prevalence of FC in children aged 0-4 years in Zunyi is 7.4%. Disease characteristics vary with age and living environment but are unrelated to gender. The gut microbiota of children with FC shows significant alterations, with higher diversity and specific phyla abundance.

What was studied?

Hyperoxaluria, including primary and secondary hyperoxaluria, is a disorder characterized by increased urinary oxalate excretion and could lead to recurrent calcium oxalate kidney stones, nephrocalcinosis and eventually end stage renal disease. For secondary hyperoxaluria, high dietary oxalate (HDOx) or its precursors intake is a key reason. Recently, accumulated studies highlight the important role of gut microbiota in the regulation of oxalate homeostasis. However, the underlying mechanisms involving gut microbiota and metabolite disruptions in secondary hyperoxaluria remain poorly understood. Here, we investigated the therapeutic efficacy of fecal microbiota transplantation (FMT) sourced from healthy rats fed with standard pellet diet against urinary oxalate excretion, renal damage and calcium oxalate (CaOx) crystal depositions via using hyperoxaluria rat models. We observed dose-dependent increases in urinary oxalate excretion and CaOx crystal depositions due to hyperoxaluria, accompanied by significant reductions in gut microbiota diversity characterized by shifts in Ruminococcaceae_UCG-014 and Parasutterella composition. Metabolomic analysis validated these findings, revealing substantial decreases in key metabolites associated with these microbial groups. Transplanting microbes from healthy rats effectively reduced HDOx-induced urinary oxalate excretion and CaOx crystal depositions meanwhile restoring Ruminococcaceae_UCG-014 and Parasutterella populations and their associated metabolites. Furthermore, FMT treatment could significantly decrease the urinary oxalate excretion and CaOx crystal depositions in rat kidneys via, at least in part, upregulating the expressions of intestinal barrier proteins and oxalate transporters in the intestine. In conclusion, our study emphasizes the effectiveness of FMT in countering HDOx-induced hyperoxaluria by restoring gut microbiota and related metabolites. These findings provide insights on the complex connection between secondary hyperoxaluria caused by high dietary oxalate and disruptions in gut microbiota, offering promising avenues for targeted therapeutic strategies.

What was studied?

This study profiled the fecal virome, bacteriome, and blood metabolome together in schizophrenia, testing whether gut viruses (mainly bacteriophages) shape the disease-associated bacterial community and whether those shifts reach the host through circulating metabolites.

Who was studied?

Forty-nine first-episode schizophrenia patients, most drug-naive or treated for fewer than five days, and 49 age-, sex-, and BMI-matched healthy controls at West China Hospital, Sichuan University (2021 to 2022). Fecal shotgun sequencing covered 95 participants and untargeted plasma metabolomics 92, with age, sex, BMI, and medication days controlled.

What were the most important findings?

Bacterial beta-diversity separated patients from controls at the family, genus, and species levels while alpha-diversity did not differ, and combining MaAsLin2 with ANCOM-BC flagged 7, 14, and 45 differentially abundant taxa respectively. The healthy viral-bacterial transkingdom correlation network was largely lost in schizophrenia, and the co-occurring metabolites were enriched in bile-acid and eicosanoid pathways linked to inflammation. A serial-mediation model supported a gut viruses to bacteria to metabolites to schizophrenia chain, with metabolites carrying most of the indirect effect.

What are the greatest implications of this study?

The results frame schizophrenia-associated dysbiosis as a virome-bacteriome-metabolome system rather than a bacterial shift alone, and highlight bile-acid and eicosanoid (COX and prostaglandin) metabolism as microbiota-linked, potentially treatable inflammatory routes. As a small cross-sectional study, it establishes associations and candidate biomarkers, not causation.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

While the urgent need for energy saving is triggering energy retrofit measures in buildings, there are still large gaps in our understanding of how these measures may impact indoor environmental quality, including particle, chemical, and microbial exposure, and ultimately human health. Here, we explore the effects of energy retrofits on the indoor microbiota characteristics of 193 apartments in 40 apartment buildings in two Northern European countries, Finland and Lithuania. Amplicon sequencing was used to characterise fungal and bacterial microbiota compositions in airborne, settled dust samples collected from apartments before and after energy retrofits, mostly targeting upgrades in insulation, heating and/or ventilation systems, and windows. Pairwise pre versus post testing of the most abundant fungal and bacterial taxa and diversity metrics, (generalized) linear mixed modelling ((G)LMM), and Analysis of Composition of Microbiomes (ANCOM) differential abundance testing were used to explore the effects of retrofits on indoor microbiota while accounting for confounding factors. The results indicated significant, country-dependent changes in the relative abundances of individual bacterial and fungal taxa, and a smaller proportion of human-sourced bacteria in Finnish buildings after compared to before retrofits. As in previous studies, factors such as outdoor temperature and type of ventilation were found to influence both bacterial and fungal composition indoors. To the best of our knowledge, this is the first dedicated, multi-country study on impacts of energy retrofits on indoor microbiota. Our novel findings offer a foundation for future research into this topic, including studies on the potential health relevance of energy retrofit associated indoor microbiome changes.

What was studied?

The human microbiome plays a vital role in human health, mediated by the gut-brain axis, with a large diversity of functions and physiological benefits. The dynamics and mechanisms of meditations on oral and gut microbiome modulations are not well understood. This study investigates the short-term modulations of the gut and oral microbiome during an Arhatic Yoga meditation retreat as well as on the role of microbiome in improving well-being through a possible gut-brain axis.

Who was studied?

A single-arm pilot clinical trial was conducted in a controlled environment during a 9-day intensive retreat of Arhatic Yoga meditation practices with vegetarian diet. Oral and fecal samples of 24 practitioners were collected at the start (Day0: T1), middle (Day3: T2), and end (Day9:T3) of the retreat. Targeted 16S rRNA gene amplicon sequencing was performed for both oral and gut samples. Functional pathway predictions was identified using phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2). DESeq2 was used to identify the differential abundant taxa. Various statistical analyses were performed to assess the significant changes in the data.

What were the most important findings?

Our findings revealed that Arhatic Yoga meditation together with a vegetarian diet led to changes in the oral and gut microbiome profiles within the 9-day retreat. Oral microbiome profile showed a significant (p < 0.05) difference in the species richness and evenness at the end of study, while non-metric multidimensional scaling (NMDS) confirmed the shift in the gut microbiome profile of the practitioners by T2 timepoint, which was further supported by PERMANOVA analysis (p < 0.05). Health-benefiting microbes known to improve the gastrointestinal and gut-barrier functions, immune modulation, and gut-brain axis were enriched. Gut microbiome of both beginner and advanced Arhatic Yoga practitioners showed similar trends of convergence by the end of study. This implies a strong selection pressure by Arhatic Yoga meditation together with a vegetarian diet on the beneficial gut microbiome.

What are the greatest implications of this study?

This pilot study demonstrates that Arhatic Yoga meditation practices combined with a vegetarian diet during a short intensive retreat resulted in enrichment of known health-promoting microbes. Such microbial consortia may be developed for potential health benefits and used as probiotics to improve the gastrointestinal and immune systems, as well as functions mediated by the gut-brain axis.

What was studied?

External factors affecting composition of the human gut microbiota have attracted considerable attention in recent years. Among these factors, habitat sharing with other humans and companion animals, especially dogs, is considered crucial together with the presence of intestinal protists. The Czech Republic, known for one of the highest rates of dog ownership in Europe, provides an ideal setting for studying such relationships. Here, we investigated the impact of dog ownership and lifestyle factors (residing in cities versus villages) on the gut microbiota (specifically bacteriome). In addition, we also investigated the influence of the common gut protist Blastocystis sp. on the human gut microbiota. Fecal DNAs from 118 humans and 54 dogs were subject to 16S rRNA gene sequencing using the Illumina MiSeq platform. Greater microbial diversity was observed in humans than in dogs. Owning a dog had no significant effect on the alpha and beta diversity of the human microbiota, although some bacterial genera were enriched in dog owners. In relation to lifestyle, urban dwellers had higher levels of Akkermansia, while people living in villages had a more diverse gut microbiota. The presence of Blastocystis sp. in humans correlated with specific microbial patterns, indicating an important role for this micro-eukaryote in the gut ecosystem. These findings highlight the intricate relationship between specific factors and the gut microbiota composition and emphasize the need for more extensive research in this area.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study investigated the smoking paradox, in which smokers tend to have lower body mass index but higher risk of obesity-related disease, through the lens of the gut microbiota. Researchers used 16S rRNA sequencing to identify smoking-related microbial genera and built a smoking-related microbiota index (SMI). They then tested whether SMI was associated with obesity indices and with incident obesity-related diseases, including analyses designed to control for shared familial and environmental confounders.

Who was studied?

The analysis drew on 4000 male participants from two cohorts, the WELL-China cohort and the Lanxi cohort. Obesity indices were derived using dual-energy X-ray absorptiometry (DEXA) scans in these participants. A subset of participants with siblings was used for sibling comparison analyses via a between-within (BW) model, allowing the researchers to account for unmeasured familial confounding.

What were the most important findings?

The smoking-related microbiota index (SMI) was positively associated with BMI and other DEXA-derived obesity indices. Higher SMI was also linked to greater risk of incident obesity-related disease, with hazard ratios of 1.97 for diabetes, 1.31 for major adverse cardiovascular events, and 1.70 for obesity-related cancers. These associations held up in sibling comparison analyses, which help rule out shared family environment or genetics as the explanation.

What are the greatest implications of this study?

The findings suggest that smoking-associated shifts in gut microbiota may help explain why smokers face elevated cardiometabolic and cancer risk despite often having lower BMI. This reframes the smoking-obesity paradox as partly a microbiome-mediated phenomenon rather than a purely anthropometric one. The sibling comparison design strengthens confidence that the microbiota signal is not simply a marker of shared family background. These results point to the gut microbiota as a potential target or biomarker for assessing metabolic and disease risk in people who smoke.

What was studied?

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.

Who was studied?

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.

What were the most important 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.

What are the greatest implications of this study?

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.

What was studied?

The gut microbiome is associated with bone mass acquisition, yet evidence in childhood remains limited. Given that lower peak bone mass predicts osteoporosis in later life, understanding early influences is important. This analysis explores the association between the early life gut microbiome and bone health in later childhood. Data were obtained from 700 children recruited in pregnancy and followed prospectively within the Copenhagen Prospective Studies on Asthma in Childhood2010 cohort, a population-based mother-child cohort. The infant gut microbiome was measured at 1 wk (n = 445), 1 mo (n = 492), 1 yr (n = 508), 4 yr (n = 350), and 6 yr (n = 327) of age by 16S ribosomal ribonucleic acid amplicon sequencing targeting the fourth variable region. Total body less head BMD and area-adjusted BMC were measured by DXA at 6 yr of age. Associations were investigated by multiple linear regression, permutational analysis of variance, differential abundance analysis, and Random Forest machine learning. There were few associations between the early-life gut microbiome and bone health outcomes at age 6. We found negative associations between alpha (within-sample) diversity and area-adjusted BMC at 4 yr. Beta (between-sample) diversity of the gut microbiome at 6 yr was associated with concurrent BMD. Escherichia-Shigella abundance at 1 mo of age was associated with lower BMD. Sutterella abundance at 1 yr was associated with lower BMD and area-adjusted BMC at 6 yr. There were no other associations between the gut microbiome and bone outcome measures at any time point. In a well-powered unselected cohort study with longitudinal sampling of the gut microbiome, there were some suggestive but no consistent associations between the early gut microbiome and bone health outcomes at 6 yr of age. Bone health in childhood is important for preventing osteoporosis later in life. This study explored whether gut bacteria (gut microbiome) during infancy and early childhood influences bone health later in childhood. We followed 700 children, measuring their gut microbiome at 1 wk, 1 mo, and at 1, 4, and 6 yr, and their bone health at age 6. While some weak links were found between specific gut microbiome and bone health, the results were inconsistent. Overall, the findings suggest that early gut microbiome may have limited impact on later childhood bone health, and further research is required to confirm this.

What was studied?

This study examined whether rifaximin, a gut-specific non-absorbable antibiotic, could reduce gut-derived systemic inflammation in severe acute pancreatitis (SAP). The researchers combined murine experimental models with a single-center, open-label randomized controlled trial (ChiCTR2100049794). They assessed pancreatic injury, systemic inflammatory markers, and gut microbiota composition, and tested whether rifaximin's effects depended on modulating the microbiota by using antibiotic-treated and germ-free mice.

Who was studied?

The animal component used murine models of severe acute pancreatitis, including antibiotic-treated and germ-free mice used to probe the mechanism. The clinical component enrolled 60 patients with predicted severe acute pancreatitis, randomized to receive rifaximin or standard control treatment. No further demographic details are given in the abstract.

What were the most important findings?

In mice, rifaximin reduced pancreatic injury and systemic inflammation and decreased mucin-degrading gut genera such as Akkermansia, but its protective effects persisted even in antibiotic-treated and germ-free mice, indicating mechanisms beyond microbiota modulation. In patients, rifaximin significantly lowered systemic inflammation, with white blood cell count falling from a median of 11.50 x10^9/L to 8.49 x10^9/L and TNF-alpha falling from 15.05 pg/mL to 11.00 pg/mL. However, the rate of culture-confirmed infection was identical between rifaximin and control groups (13.3% vs 13.3%), and adverse events were comparable between groups.

What are the greatest implications of this study?

The findings suggest rifaximin can dampen systemic inflammation in severe acute pancreatitis through mechanisms that are not solely dependent on reshaping the gut microbiota, pointing to a possible direct anti-inflammatory or barrier-protective effect. Because inflammation markers improved without any change in infection risk, rifaximin may offer a safe adjunct for controlling inflammatory injury in SAP without added infectious risk. This supports further investigation of rifaximin as a therapeutic strategy for gut-derived inflammation in acute pancreatitis, alongside continued study of its non-microbiota-dependent mechanisms.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

Who was studied?

A rat model of CHD and depression was established using a high-fat diet and chronic unpredictable mild stress and verified by electrocardiogram, behavioral assessments, and cardiac marker analysis. Fecal microbiota transplantation (FMT) was performed by transferring microbiota from diseased rats to healthy rats (FMT-Disease group); the fecal microbiota of the rats from the FMT-Disease and FMT-Normal groups were compared. The TLR4 inhibitor TAK-242 was administered, creating the Disease + TAK-242 and FMT-Disease-TAK-242 groups. Gut microbiota composition was analyzed using 16 S rRNA high-throughput sequencing; LPS levels were measured using enzyme-linked immunosorbent assay. Polymerase chain reaction and western blotting were used to detect the expression of genes and proteins related to the TLR4/MYD88/NF-κB pathway in the heart and hippocampus, respectively.

What were the most important findings?

We confirmed that in the FMT-Disease group, the gut microbiota of diseased rats altered the gut microbial composition of healthy rats in terms of β-diversity, α-diversity, and community structure. Notably, LPS levels in the serum of FMT-Disease rats were elevated, thereby activating the TLR4/MYD88/NF-κB inflammatory pathway and increasing susceptibility to CHD comorbid with depression. Additionally, after receiving fecal microbiota from healthy rats, the Disease group showed a restoration of gut microbiota balance, improvement in general condition, and normalization of pathological, biochemical, and inflammatory indicators, indicating a suppressive effect on the progression of CHD with depression.

What are the greatest implications of this study?

Our findings further clarify the interrelationship between gut microbiota and CHD comorbid with depression, enhancing our understanding of its pathogenesis. Moreover, we propose a potential novel therapeutic strategy that focuses on modulating gut microbiota composition to block the TLR4/MYD88/NF-κB inflammatory pathway.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

Most research into the development of the canine gut microbiota has featured cross-sectional studies, and there has been limited exploratory research into how it is affected by external factors. We aimed to longitudinally characterise the gut microbiota and its development in Labrador Retriever puppies and identify whether alterations in the gut microbiota are associated with factors related to demography, lifestyle, antibiotic usage and gastrointestinal health.

What were the most important findings?

76 Labrador Retriever puppies were recruited via Dogslife, a UK-based online cohort study. Faecal samples were collected at three to four, seven, and 12 months of age and analysed using 16 S rRNA gene sequencing alongside questionnaire data. Alpha and beta diversity were assessed using linear mixed effects models and permutational multivariate analysis, accounting for repeated measures. Differential abundance was evaluated using multivariable association with linear models. Associations were identified between puppies' gut microbiota and age, sex, coat colour, household smoking status, dietary indiscretions (e.g. household waste, coprophagia), contact with other dogs and horses, recent oral/injected antibiotic use, and recent vomiting and diarrhoea. The greatest source of variation was individual identity, explaining approximately 25% of alpha diversity and 50% of beta diversity. Alpha diversity declined between three and 12 months, with age-related shifts in community composition and dispersion. Coprophagia was associated with increased alpha diversity and contributed to variation in community structure. Antibiotic use was associated with reduced alpha diversity, altered composition, and changes in taxa across Firmicutes, Proteobacteria, and Tenericutes. These effects were largely transient, with the largest shifts occurring within one week of treatment. Puppies with recent diarrhoea showed increased alpha diversity and differential abundance in several taxa within four weeks of the episode. Helicobacter was more frequently detected in samples from puppies with recent diarrhoea.

What are the greatest implications of this study?

This longitudinal study characterises the development of gut microbiota in Labrador Retriever puppies and identifies associations with demographic, environmental, and health-related factors. These findings underscore the value of longitudinal sampling in microbiome research, offer novel insights for owners and veterinarians, and lay a foundation for future studies investigating causal mechanisms and potential interventions.

What was studied?

Sini-San (SNS), a classical traditional Chinese medicinal formula, has demonstrated promising potential in mitigating the progression of liver fibrosis (LF). Increasing evidence highlights that disruption of bile acids (BAs) homeostasis is critically involved in the pathogenesis and progression of LF, suggesting that targeting BAs metabolism could represent a therapeutic strategy. This study aimed to explore whether the protective effects of SNS against LF are mediated through modulation of BAs metabolism and associated regulatory pathways.

Who was studied?

The chemical constituents of SNS were characterized using high-performance liquid chromatography (HPLC). LF models were established in mice through intraperitoneal injection of carbon tetrachloride (CCl4) or feeding a high-fat, high-sugar (HFHS) diet. SNS was administered orally. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and hydroxyproline (HYP) levels were measured, and liver histopathology was evaluated by hematoxylin-eosin (HE), Masson and TUNEL staining. The expression of fibrosis- and apoptosis-associated markers (Collagen-1, α-SMA, Bcl-2, Bax, and Caspase-3) was assessed by RT-qPCR and Western blotting. Serum BAs profiles were analyzed using LC-MS/MS, and molecules involved in BA metabolism (Fxr, Cyp7a1, Cyp27a1, Bsep, Ntcp, Asbt and OATP) were examined. Gut microbiota composition was analyzed through 16S rRNA gene sequencing. To investigate the mechanisms by which SNS regulates BAs homeostasis, additional experiments were conducted under choline chelation, pseudo-sterile conditions, and in fxr-/- mice.

What were the most important findings?

In LF mice induced by CCl4 or HFHS diet, significant alterations were observed in BAs levels and composition. The expression of BAs-synthesizing enzymes (CYP7A1, CYP27A1), BAs transporters (Bsep, Ntcp, Asbt and Oatp), and the feedback regulatory receptor FXR was markedly dysregulated. Meanwhile, gut microbiota abundance and composition were also significantly disrupted, indicating a disturbance of BAs homeostasis. SNS treatment effectively alleviated liver injury and fibrosis, corrected BAs imbalance, regulated the expression of BAs-related genes, and restored microbial diversity. However, the antifibrotic effects of SNS were reversed by choline chelation, antibiotic treatment, and fxr knockout.

What are the greatest implications of this study?

SNS may exert anti-hepatic fibrosis effects by modulating BAs metabolism and gut-liver axis pathways, ultimately restoring BAs homeostasis. These findings provide new insights into the therapeutic mechanisms of SNS and suggest its potential as a multitargeted strategy for LF treatment.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study examined whether the intestinal microbiota differs between men and women who have coronary heart disease (CHD). The researchers compared microbiota composition in CHD patients against non-CVD controls, analyzing each sex separately. Intestinal bacteria were profiled using 16S metagenomic sequencing on the Illumina MiSeq platform, with data processed in Qiime2. The goal was to identify sex-specific microbial patterns tied to cardiovascular disease.

Who was studied?

The study drew on the CORDIOPREV clinical trial cohort, which included 837 men and 165 women with CHD. These CHD patients were compared against a reference group of 375 individuals without cardiovascular disease, consisting of 270 men and 105 women. In total, the analysis spanned over 1,300 participants across both sexes and disease status.

What were the most important findings?

Beta diversity, reflecting differences in microbial community composition, varied by sex, while alpha diversity (within-sample richness) remained similar between men and women. LEfSe analysis identified sex-specific alterations in the gut microbiota associated with CVD. Using random forest modeling, the researchers pinpointed seven bacterial taxa as key discriminators: g_UBA1819 (Ruminococcaceae), g_Bilophila, g_Subdoligranulum, g_Phascolarctobacterium, f_Barnesiellaceae, g_Ruminococcus, and an unidentified genus within Ruminococcaceae (Ruminococcaceae incertae sedis).

What are the greatest implications of this study?

These findings suggest that cardiovascular disease is linked to distinct microbial signatures depending on sex, rather than a single universal gut microbiota pattern. This implies that future microbiome-based research or risk assessment for CHD may need to account for sex as a variable rather than treating cohorts as uniform. The identified taxa, several from the Ruminococcaceae family and related groups, may serve as candidate markers warranting further investigation in sex-stratified cardiovascular studies.

What was studied?

This study used species-level shotgun metagenomic sequencing to characterize the gut microbiota of men who have sex with men (MSM). It investigated why the MSM gut microbiome, previously shown to differ from that of non-MSM, so often resembles the microbial communities seen in non-Westernized populations. The researchers also used questionnaire data and machine learning to link specific sexual practices to variation in microbiota composition among MSM.

Who was studied?

The study population was men who have sex with men of Western origin, compared against patterns typical of non-Westernized populations. The abstract does not give an exact sample size, but participants contributed both stool samples for shotgun metagenomics and questionnaire responses on sexual practices. This design allowed the authors to relate individual behavioral data to individual gut microbiome profiles within the MSM cohort.

What were the most important findings?

Many MSM with Western origin had gut microbiomes resembling those of non-Westernized populations rather than typical Western gut profiles. These microbiomes were frequently dominated by Prevotellaceae family members, including co-colonization by species from the Segatella copri complex alongside unknown Prevotellaceae members. Questionnaire analysis and machine learning further identified specific sexual practices as microbial features associated with this altered, Prevotellaceae-rich composition.

What are the greatest implications of this study?

The findings show that sexual activity itself can be a driver of major gut microbiome alterations, independent of the diet and lifestyle factors usually invoked to explain Westernized versus non-Westernized microbiota differences. Because MSM gut microbiomes can resemble non-Westernized profiles, sexual practice becomes an important variable that population-based microbiota studies may need to account for. This has implications for how researchers select and interpret control or reference populations in microbiome research and for disentangling behavioral from dietary or geographic influences on gut microbial composition.

What was studied?

Adequate consumption of fiber has a positive effect on health. The crossover study examined the effect of a pectin-enriched smoothie on gut microbiota and health parameters. During 3 weeks, 31 adults consumed two smoothies (11.6 or 4.8 g of fiber/day), alternating with washout periods in different order. At the end of each period, weekly food diaries, blood samples, and stool microbiota were collected. Changes in the microbiota during smoothie consumption were associated with baseline fiber intake. A greater proportion of up- (Lachnospira, Colidextribacter, and Bacteroides) or down-shifts (Streptococcus, Holdemanella) was observed in low-fiber (n = 22) compared to high-fiber consumers (n = 9). In both groups, the pectin-enriched smoothie reduced the number of the Ruminococcus torques group bacteria. Our results showed that the short-term approach is effective to estimate relationships between food components and gut bacteria.

What was studied?

This study aimed to reveal the association between the gut microbiota (GM) and six diabetic complications: diabetic hypoglycemia; ketoacidosis; nephropathy; neuropathy; retinopathy; and Charcot's foot.

Who was studied?

GM data were obtained from the MiBioGen consortium and Dutch Microbiome Project while data on the six diabetic complications were obtained from the FinnGen consortium. Two-sample Mendelian randomization (TSMR) was performed to explore the association between GM and the common diabetic complications. Inverse MR analysis was conducted to examine the effect of diabetic complications on the identified GM. Sensitivity tests were conducted to validate the stability of the results. Finally, multivariate MR (MVMR) was performed to determine whether GM had a direct influence on the diabetic complications.

What were the most important findings?

After multiple corrections, the inverse variance weighted (IVW) results predicted 61 suggestive markers between GM and six diabetic complications. In particular, the IVW results revealed that the Bacteroidia class and Bacteroidales order were positively associated with diabetic hypoglycemia while the Verrucomicrobiae class and Verrucomicrobiales order were positively associated with diabetic nephropathy. Based on the replication analysis, these results were identified to be stable. MVMR showed that the results remained stable after accounting for traditional risk factors.

What are the greatest implications of this study?

Extensive causal associations were found between GM and diabetic complications, which may provide new insights into the mechanisms of microbiome-mediated complications of diabetes.

What was studied?

The study examined how peripheral neurons connected to the gastrointestinal tract influence the gut microbiome and gut physiology. Researchers activated choline acetyltransferase (ChAT)-expressing or tyrosine hydroxylase (TH)-expressing gut-associated neurons in mice. They then measured effects on intestinal microbial communities, microbial metabolites (including bile acid profiles), and host physiological responses using multi-omics approaches.

Who was studied?

The subjects were mice in which ChAT+ or TH+ gut-associated neurons were experimentally activated. The abstract does not give a specific sample size or strain detail, so no cohort numbers can be stated. This was an animal model study, not a human cohort, and it generated multi-omics datasets from these mice rather than drawing on a public metagenomic dataset.

What were the most important findings?

Activating either ChAT+ or TH+ neurons reshaped the structure of the intestinal microbiome, including changes to bile acid profiles and fungal colonization. Physiologically, activation of either neuron type increased fecal output, showing a shared downstream effect on gut transit. Only ChAT+ neuron activation additionally increased colonic contractility and produced diarrhea-like fluid secretion, indicating that these two neuronal subtypes act through distinct physiological pathways despite some overlapping effects.

What are the greatest implications of this study?

The findings show that distinct subsets of peripheral, gut-associated neurons can independently shape microbiome composition and gastrointestinal physiology without requiring signals from the brain. This suggests the enteric and peripheral nervous system directly sculpts microbial ecology, including bacterial and fungal populations and bile acid metabolism, rather than the microbiome being shaped only by diet or host genetics. Because different neuron subtypes produce different physiological outcomes (fecal output alone versus contractility and diarrhea-like secretion), this points to neuron-specific pathways as potential targets for understanding or treating GI motility and secretory disorders.

What was studied?

It has been suggested that dysbiosis of the gut microbiota is associated with the pathogenesis of Polycystic Ovary Syndrome (PCOS), and that improper diet can aggravate these changes. This study thus aimed to investigate the effects of a high-fat/high-fructose (HF/HFr) diet on the gut microbial community and their metabolites in prepubertal female mice with letrozole (LET)-induced PCOS. We also tested the correlations between the relative abundance of microbial taxa and selected PCOS parameters. RESEARCH METHODS &

What were the most important findings?

Placebo + HF/HFr and LET + HF/HFr had significantly higher microbial alpha diversity than either group fed StD. The LET-implanted mice fed StD had a significantly higher abundance of Prevotellaceae_UCG-001 than the placebo mice fed StD. Both groups fed the HF/HFr diet had significantly lower fecal levels of short-chain fatty acids than the placebo mice fed StD, while the LET + HF/HFr animals had significantly higher concentrations of lipopolysaccharides in blood serum than either the placebo or LET mice fed StD. Opposite correlations were observed between Turicibacter and Lactobacillus and the lipid profile,

What are the greatest implications of this study?

HF/HFr diet had a much stronger effect on the composition of the intestinal microbiota of prepubertal mice than LET itself.

What was studied?

This pilot prospective cohort study examined whether ethnicity influences gut microbiome dysbiosis in pregnancies complicated by gestational diabetes mellitus (GDM). The researchers also investigated whether diet and lifestyle modifications made after a GDM diagnosis could modulate the gut microbiome. Fecal samples were collected at two time points, 24 to 28 weeks and 36 to 40 weeks of gestation, and analyzed using targeted 16S rRNA gene-based amplicon sequencing. Statistical comparisons between groups used PERMANOVA, differential abundance testing used DeSeq2, and functional predictions were generated with PICRUSt2.

Who was studied?

The cohort included 53 women with GDM and 16 women without GDM, all residing in Singapore. Participants belonged to three Asian ethnic groups: Chinese, Malay, and Indian. This design allowed comparison of gut dysbiosis patterns both across GDM status and across ethnic background within the same population.

What were the most important findings?

Among women with GDM, gut microbiomes from the different ethnic groups shared common features rather than diverging by ethnicity. This suggests that GDM-related dysbiosis is a relatively consistent phenomenon across the Chinese, Malay, and Indian groups studied. The abstract indicates that ethnicity was not a major driver of the microbiome differences observed in these GDM pregnancies.

What are the greatest implications of this study?

If GDM-associated gut dysbiosis is largely independent of Asian ethnic background, microbiome-targeted strategies for GDM may generalize across these ethnic groups rather than needing ethnicity-specific approaches. This supports the idea that dietary and lifestyle interventions after a GDM diagnosis could be evaluated and applied similarly across diverse populations. As a pilot study, these findings point to the need for larger cohorts to confirm whether microbiome-based interventions can be standardized across ethnicities.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

Polycystic ovary syndrome (PCOS) is an endocrinopathy in childbearing-age females which can cause many complications, such as diabetes, obesity, and dyslipidemia. The metabolic disorders in patients with PCOS were linked to gut microbial dysbiosis. However, the correlation between the gut microbial community and dyslipidemia in PCOS remains unillustrated. Our study elucidated the different gut microbiota in patients with PCOS and dyslipidemia (PCOS.D) compared to those with only PCOS and healthy women.

What were the most important findings?

In total, 18 patients with PCOS, 16 healthy females, and 18 patients with PCOS.D were enrolled. The 16 S rRNA sequencing in V3-V4 region was utilized for identifying the gut microbiota, which analyzes species annotation, community diversity, and community functions. Our results showed that the β diversity of gut microbiota did not differ significantly among the three groups. Regarding gut microbiota dysbiosis, patients with PCOS showed a decreased abundance of Proteobacteria, and patients with PCOS.D showed an increased abundance of Bacteroidota compared to other groups. With respect to the gut microbial imbalance at genus level, the PCOS.D group showed a higher abundance of Clostridium_sensu_stricto_1 compared to other two groups. Furthermore, the abundances of Faecalibacterium and Holdemanella were lower in the PCOS.D than those in the PCOS group. Several genera, including Faecalibacterium and Holdemanella, were negatively correlated with the lipid profiles. Pseudomonas was negatively correlated with luteinizing hormone levels. Using PICRUSt analysis, the gut microbiota community functions suggested that certain metabolic pathways (e.g., amino acids, glycolysis, and lipid) were altered in PCOS.D patients as compared to those in PCOS patients.

What are the greatest implications of this study?

The gut microbiota characterizations in patients with PCOS.D differ from those in patients with PCOS and controls, and those might also be related to clinical parameters. This may have the potential to become an alternative therapy to regulate the clinical lipid levels of patients with PCOS in the future.

What was studied?

This study examined gut microbial features associated with Parkinson's disease (PD) by meta-analyzing shotgun metagenomic sequencing data across six independent datasets from different countries. The researchers also established GC-MS and LC-MS/MS assays to directly quantify fecal short-chain fatty acids (SCFAs) and fecal polyamines. They analyzed taxonomic composition, functional gene pathways, and carbohydrate-active enzymes (CAZymes) in relation to PD status, adjusting for confounding factors.

Who was studied?

The core dataset consisted of 94 PD patients and 73 controls whose fecal samples were shotgun sequenced in Japan. This Japanese cohort was combined with five previously reported datasets from the USA, Germany, China (two separate cohorts), and Taiwan. In total, the meta-analysis spanned six countries, giving the study an international, multi-cohort scope rather than a single-population sample.

What were the most important findings?

Across all six datasets, alpha-diversity was consistently increased in PD. Taxonomic analysis showed Akkermansia muciniphila was increased in PD, while Roseburia intestinalis and Faecalibacterium prausnitzii, both associated with anti-inflammatory, butyrate-related commensal activity, were decreased. Genes for riboflavin and biotin biosynthesis and five of six CAZyme categories were markedly decreased in PD, and fecal SCFAs and polyamines were significantly reduced, with riboflavin/biotin gene abundance positively correlated with these metabolite levels.

What are the greatest implications of this study?

The convergent, cross-country decrease in Faecalibacterium prausnitzii, Roseburia intestinalis, SCFAs, and polyamines suggests a reproducible loss of beneficial, anti-inflammatory commensal function in PD gut microbiota. Because the specific bacteria driving reduced riboflavin biosynthesis differed between Japan/USA/Germany and China1/China2/Taiwan, the findings imply that shared functional deficits in PD can arise from different taxonomic routes depending on population. This points toward B-vitamin biosynthesis and short-chain fatty acid/polyamine metabolism as potential functional biomarkers or intervention targets for PD that generalize better across populations than single-taxon signatures.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study used deep shotgun metagenomic sequencing to characterize the taxonomic and functional composition of the gut microbiome in older adults from Singapore. The researchers examined how gut microbial communities and their metabolic capabilities relate to aging phenotypes. They performed joint species-level analysis together with other Asian cohorts to identify age-associated shifts in microbial composition and function. The work also linked microbiome features to clinical markers of inflammation, cardiometabolic health, and liver health.

Who was studied?

The cohort consisted of 234 community-living octogenarians in Singapore who were described as well-phenotyped. Their gut microbiomes were compared jointly against data from other Asian cohorts to identify consistent age-associated species shifts. The abstract does not specify sex distribution, exact age range beyond octogenarian status, or additional demographic details.

What were the most important findings?

Aging was associated with reduced microbial richness and enrichment of specific Alistipes and Bacteroides species, including Alistipes shahii and Bacteroides xylanisolvens. Functional analysis showed a corresponding expansion of metabolic potential toward pathways synthesizing and utilizing amino-acid precursors, in contrast to the dominant butyrate-producing guilds such as Faecalibacterium prausnitzii and Roseburia inulinivorans that generate butyrate from pyruvate. The study also identified more than ten robust microbial associations with inflammation and with cardiometabolic and liver health markers, including a potential probiotic species, Parabacteroides goldsteinii.

What are the greatest implications of this study?

The findings suggest that healthy aging in this population is accompanied by a measurable shift away from butyrate-producing commensals like Faecalibacterium prausnitzii toward microbes with alternate amino-acid metabolic capacity. This shift, combined with the identified links to inflammation and cardiometabolic and liver health markers, points to specific microbial species and pathways that could serve as biomarkers or targets for supporting healthy aging. The results also highlight potential probiotic candidates, such as Parabacteroides goldsteinii, for further investigation in aging-related interventions.

What was studied?

IgA nephropathy (IgAN) is intimately linked to mucosal immune responses, with nasopharyngeal and intestinal lymphoid tissues being crucial for its abnormal mucosal immunity. The specific pathogenic bacteria in these sites associated with IgAN, however, remain elusive. Our study employs 16S rRNA sequencing and machine learning (ML) approaches to identify specific pathogenic bacteria in these locations and to investigate common pathogens that may exacerbate IgAN.

Who was studied?

In this cross-sectional analysis, we collected pharyngeal swabs and stool specimens from IgAN patients and healthy controls. We applied 16SrRNA sequencing to identify differential microbial populations. ML algorithms were then used to classify IgAN based on these microbial differences. Spearman correlation analysis was employed to link key bacteria with clinical parameters.

What were the most important findings?

We observed a reduced microbial diversity in IgAN patients compared to healthy controls. In the gut microbiota of IgAN patients, increases in Bacteroides, Escherichia-Shigella, and Parabacteroides, and decreases in Parasutterella, Dialister, Faecalibacterium, and Subdoligranulum were notable. In the respiratory microbiota, increases in Neisseria, Streptococcus, Fusobacterium, Porphyromonas, and Ralstonia, and decreases in Prevotella, Leptotrichia, and Veillonella were observed. Post-immunosuppressive therapy, Oxalobacter and Butyricoccus levels were significantly reduced in the gut, while Neisseria and Actinobacillus levels decreased in the respiratory tract. Veillonella and Fusobacterium appeared to influence IgAN through dual immune loci, with Fusobacterium abundance correlating with IgAN severity.

What are the greatest implications of this study?

This study revealing that changes in flora structure could provide important pathological insights for identifying therapeutic targets, and ML could facilitate noninvasive diagnostic methods for IgAN.

What was studied?

Dysbiosis of the microbiome is a key hallmark of polycystic ovary syndrome (PCOS). However, the interaction between the host and microbiome and its relevance to the pathogenesis of PCOS remain unclear.

Who was studied?

To evaluate the role of the commensal gut microbiome in PCOS, we gavaged germ-free mice with the fecal microbiota from patients with PCOS or healthy individuals and evaluated the reproductive endocrine features of the recipient mice.

What were the most important findings?

Mice transplanted with fecal microbiota from PCOS patients and those transplanted from healthy controls presented different bacterial profiles and reproductive endocrine features. The fecal microbiota of the mice in the PCOS group was enriched in Phocaeicola, Mediterraneibacter, Oscillospiraceae, Lawsonibacter and Rikenellaceae. Fecal microbiota transplantation (FMT) from PCOS patients induced increased disruption of ovarian functions, lipo-metabolic disturbance, insulin resistance and an obese-like phenotype in recipient mice.

What are the greatest implications of this study?

Our findings suggest that the microbiome may govern the set point of PCOS-bearing individuals and that gut ecosystem manipulation may be a useful marker and target for the management of PCOS.

What was studied?

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.

Who was studied?

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.

What were the most important 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.

What are the greatest implications of this study?

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.

What was studied?

This study examined whether iron overload in thalassemia patients is linked to gut dysbiosis and cognitive impairment through the gut-brain axis. Researchers assessed iron burden, cognitive function, and both gut and blood microbiome composition across different blood-transfusion regimens. The goal was to determine whether specific microbial shifts track with iron accumulation and cognitive status in this population.

Who was studied?

Sixty participants were recruited, comprising healthy controls, transfusion-dependent thalassemia (TDT) patients, and non-transfusion-dependent thalassemia (NTDT) patients. TDT patients receive more frequent blood transfusions and, consistent with this, showed greater iron overload than NTDT patients. This design allowed comparisons of gut and blood microbiota across a spectrum of iron-overload severity within the same disease population.

What were the most important findings?

Most thalassemia patients developed gut dysbiosis, and about 25% developed minor cognitive impairment. Both TDT and NTDT groups showed increased Fusobacteriota and Verrucomicrobiota with decreased Fibrobacterota, and TDT patients had more abundant Verrucomicrobia, described as beneficial bacteria. Iron overload correlated with cognitive impairment, and increased Butyricimonas with decreased Paraclostridium was associated with higher cognitive function. No blood microbiota was detected, and blood bacterial profiles did not differ significantly between thalassemia patients and controls.

What are the greatest implications of this study?

The findings suggest that iron overload in thalassemia is associated with gut microbial imbalance that may relate to cognitive outcomes through the gut-brain axis. Specific gut taxa such as Butyricimonas and Paraclostridium emerge as candidate markers linked to cognitive function, while the blood compartment appears not to harbor a distinct microbiome signal in this context. This points to the gut, rather than blood, as the more relevant site for future investigation of microbiome-cognition relationships in iron-overloaded thalassemia patients.

What was studied?

This study examined the biogeography of the mucosa-associated microbiome (MAM) across different segments of the upper and lower gastrointestinal tract. Researchers compared microbial composition and bacterial load between patients with inflammatory bowel disease (IBD) and controls. They also looked at how the MAM related to proton pump inhibitor (PPI) use, gastrointestinal symptom severity, and symptom response to a standardised nutrient challenge. Microbial composition was assessed with 16S rRNA gene amplicon sequencing, and bacterial load was measured by qPCR on mucosal biopsies.

Who was studied?

The study included 59 controls without structural gastrointestinal abnormalities or symptoms, 44 patients with ulcerative colitis, and 31 patients with Crohn's disease. Biopsies were collected from multiple segments of both the upper and lower gastrointestinal tract in these participants. This gives a total of 134 individuals across three clinical groups.

What were the most important findings?

Microbial communities differed between the upper and lower gastrointestinal tract in their mucosal composition. IBD patients showed relative and absolute depletion of numerous genera known to produce butyrate and/or propionate compared with controls. The largest difference observed was depletion of Faecalibacterium in the lower gastrointestinal tract of patients with Crohn's disease. The abstract also indicates that PPI users showed a notable difference in the MAM, though the specific finding is cut off in the provided text.

What are the greatest implications of this study?

The findings suggest that loss of short-chain fatty acid producing bacteria, particularly Faecalibacterium, is a hallmark of mucosal dysbiosis in Crohn's disease at the site of tissue contact rather than only in stool. Mapping microbiome differences by gastrointestinal segment highlights that biogeography matters when interpreting mucosal microbiome studies in IBD. The association with PPI use also points to medication exposure as a factor that should be accounted for when characterizing the mucosa-associated microbiome in these patients.

What was studied?

This study investigated the microbial and metabolic profile of the gut-lung axis in children with pulmonary arterial hypertension associated with congenital heart disease (PAH-CHD). The researchers used an integrated multi-omics approach, analyzing metabolites and microbiota from both the gut and lower respiratory tract. Their goal was to characterize how gut and pulmonary microbiome and metabolome profiles relate to each other in PAH-CHD and to explore the potential diagnostic value of these profiles.

Who was studied?

The study recruited 15 healthy individuals and 15 patients with pulmonary arterial hypertension due to congenital heart disease. Participants were drawn from Fuwai Yunnan Hospital, Chinese Academy of Medical Sciences, and Kunming Children's Hospital. This design allowed direct comparison of gut and lower respiratory tract samples between affected children and healthy controls.

What were the most important findings?

The gut and pulmonary microbiota of children with PAH-CHD showed an increased abundance of beneficial symbionts compared to healthy individuals. These microbial shifts were closely linked to accompanying metabolite changes, indicating coordinated alterations across the gut-lung axis. The abstract does not specify particular taxa such as Salmonella, Salmonella enterica, typhoid-associated organisms, or the Enterobacteriaceae, so no claims about those groups can be made from this study.

What are the greatest implications of this study?

The findings support the idea that the gut-lung axis is disrupted in pediatric PAH-CHD and may play a role in disease progression through immune and metabolic pathways. Because distinct microbiome and metabolome signatures were identified, these profiles could potentially serve as aids in diagnosing PAH-CHD. Further validation would be needed before such profiles could be used clinically, but the results point toward the microbiome as a relevant factor in this cardiopulmonary condition.

What was studied?

Constipation is a common symptom in maintenance hemodialysis patients and greatly affects the quality of survival of hemodialysis patients. Fecal microbiota transplantation and probiotics are feasible treatments for functional constipation, but there is still a gap in the research on the characteristics of gut flora in patients with maintenance hemodialysis combined with constipation. The aim of this study is to clarify the characteristics of the intestinal flora and its changes in maintenance hemodialysis patients with constipation.

Who was studied?

Fecal samples were collected from 45 participants, containing 15 in the maintenance hemodialysis constipation group,15 in the maintenance hemodialysis non-constipation group and 15 in the healthy control group. These samples were analyzed using 16S rRNA gene sequencing. The feature of the intestinal microbiome of maintenance hemodialysis constipation group and the microbiome differences among the three groups were elucidated by species annotation analysis, α-diversity analysis, β-diversity analysis, species difference analysis, and predictive functional analysis.

What were the most important findings?

The alpha diversity analysis indicated that maintenance hemodialysis constipation group was less diverse and homogeneous than maintenance hemodialysis non-constipation group and healthy control group. At the genus level, the top ten dominant genera in maintenance hemodialysis constipation group patients were Enterococcus, Escherichia-Shigella, Bacteroides, Streptococcus, Bifidobacterium, Ruminococcus_gnavus_group, Lachnospiraceae_unclassified, Faecalibacterium, Akkermansia and UCG-002. Compared with non-constipation group, the Enterococcus, Rhizobiales_unclassified, Filomicrobium, Eggerthella, Allobaculum, Prevotella_7, Gordonibacter, Mitochondria_unclassified, Lachnoanaerobaculum were significantly higher in constipation group (p<0.05). Compared with non-constipation group, the Kineothrix, Rhodopirellula, Weissella were significantly lower in constipation group (p<0.05). The predictive functional analysis revealed that compared with non-constipation group, constipation group was significantly enriched in pathways associated with pyruate metabolism, flavonoid biosynthesis.

What are the greatest implications of this study?

This study describes for the first time the intestinal microbiome characteristics of maintenance hemodialysis patients with constipation. The results of this study suggest that there is a difference in the intestinal flora between maintenance hemodialysis patients with constipation and maintenance hemodialysis patients without constipation.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

The gut microbiota plays a pivotal role in ulcerative colitis (UC) development. This study explores the impact of latent tuberculosis infection (LTBI) on the gut microbiota in UC and assesses changes during vedolizumab treatment, investigating prophylactic anti-tuberculosis therapy.

What were the most important findings?

This cohort study included adult patients with UC receiving vedolizumab treatment at Jinhua Hospital, Zhejiang University from April 2021 to December 2022. Patients were divided into LTBI (n = 24) and non-LTBI (n = 21) groups. Patients in the LTBI group were further subdivided into prophylactic (n = 13) and non-prophylactic (n = 11) groups. Clinical and fecal samples were collected pre- and post-vedolizumab treatment for the LTBI groups and pre-treatment for the non-LTBI group. The gut microbiota was analyzed using 16 S rRNA sequencing. Patients in the non-LTBI group exhibited higher diversity indices. Vedolizumab demonstrated efficacy in the LTBI group, with clinical response and remission rates of 83.3% and 75.0%, respectively. The gut microbiota diversity in the LTBI group increased post-vedolizumab treatment, and receiving prophylactic isoniazid showed no significant difference in vedolizumab treatment response compared to not receiving prophylactic isoniazid. Microbiota changes were similar between groups, with an increase in [Ruminococcus] expression after vedolizumab treatment.

What are the greatest implications of this study?

This cohort study, conducted at a single center, highlights that LTBI can reduce gut microbiota diversity among adult patient with UC. The observed efficacy of vedolizumab treatment in the LTBI group indicates a potential association with microbiota changes. However, mono-isoniazid exhibited limited impact, underscoring the potential of vedolizumab as a promising candidate for prophylactic anti-tuberculosis treatment in the context of UC.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study investigated the microbiome associated with ovarian cancer (OC) and its potential role in detection, disease progression, and prognosis. Researchers examined microbial taxa across multiple body sites in OC patients compared with a benign cohort. The aim was to identify microbial indicators that could aid early detection, track disease stage and grade, and predict treatment response.

Who was studied?

The abstract does not give a specific cohort size or demographic description. It describes an OC patient cohort compared against a benign cohort, with sampling across several body sites; stool and omentum were sampled in the OC cohort but not in the benign cohort. Beyond this, the population can only be described in general terms as ovarian cancer patients versus patients with benign gynecological conditions.

What were the most important findings?

The researchers identified a distinct OC microbiome with general enrichment of several microbial taxa, including Dialister, Corynebacterium, Prevotella, and Peptoniphilus, across body sites in the OC cohort. These same taxa were depleted in advanced-stage and high-grade OC patients compared with early-stage and low-grade patients, suggesting decreased accumulation as disease advances. The mainly pathogenic taxa were also more abundant in OC patients with adverse treatment outcomes compared to those without treatment-related events.

What are the greatest implications of this study?

The enrichment and depletion patterns of these taxa suggest they could serve as potential indicators for early detection of ovarian cancer. Their accumulation in patients with adverse treatment outcomes suggests they could also help predict how patients will respond to treatment. Together these findings point to a possible diagnostic and prognostic role for the OC-associated microbiome, though the abstract does not describe validation in an independent cohort.

What was studied?

Colorectal polyps are common precursors of colorectal cancer (CRC) and are influenced by various lifestyle and environmental factors. Increasing evidence highlights the role of gut microbiota in the development of intestinal diseases, including CRC. Previous studies have reported differences between mucosal and faecal microbiota, with certain taxa such as Fusobacterium and Bacteroides fragilis being implicated in disease progression. However, microbiota signatures across different sampling sites in individuals with colorectal polyps remain unclear. This study aimed to characterize and compare the gut microbiota in faecal samples, normal colorectal mucosa, and polyp tissues from patients with colorectal polyps, as well as in healthy individuals. Using 16S rRNA gene sequencing and bioinformatic analysis, the study evaluates differences in microbial composition across these sites. The findings are expected to provide insight into site-specific microbiota variations and contribute to understanding microbial changes involved in the progression from colorectal polyps to colorectal cancer.

What were the most important findings?

Transplantation of the SD-gut microbiota into normal mice induced microglia overactivation and neuronal apoptosis in the hippocampus, cognitive decline, and colonic microbiota disorder, manifesting as increased levels of Aeromonas and LPS and decreased levels of Lachnospiraceae_NK4A136 and butyrate. All these events were reversed with the transplantation of SD + melatonin-gut microbiota. Colonization with Aeromonas and the addition of LPS produced an inflammatory response in the hippocampus and spatial memory impairment in mice. These changes were reversed by supplementation with melatonin, accompanied by decreased levels of Aeromonas and LPS. Butyrate administration to sleep-deprived mice restored inflammatory responses and memory impairment. In vitro, LPS supplementation caused an inflammatory response in BV2 cells, which was improved by butyrate supplementation. This ameliorative effect of butyrate was blocked by pretreatment with MCT1 inhibitor and HDAC3 agonist but was mimicked by TLR4 and p-P65 antagonists.

What are the greatest implications of this study?

Gut microbes and their metabolites mediate the ameliorative effects of melatonin on SD-induced cognitive impairment. A feasible mechanism is that melatonin downregulates the levels of Aeromonas and constituent LPS and upregulates the levels of Lachnospiraceae_NK4A136 and butyrate in the colon. These changes lessen the inflammatory response and neuronal apoptosis in the hippocampus through crosstalk between the TLR4/NF-κB and MCT1/ HDAC3 signaling pathways. Video Abstract.

What was studied?

Metabolites secreted by the gut microbiota may play an essential role in microbiota-gut-central nervous system crosstalk. In this study, we explored the changes occurring in the gut microbiota and their metabolites in patients with spinal cord injury (SCI) and analyzed the correlations among them.

Who was studied?

The structure and composition of the gut microbiota derived from fecal samples collected from patients with SCI (n = 11) and matched control individuals (n = 10) were evaluated using 16S rRNA gene sequencing. Additionally, an untargeted metabolomics approach was used to compare the serum metabolite profiles of both groups. Meanwhile, the association among serum metabolites, the gut microbiota, and clinical parameters (including injury duration and neurological grade) was also analyzed. Finally, metabolites with the potential for use in the treatment of SCI were identified based on the differential metabolite abundance analysis.

What were the most important findings?

The composition of the gut microbiota was different between patients with SCI and healthy controls. At the genus level, compared with the control group, the abundance of UBA1819, Anaerostignum, Eggerthella, and Enterococcus was significantly increased in the SCI group, whereas that of Faecalibacterium, Blautia, Escherichia-Shigella, Agathobacter, Collinsella, Dorea, Ruminococcus, Fusicatenibacter, and Eubacterium was decreased. Forty-one named metabolites displayed significant differential abundance between SCI patients and healthy controls, including 18 that were upregulated and 23 that were downregulated. Correlation analysis further indicated that the variation in gut microbiota abundance was associated with changes in serum metabolite levels, suggesting that gut dysbiosis is an important cause of metabolic disorders in SCI. Finally, gut dysbiosis and serum metabolite dysregulation was found to be associated with injury duration and severity of motor dysfunction after SCI.

What are the greatest implications of this study?

We present a comprehensive landscape of the gut microbiota and metabolite profiles in patients with SCI and provide evidence that their interaction plays a role in the pathogenesis of SCI. Furthermore, our findings suggested that uridine, hypoxanthine, PC(18:2/0:0), and kojic acid may be important therapeutic targets for the treatment of this condition.

What was studied?

The microbiome-gut-brain axis plays a role in anxiety, the stress response and social development, and is of growing interest in neuropsychiatric conditions. The gut microbiota shows compositional alterations in a variety of psychiatric disorders including depression, generalised anxiety disorder (GAD), autism spectrum disorder (ASD) and schizophrenia but studies investigating the gut microbiome in social anxiety disorder (SAD) are very limited. Using whole-genome shotgun analysis of 49 faecal samples (31 cases and 18 sex- and age-matched controls), we analysed compositional and functional differences in the gut microbiome of patients with SAD in comparison to healthy controls. Overall microbiota composition, as measured by beta-diversity, was found to be different between the SAD and control groups and several taxonomic differences were seen at a genus- and species-level. The relative abundance of the genera Anaeromassillibacillus and Gordonibacter were elevated in SAD, while Parasuterella was enriched in healthy controls. At a species-level, Anaeromassilibacillus sp An250 was found to be more abundant in SAD patients while Parasutterella excrementihominis was higher in controls. No differences were seen in alpha diversity. In relation to functional differences, the gut metabolic module 'aspartate degradation I' was elevated in SAD patients. In conclusion, the gut microbiome of patients with SAD differs in composition and function to that of healthy controls. Larger, longitudinal studies are warranted to validate these preliminary results and explore the clinical implications of these microbiome changes.

What was studied?

Type 2 diabetes mellitus (T2DM) is an independent risk factor for colorectal cancer (CRC), and the patients with CRC and T2DM have worse survival. The human gut microbiota (GM) is linked to the development of CRC and T2DM, respectively. However, the GM characteristics in patients with CRC and T2DM remain unclear.

Who was studied?

We performed fecal metagenomic and targeted metabolomics studies on 36 samples from CRC patients with T2DM (DCRC group, n = 12), CRC patients without diabetes (CRC group, n = 12), and healthy controls (Health group, n = 12). We analyzed the fecal microbiomes, characterized the composition and function based on the metagenomics of DCRC patients, and detected the short-chain fatty acids (SCFAs) and bile acids (BAs) levels in all fecal samples. Finally, we performed a correlation analysis of the differential bacteria and metabolites between different groups.

What were the most important findings?

Compared with the CRC group, LefSe analysis showed that there is a specific GM community in DCRC group, including an increased abundance of Eggerthella , Hungatella , Peptostreptococcus , and Parvimonas , and decreased Butyricicoccus , Lactobacillus , and Paraprevotella . The metabolomics analysis results revealed that the butyric acid level was lower but the deoxycholic acid and 12-keto-lithocholic acid levels were higher in the DCRC group than other groups ( P < 0.05). The correlation analysis showed that the dominant bacterial abundance in the DCRC group ( Parvimonas , Desulfurispora , Sebaldella , and Veillonellales , among others) was negatively correlated with butyric acid, hyodeoxycholic acid, ursodeoxycholic acid, glycochenodeoxycholic acid, chenodeoxycholic acid, cholic acid and glycocholate. However, the abundance of mostly inferior bacteria was positively correlated with these metabolic acid levels, including Faecalibacterium , Thermococci , and Cellulophaga .

What are the greatest implications of this study?

Unique fecal microbiome signatures exist in CRC patients with T2DM compared to those with non-diabetic CRC. Alterations in GM composition and SCFAs and secondary BAs levels may promote CRC development.

What was studied?

This study examined whether Faecalibacterium prausnitzii, a next-generation probiotic candidate, could mitigate nonalcoholic steatohepatitis (NASH). The researchers used 16S rRNA sequencing to analyze gut microbiota composition and tested oral administration of F. prausnitzii strains in a mouse model of NASH induced by a high-fructose high-fat diet over 16 weeks. Outcomes were assessed using oral glucose tolerance tests, biochemical assays, and histological analyses of liver tissue.

Who was studied?

The abstract describes two study populations. First, patients with NASH and healthy controls underwent 16S rRNA sequencing analysis of their gut microbiota. Second, four F. prausnitzii strains (EB-FPDK3, EB-FPDK9, EB-FPDK11, and EB-FPYYK1) were isolated from fecal samples of four healthy individuals and then tested in mice fed a high-fructose high-fat diet to induce NASH.

What were the most important findings?

The 16S rRNA sequencing analyses confirmed differences in gut microbiota between NASH patients and healthy controls, supporting a link between dysbiosis and NASH pathophysiology. The abstract text is truncated before the specific results of the mouse experiments are given, so the precise magnitude of hepatic protection cannot be stated. However, the study's framing indicates that F. prausnitzii administration was evaluated for its ability to alleviate characteristic NASH phenotypes, including glucose tolerance, biochemical markers, and liver histology.

What are the greatest implications of this study?

The findings support the premise that F. prausnitzii, a commensal gut bacterium, may serve as a next-generation probiotic for the prevention or treatment of NASH. This work extends probiotic research beyond traditional strains and highlights gut dysbiosis as a therapeutic target in fatty liver disease. If confirmed, it points toward microbiome-based interventions as a strategy for mitigating hepatic damage in metabolic liver disease.

What was studied?

Constipation is a common disease affecting humans. Bifidobacterium longum is reportedly effective in relieving constipation. Current studies generally focus on the dose–response relationship of oral doses; however, the dose–effect relationship of B. longum in the colon, which is the primary site where B. longum exerts constipation-relieving effects, to treat constipation has not been studied. Herein, three strains of B. longum (FGSZY6M4, FJSWXJ10M2, and FSDJN6M3) were packaged in colon-released capsules to explore the dose–effect relationship in the colon. For each strain, three groups of capsules (104, 106, and 108 CFU/capsule, respectively) and one group of free probiotics (108 CFU/mL) were used to explore the colonic dose effect of B. longum. The results showed that the three strains of B. longum improved fecal water content and promoted intestinal motility by regulating gastrointestinal peptide (MTL, GAS, and VIP), aquaporin-3, and 5-hydroxytryptamine levels while promoting gastrointestinal motility and relieving constipation by regulating the intestinal flora composition of constipated rats and changing their metabolite content (short-chain fatty acids). Among the three free bacterial solution groups (108 CFU/mL), FGSZY6M4 was the most effective in relieving constipation caused by loperamide hydrochloride in rats. The optimal effective dose of each strain was 6M4 (104 CFU/day), 10M2 (106 CFU/day), and S3 (108 CFU/day) of the colon-released capsules. Therefore, for some effective strains, the dose of oral probiotics can be reduced by colon-released capsules, and constipation can be relieved without administering a great number of bacterial solutions. Therefore, investigating the most effective dose of B. longum at the colon site can help to improve the efficiency of relieving constipation.

What was studied?

This study examined the gut microbiome and serum metabolome in patients with functional constipation (FC), a common gastrointestinal disorder that significantly affects physical and mental health. The researchers used 16S rRNA microbial genomics to profile gut microbiota composition and non-target metabolomics based on liquid chromatography-mass spectrometry to characterize serum metabolic profiles. The study was designed to address inconsistent prior findings on the gut microbiome and FC, and to better link microbiome changes to host metabolites.

Who was studied?

The study included 30 patients with functional constipation and 28 healthy individuals as a comparison group. Fecal samples were used for 16S rRNA gut microbiota analysis and serum samples were used for metabolomic profiling in these participants. The abstract does not specify additional demographic details such as age or sex distribution.

What were the most important findings?

FC patients had distinct gut microbiota structures and serum metabolic profiles compared to healthy individuals. Patients with FC showed increased levels of Bacteroides and of several butyrate-producing bacteria, including Roseburia, Faecalibacterium, and Butyricicoccus. Serum levels of upstream products of host arginine biosynthesis, specifically 2-oxoglutaric acid, L-glutamic acid, N-acetylornithine, and L-ornithine, were significantly reduced in FC patients.

What are the greatest implications of this study?

The findings suggest that functional constipation may be associated with an altered gut microbiota, including increased Bacteroidetes, alongside downregulation of host arginine biosynthesis intermediates. This points to a potential link between specific gut bacteria and disrupted host amino acid metabolism in FC. The pairing of microbiome and metabolome data offers a more integrated view of FC pathophysiology than microbiome data alone, which could inform future mechanistic or therapeutic research.

What was studied?

The microbiome has been implicated in the initiation and progression of colorectal cancer (CRC) in cross-sectional studies. However, there is a lack of studies using prospectively collected samples.

Who was studied?

From the Norwegian Colorectal Cancer Prevention (NORCCAP) trial, we analyzed 144 archived fecal samples from participants who were diagnosed with CRC or high-risk adenoma (HRA) at screening and from participants who remained cancer-free during 17 years of follow-up. We performed 16S rRNA sequencing of all the samples and metagenome sequencing on a subset of 47 samples. Differences in taxonomy and gene content between outcome groups were assessed for alpha and beta diversity and differential abundance.

What were the most important findings?

Diversity and composition analyses showed no significant differences between CRC, HRA, and healthy controls. Phascolarctobacterium succinatutens was more abundant in CRC compared with healthy controls in both the 16S and metagenome data. The abundance of Bifidobacterium and Lachnospiraceae spp. was associated with time to CRC diagnosis.

What are the greatest implications of this study?

Using a longitudinal study design, we identified three taxa as being potentially associated with CRC. These should be the focus of further studies of microbial changes occurring prior to CRC diagnosis.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

The ketogenic diet (KD) is recommended to improve polycystic ovary syndrome (PCOS); however, its mechanisms of action are unclear. We aimed to study the effects and mechanisms of action of the KD on the gut microbiome and metabolites in PCOS rats and determine whether the sex hormone regulatory effects are related to modulations of the gut microbiota and metabolites.

Who was studied?

PCOS was induced with a high-fat diet and letrozole in the rats. A KD was fed to rats for 8 wk, serum samples were collected for biochemical analysis, and the rats' fecal samples were subjected to 16S ribosomal RNA sequencing and metabolomic analysis.

What were the most important findings?

Feeding with a KD for 8 wk suppressed body weight gain, decreased luteinizing hormone and androgen levels, and improved insulin levels. Furthermore, the KD reversed the dysregulation of the gut microbiota in PCOS rats by adjusting the ratio of firmicutes and bacteroidetes. Also, the KD was involved in hormonal metabolic pathways by reducing the levels of some metabolites (such as testosterone and 7α-hydroxytestosterone) that are closely related to gut microbes.

What are the greatest implications of this study?

The KD improved the clinical phenotype and insulin resistance in PCOS rats and altered the composition of the gut microbiome and metabolites, which were associated with androgen metabolism, representing a potential mechanism for mediating the effects of the KD on sex hormone metabolism in PCOS. However, our study found contradictory effects of KD on the gut microbiome in PCOS, which need further research.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

Gastric cancer is one of the leading causes of death worldwide, and resections are performed to cure the disease. We have previously reported the changes in the gastric microbiota after gastric cancer resection, which may be associated with the oral microbiota; however, the changes in the oral microbiota remain uncharacterized. This study aimed to characterize the changes in the salivary microbiota caused by gastric cancer resection and to evaluate their association with the gastric fluid microbiota. Saliva and gastric fluid samples were collected from 63 patients who underwent gastrectomy before and after surgery, and a 16S rRNA metagenomic analysis was performed to compare the microbiota composition. The number of bacterial species in the salivary microbiota decreased, and the bacterial composition changed after the resection of gastric cancer. In addition, we identified several bacterial genera that varied significantly in the salivary microbiota, some of which also showed similar changes in the gastric fluid microbiota. These findings indicate that changes in the gastric environment affect the oral microbiota, emphasizing the close association between the oral and gastric fluid microbiota. Our study signifies the importance of focusing on the oral microbiota in the perioperative period of gastrectomy in patients with gastric cancer.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

The most common toxic side effect after chemotherapy, one of the main treatments for colorectal cancer (CRC), is myelosuppression. To analyze the correlation between gut microbiota and leukopenia after chemotherapy in CRC patients.

Who was studied?

Stool samples were collected from 56 healthy individuals and 55 CRC patients. According to the leukocytes levels in peripheral blood, the CRC patients were divided into hypoleukocytes group (n = 13) and normal leukocytes group (n = 42). Shannon index, Simpson index, Ace index, Chao index and Coverage index were used to analyze the diversity of gut microbiota. LDA and Student's t-test(St test) were used for analysis of differences. Six machine learning algorithms, including logistic regression (LR) algorithm, random forest (RF) algorithm, neural network (NN) algorithm, support vector machine (SVM) algorithm, catboost algorithm and gradient boosting tree algorithm, were used to construct the prediction model of gut microbiota with leukopenia after chemotherapy for CRC.

What were the most important findings?

Compared with healthy group, the microbiota alpha diversity of CRC patients was significantly decreased (p < 0.05). After analyzing the gut microbiota differences of the two groups, 15 differential bacteria, such as Bacteroides, Faecalibacterium and Streptococcus, were screened. RF prediction model had the highest accuracy, and the gut microbiota with the highest predictive value were Peptostreptococcus, Faecalibacterium, and norank_f__Ruminococcaceae, respectively. Compared with normal leukocytes group, the microbiota alpha diversity of hypoleukocytes group was significantly decreased (p < 0.05). The proportion of Escherichia-Shigella was significantly decreased in the hypoleukocytes group. After analyzing the gut microbiota differences of the two groups, 9 differential bacteria, such as Escherichia-Shigella, Fusicatenibacter and Cetobacterium, were screened. RF prediction model had the highest accuracy, and the gut microbiota with the highest predictive value were Fusicatenibacte, Cetobacterium, and Paraeggerthella.

What are the greatest implications of this study?

Gut microbiota is related to leukopenia after chemotherapy. The gut microbiota may provide a novel method for predicting myelosuppression after chemotherapy in CRC patients.

What was studied?

Amphibian skin harbors microorganisms that are associated with the fungal pathogen Batrachochytrium dendrobatidis (Bd), which causes chytridiomycosis, one of the most significant wildlife diseases known. This pathogen originated in Asia, where diverse Bd lineages exist; hence, native amphibian hosts have co-existed with Bd over long time periods. Determining the nuances of this co-existence is crucial for understanding the prevalence and spread of Bd from a microbial context. However, associations of Bd with the natural skin microbiome remain poorly understood for Asian hosts, especially in relation to skin-associated fungi. We used 16 S rRNA and fungal internal transcribed spacer (ITS) gene sequencing to characterize the skin microbiome of four native Asian amphibian species and examined the relationships between Bd infection and their skin bacterial and fungal communities; we also analyzed the correlates of the putative anti-Bd bacteria. We show that both skin bacterial and fungal community structure and composition had significant associations with infection status (Bd presence/absence) and infection intensity (frequency of Bd sequence reads). We also found that the putative anti-Bd bacterial richness was correlated with Bd infection status and infection intensity, and observed that the relative abundance of anti-Bd bacteria roughly correspond with changes in both Bd prevalence and mean infection intensity in populations. Additionally, the microbial co-occurrence network of infected frogs was significantly different from that of uninfected frogs that were characterized by more keystone nodes (connectors) and larger proportions in correlations between bacteria, suggesting stronger inter-module bacterial interactions. These results indicate that the mutual effects between Bd and skin-associated microbiome, including the interplay between bacteria and fungi, might vary with Bd infection in susceptible amphibian species. This knowledge will help in understanding the dynamics of Bd from a microbial perspective, potentially contributing to mitigate chytridiomycosis in other regions of the world.

What was studied?

Growing evidence has demonstrated that patients undergoing peritoneal dialysis (PD) are more likely to experience cognitive impairment than patients with non-dialysis end-stage renal disease (ESRD); however, the underlying mechanisms remain unclear. This study aimed to identify the role and predictive significance of gut microbiome alterations in PD-associated cognitive impairment.

Who was studied?

A total of 29 non-dialysis ESRD patients and 28 PD patients were enrolled in this study and divided into subgroups according to the Montreal Cognitive Assessment (MoCA). Faecal samples were analyzed using 16 S rRNA. Mini-Mental State Examination (MMSE) and MoCA scores were used to assess the degree of cognitive impairment in patients.

What were the most important findings?

The 16 S rRNA analysis demonstrated differences in gut microbiome abundance and structure between PD and non-dialysis ESRD patients and between PD patients with cognitive impairment (PCI) and PD patients with normal cognition (PNCI). At family and genus levels, Prevotellaceae exhibited the greatest structure difference, while Lactobacillus exhibited the greatest abundance difference between PCI and PNCI. Altered microbiota abundance significantly correlated with cognitive function and serum indicators in PD. In addition, different modules related to fatty acid, lipid, pantothenate, and coenzyme A biosynthesis, and tyrosine and tryptophan metabolism were inferred from 16 S rRNA data between PCI and PNCI. Both groups could be distinguished using models based on the abundance of Lactobacillaceae (Area under curve [AUC] = 0.83), Actinomycetaceae (AUC = 0.798), and Prevotellaceae (AUC = 0.778) families and Lactobacillus (AUC = 0.848) and Actinomyces (AUC = 0.798) genera.

What are the greatest implications of this study?

Gut microbiome evaluation could aid early cognitive impairment diagnosis in patients undergoing PD.

What was studied?

Autism spectrum disorder (ASD) is associated with alterations in the gut microbiome. However, there are few studies on gut microbiota of children with ASD in China, and there is a lack of consensus on the changes of bacterial species. Autism spectrum disorder (ASD) is associated with alterations in the gut microbiome. However, there are few studies on gut microbiota of children with ASD in China, and there is a lack of consensus on the changes of bacterial species.

Who was studied?

We used 16S rRNA sequencing to analyze ASD children (2 to 12 years), HC (2 to 12 years).

What were the most important findings?

Our findings showed that the α-diversity, composition, and relative abundance of gut microbiota in the ASD group were significantly different from those in the HC groups. Compared with the HC group, the α-diversity in the ASD group was significantly decreased. At the genus level, the relative abundance of g_Faecalibacterium, g_Blautia, g_Eubacterium_eligens_group, g_Parasutterella, g_Lachnospiraceae_NK4A136_group and g_Veillonella in ASD group was significantly increased than that in HC groups, while the relative abundance of g_Prevotella 9 and g_Agathobacter was significantly decreased than that in HC groups. In addition, KEGG pathway analysis showed that the microbial functional abnormalities in ASD patients were mainly concentrated in metabolic pathways related to fatty acid, amino acid metabolism and aromatic compound metabolism, and were partially involved in neurotransmitter metabolism.

What are the greatest implications of this study?

This study revealed the characteristics of gut microbiota of Chinese children with ASD and provided further evidence of gut microbial dysbiosis in ASD.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

Alzheimer's disease (AD) is a heterogeneous disorder that spans a continuum with multiple phases, including preclinical, mild cognitive impairment, and dementia. Unlike for most other chronic diseases, human studies reporting on AD gut microbiota in the literature are very limited. With the scarcity of approved drugs for AD therapies, the rational and precise modulation of gut microbiota composition using diet and other tools is a promising approach to the management of AD. Such an approach could be personalized if an AD continuum can first be deconstructed into multiple strata based on specific microbiota features by using single or multiomics techniques. However, stratification of AD gut microbiota has not been systematically investigated before, leaving an important research gap for gut microbiota-based therapeutic approaches. Here, we analyze 16S rRNA amplicon sequencing of stool samples from 27 patients with mild cognitive impairment, 47 patients with AD, and 51 nondemented control subjects by using tools compatible with the compositional nature of microbiota. To stratify the AD gut microbiota community, we applied four machine learning techniques, including partitioning around the medoid clustering and fitting a probabilistic Dirichlet mixture model, the latent Dirichlet allocation model, and we performed topological data analysis for population-scale microbiome stratification based on the Mapper algorithm. These four distinct techniques all converge on Prevotella and Bacteroides stratification of the gut microbiota across the AD continuum, while some methods provided fine-scale resolution in stratifying the community landscape. Finally, we demonstrate that the signature taxa and neuropsychometric parameters together robustly classify the groups. Our results provide a framework for precision nutrition approaches aiming to modulate the AD gut microbiota. IMPORTANCE The prevalence of AD worldwide is estimated to reach 131 million by 2050. Most disease-modifying treatments and drug trials have failed, due partly to the heterogeneous and complex nature of the disease. Recent studies demonstrated that gut dybiosis can influence normal brain function through the so-called "gut-brain axis." Modulation of the gut microbiota, therefore, has drawn strong interest in the clinic in the management of the disease. However, there is unmet need for microbiota-informed stratification of AD clinical cohorts for intervention studies aiming to modulate the gut microbiota. Our study fills in this gap and draws attention to the need for microbiota stratification as the first step for microbiota-based therapy. We demonstrate that while Prevotella and Bacteroides clusters are the consensus partitions, the newly developed probabilistic methods can provide fine-scale resolution in partitioning the AD gut microbiome landscape.

What was studied?

The gut microbiota is implicated in the adverse developmental outcomes of postnatal iron supplementation. To generate hypotheses on how changes to the gut microbiota by iron adversely affect development, and to determine whether the form of iron influences microbiota outcomes, we characterized gut microbiome and metabolome changes in Sprague-Dawley rat pups given oral supplements of ferrous sulfate (FS), ferrous bis-glycinate chelate (FC), or vehicle control (CON) on postnatal day (PD) 2−14. Iron supplementation reduced microbiome alpha-diversity (p < 0.0001) and altered short-chain fatty acids (SCFAs) and trimethylamine (TMA) in a form-dependent manner. To investigate the long-term effects of iron provision in early life, an additional cohort was supplemented with FS, FC, or CON until PD 21 and then weaned onto standard chow. At ~8 weeks of age, young adult (YA) rats that received FS exhibited more diverse microbiomes compared to CON (p < 0.05), whereas FC microbiomes were less diverse (p < 0.05). Iron provision resulted in 10,000-fold reduced abundance of Lactobacilli in pre-weanling and YA animals provided iron in early life (p < 0.0001). Our results suggest that in pre-weanling rats, supplemental iron form can generate differential effects on the gut microbiota and microbial metabolism that persist into adulthood.

What was studied?

This pilot study examined the gut microbiota of patients with brain tumors to determine whether benign and malignant tumors are associated with distinct microbial patterns. It compared microbial diversity and composition across benign meningioma, malignant glioma, and healthy control groups. The work builds on prior evidence linking gut microbiota to tumor growth, including malignant gliomas, via the brain-gut axis.

Who was studied?

The study included 32 patients with benign meningioma, 27 patients with malignant glioma, and 41 healthy individuals as controls. This gives a total pilot cohort of 100 participants across the three groups. No further demographic details are provided in the abstract.

What were the most important findings?

Brain tumor patients, both meningioma and glioma groups, showed lower gut microbial diversity than healthy controls, with no significant diversity difference between the two tumor groups. Microbial composition differed significantly between tumor patients and healthy participants. Meningioma patients had increased pathogenic bacteria such as Enterobacteriaceae, while glioma patients showed overrepresentation of carcinogenic bacteria including Fusobacterium and Akkermansia. Both benign and malignant tumor groups lacked SCFA-producing probiotic bacteria.

What are the greatest implications of this study?

The findings suggest that gut microbial alterations, including reduced diversity and loss of SCFA-producing bacteria, are associated with the presence of brain tumors generally, while specific taxa may distinguish benign from malignant disease. The identification of a candidate microbial biomarker panel, including Fusobacterium, Akkermansia, Escherichia/Shigella, Lachnospira, and Agathobacter, points toward potential non-invasive markers for differentiating tumor types. As a pilot study, these results support further investigation into the brain-gut axis as a factor in brain tumor pathology.

What was studied?

This study examined the role of gut microbiota in two autoimmune thyroid conditions, Graves' disease (GD) and Hashimoto's thyroiditis (HT). Researchers used 16S sequencing to characterize fecal bacterial communities and chemiluminescence to measure thyroid function and autoantibodies (FT3, FT4, TSH, TRAb, TGAb, and TPOAb). Thyroid ultrasound was also used, and functional prediction of the microbiota was carried out using KEGG and COG analyses to explore possible mechanisms linking gut bacteria to disease.

Who was studied?

Seventy fecal samples were collected in total. These included 27 patients with Graves' disease, 27 patients with Hashimoto's thyroiditis, and 16 samples from healthy volunteers who served as controls.

What were the most important findings?

The overall structure of the gut microbiota in both the GD and HT groups differed significantly from that of the healthy control group. Proteobacteria and Actinobacteria were most abundant in the HT group, while both the GD and HT groups showed higher levels of Erysipelotrichia, Cyanobacteria, and Ruminococcus_2 and lower levels of Bacillaceae and Megamonas compared to controls. Functional analysis linked the ABC transporter pathway strongly to GD and HT, and COG analysis showed enrichment in carbohydrate transport and metabolism, but not amino acid transport and metabolism, in both patient groups.

What are the greatest implications of this study?

The findings suggest that gut microbiota alterations, particularly shifts in carbohydrate transport and metabolism pathways, may be mechanistically involved in the development of Graves' disease and Hashimoto's thyroiditis. This supports a role for the gut microbiome in autoimmune thyroid disease pathogenesis and points to specific bacterial taxa and metabolic pathways as potential targets for further mechanistic study. Because the abstract does not specify additional cohort details or long-term outcomes, further research is needed to confirm causality and clinical relevance.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study investigated whether the gut microbiota differs in patients with brain tumors compared to healthy people. The researchers characterized the fecal microbial community using 16S rRNA gene amplicon sequencing. They then examined correlations between microbiota composition and clinical features of the tumors, and explored whether specific microbial markers could help diagnose brain tumors.

Who was studied?

The study recruited 158 participants in total. This included 101 patients with brain tumors, made up of 65 benign and 36 malignant cases, along with 57 age- and sex-matched healthy controls.

What were the most important findings?

Patients with brain tumors had markedly lower gut microbial ecosystem richness and evenness than healthy controls. The overall structure of the gut microbiota community was also profoundly altered in the brain tumor group. This shift included increased abundance of pathogenic bacteria such as Fusobacteriota and Proteobacteria, alongside a reduction in other taxa.

What are the greatest implications of this study?

These findings support a gut-brain crosstalk in which gut dysbiosis is associated with the presence of brain tumors, extending prior work on microbiota alterations in other CNS diseases to this tumor context. The distinct shifts toward pathogenic taxa such as Fusobacteriota and Proteobacteria suggest the gut microbiota could potentially serve as a diagnostic marker for brain tumors. Further work would be needed to determine whether these microbial changes are a cause, consequence, or bystander effect of tumor presence.

What was studied?

The purpose of this study was to elucidate the characteristics of the gut microbiome in patients with Polycystic ovary syndrome (PCOS) and analyze the alterations of fecal fatty acid metabolism, so as to further provide the pathogenesis of PCOS.

Who was studied?

Fecal samples from the PCOS group (n = 31) and healthy control group (n = 27) were analyzed by 16S rRNA gene sequencing and untargeted metabolomics. Peripheral venous blood was collected to measure serum inflammation and intestinal permeability. Finally, the correlation analysis of intestinal flora, fecal metabolites, and laboratory indicators was carried out.

What were the most important findings?

Serum D-lactate content in the PCOS group was higher than that in the control group. There was no significant difference in microbial α diversity and β diversity between PCOS patients and healthy controls. Peptostreptococcaceae and Bacteroidales S24-7 group existed significant differences between PCOS patients and healthy controls. Based on linear discriminant analysis selection, 14 genera including Klebsiella, Enterobacteriaceae, and Gammaproteobacteria were dominant in patients with PCOS, while 4 genera, including rumenococcus (Ruminocaccaceae UCG 013), prewortella (Prevotellaceae UCG 001), and erysipelas (Erysipelatoclostridium), were dominant in healthy controls. Compared with PCOS with Body mass index (BMI) < 24, patients with BMI ≥ 24 have multiple dominant genera including Abiotrophia and Peptostreptococcaceae. Moreover, serum levels of free testosterone and androstenedione were positively correlated with Megamonas, while total testosterone was negatively correlated with Alistipes. Additionally, fecal contents of acetic acid and propionic acid in patients with PCOS were significantly higher than those in healthy controls. Eubacterium_coprostanoligenes_group and Alistipes were positively correlated with 6 kinds of fatty acids.

What are the greatest implications of this study?

Specific intestinal flora fecal fatty acids and serum metabolites may mediate the occurrence and development of PCOS. PCOS patients with different body sizes have specific intestinal flora.

What was studied?

CKD is characterized by a sustained proinflammatory response of the immune system, promoting hypertension and cardiovascular disease. The underlying mechanisms are incompletely understood but may be linked to gut dysbiosis. Dysbiosis has been described in adults with CKD; however, comorbidities limit CKD-specific conclusions.

Who was studied?

We analyzed the fecal microbiome, metabolites, and immune phenotypes in 48 children (with normal kidney function, CKD stage G3-G4, G5 treated by hemodialysis [HD], or kidney transplantation) with a mean±SD age of 10.6±3.8 years.

What were the most important findings?

Serum TNF-α and sCD14 were stage-dependently elevated, indicating inflammation, gut barrier dysfunction, and endotoxemia. We observed compositional and functional alterations of the microbiome, including diminished production of short-chain fatty acids. Plasma metabolite analysis revealed a stage-dependent increase of tryptophan metabolites of bacterial origin. Serum from patients on HD activated the aryl hydrocarbon receptor and stimulated TNF-α production in monocytes, corresponding to a proinflammatory shift from classic to nonclassic and intermediate monocytes. Unsupervised analysis of T cells revealed a loss of mucosa-associated invariant T (MAIT) cells and regulatory T cell subtypes in patients on HD.

What are the greatest implications of this study?

Gut barrier dysfunction and microbial metabolite imbalance apparently mediate the proinflammatory immune phenotype, thereby driving the susceptibility to cardiovascular disease. The data highlight the importance of the microbiota-immune axis in CKD, irrespective of confounding comorbidities.

What was studied?

This scoping review examined the human gut microbiota and its relation to glucose metabolism, insulin resistance, and type 2 diabetes risk. The authors searched PubMed and screened 5983 records down to 45 original observational studies. They focused on identifying key bacterial taxa associated with markers and stages of glucose dysregulation, independent of overweight, obesity, and metabolic drugs. The review also considered the potential mediating role of short-chain fatty acids (SCFAs) and the influence of diet and diet-microbiota derived metabolites.

Who was studied?

The review drew on human observational studies conducted in healthy adults as well as adults with metabolic disease and associated risk factors. Rather than a single cohort, the evidence base was pooled across 45 separate original studies identified from the PubMed literature. Specific sample sizes or demographic details for individual cohorts are not given in the abstract.

What were the most important findings?

Across the reviewed studies, alpha diversity and 45 distinct bacterial taxa were associated with glucose metabolism outcomes. Six taxa emerged as most frequently linked to glucose metabolism, including Akkermansia muciniphila, Bifidobacterium longum, the Clostridium leptum group, and Faecalibacterium prausnitzii. The authors present evidence supporting SCFAs as a mechanism that may mediate the relationship between these gut bacteria and glucose regulation. Diet and microbiota-derived metabolites are also highlighted as relevant contributors to these associations.

What are the greatest implications of this study?

Identifying specific gut bacteria, including SCFA-associated and anti-inflammatory commensals such as Faecalibacterium prausnitzii, consistently linked to glucose metabolism could open new avenues for type 2 diabetes prevention. Because these associations were found independent of obesity and metabolic drug use, the gut microbiota may represent an independent target for intervention. The proposed role of SCFAs and diet-derived metabolites suggests that dietary strategies aimed at shaping the microbiota could be a practical entry point for future prevention efforts. Overall, the findings support further mechanistic and interventional research into these key taxa and their metabolic products.

What was studied?

HIV-exposed uninfected infants (HEU) have abnormal immunologic functions and increased infectious morbidity in the first 6 months of life, which gradually decreases thereafter. The mechanisms underlying HEU immune dysfunctions are unknown. We hypothesized that unique characteristics of the HEU gut microbiota associated with maternal HIV status may underlie the HEU immunologic dysfunctions. We characterized the infant gut, maternal gut, and breast milk microbiomes of mother-infant pairs, including 123 with HEU and 117 with HIV-uninfected infants (HUU), from South Africa. Pan-bacterial 16S rRNA gene sequencing was performed on (i) infant stool at 6, 28, and 62 weeks; (ii) maternal stool at delivery and 62 weeks; and (iii) breast milk at 6 weeks. Infant gut alpha and beta diversities were similar between groups. Microbial composition significantly differed, including 12 genera, 5 families and 1 phylum at 6 weeks; 12 genera and 2 families at 28 weeks; and 2 genera and 2 families at 62 weeks of life. Maternal gut microbiomes significantly differed in beta diversity and microbial composition, and breast milk microbiomes differed in microbial composition only. Infant gut microbiotas extensively overlapped with maternal gut and minimally with breast milk microbiotas. Nevertheless, exclusively breastfed HEU and HUU had less divergent microbiomes than nonexclusively breastfed infants. Feeding pattern and maternal gut microbiome imprint the HEU gut microbiome. Compared to HUU, the HEU gut microbiome prominently differs in early infancy, including increased abundance of taxa previously observed to be present in excess in adults with HIV. The HEU and HUU gut microbiome compositions converge over time, mirroring the kinetics of HEU infectious morbidity risk. IMPORTANCE HIV-exposed uninfected infants (HEU) are highly vulnerable to infections in the first 6 months of life, and this vulnerability decreases to the age of 24 months. Because the microbiome plays a critical role in the education of the infant immune system, which protects them against infections, we characterized the gut microbiomes of HEU and HIV-unexposed infants (HUU) in the first year of life. The HEU and HUU gut microbiomes showed prominent differences at 6 and 28 weeks of life but converged at 62 weeks of life, mirroring the time course of the HEU excess infectious morbidity and suggesting a potential association between the infant gut microbiome structure and susceptibility to infections. Infant gut microbiotas extensively overlapped with maternal gut and minimally with breast milk microbiotas. Moreover, exclusively breastfed HEU and HUU had less divergent microbiomes at 6 and 28 weeks than nonexclusively breastfed HEU and HUU. The factors that affect the HEU gut microbiome, maternal gut microbiome and exclusive breastfeeding, may be targeted by interventions.

What was studied?

MaZiRenWan (MZRW) is the most frequently used Traditional Chinese Medicine formula to treat chronic constipation, Cannabis sativa L. is regarded as a monarch drug in MZRW. However, the targets of Cannabis sativa L. that enhance colonic motility and improve constipation symptoms remain unknown. This study was designed to investigate the laxative effect and underlying mechanism of the water extract of Cannabis sativa L. (WECSL) using a loperamide-induced constipation mouse model. We found that WECSL treatment significantly improved intestinal motility and water-electrolyte metabolism, decreased inflammatory responses, prevented gut barrier damage, and relieved anxiety and depression in constipated mice. WECSL also structurally remodeled the composition of the gut microbiota and altered the abundance of bacteria related to inflammation, specifically Butyricicoccus and Parasutterella. Moreover, WECSL failed to relieve constipation symptoms following intestinal flora depletion, indicating that WECSL alleviates constipation symptoms depending on the gut microbiota. Our research provides a basis for WECSL to be further investigated in the treatment of constipation from the perspective of modern medicine.

What was studied?

Although gut microbiota dysbiosis has been reported in HIV infected individuals recently, the relationship between the gut microbiota and immune activation in patients with different immune responses to highly active antiretroviral therapy (HAART) is still not well understood. Gut microbiota and immune activation were studied in 36 non-HIV-infected subjects (healthy controls) and 58 HIV-infected individuals, including 28 immunological responders (IR) and 30 immunological non-responders (INR) (≥500 and < 200 CD4+ T-cell counts/μl after 2 years of HIV-1 viral suppression respectively) without comorbidities.

What were the most important findings?

Metagenome sequencing revealed that HIV-infected immunological responders and immunological non-responders could not recover completely from the gut microbiota dysbiosis. At a 97% similarity level, the relative abundances of Fusobacterium, Ruminococcus gnavus and Megamonas were greater, whereas Faecalibacterium, Alistipes, Bifidobacterium, Eubacterium rectale and Roseburia were more depleted in the IR and INR groups than those in the healthy controls. Ruminococcaceae and Alistipes were positively correlated with nadir and current CD4+ T-cell counts, but negatively correlated with CD8 + CD57+ T-cell counts. Inflammation markers and translocation biomarkers (LPS) levels were positively correlated with the abundances of genera Ruminococcus and Fusobacterium but were negatively correlated with the genus Faecalibacterium. The relative abundances of Escherichia-Shigella and Blautia were significantly higher in the IR than those in the INR group. Escherichia-Shigella were negatively correlated with the CD4/CD8 ratio but positively correlated with the amount of CD8 + CD57+ T-cells. Roseburia and Blautia were negatively associated with nadir CD4+ T-cell and positively associated with CD8 + CD57+ T-cell counts.

What are the greatest implications of this study?

Gut microbiota dysbiosis may be one of the factors contributing to different immune responses and treatment outcomes to HAART.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

To characterise the oral microbiome, gut microbiome and serum lipid profiles in patients with active COVID-19 and recovered patients; evaluate the potential of the microbiome as a non-invasive biomarker for COVID-19; and explore correlations between the microbiome and lipid profile.

Who was studied?

We collected and sequenced 392 tongue-coating samples, 172 faecal samples and 155 serum samples from Central China and East China. We characterised microbiome and lipid molecules, constructed microbial classifiers in discovery cohort and verified their diagnostic potential in 74 confirmed patients (CPs) from East China and 37 suspected patients (SPs) with IgG positivity.

What were the most important findings?

Oral and faecal microbial diversity was significantly decreased in CPs versus healthy controls (HCs). Compared with HCs, butyric acid-producing bacteria were decreased and lipopolysaccharide-producing bacteria were increased in CPs in oral cavity. The classifiers based on 8 optimal oral microbial markers (7 faecal microbial markers) achieved good diagnostic efficiency in different cohorts. Importantly, diagnostic efficacy reached 87.24% in the cross-regional cohort. Moreover, the classifiers successfully diagnosed SPs with IgG antibody positivity as CPs, and diagnostic efficacy reached 92.11% (98.01% of faecal microbiome). Compared with CPs, 47 lipid molecules, including sphingomyelin (SM)(d40:4), SM(d38:5) and monoglyceride(33:5), were depleted, and 122 lipid molecules, including phosphatidylcholine(36:4p), phosphatidylethanolamine (PE)(16:0p/20:5) and diglyceride(20:1/18:2), were enriched in confirmed patients recovery.

What are the greatest implications of this study?

This study is the first to characterise the oral microbiome in COVID-19, and oral microbiomes and lipid alterations in recovered patients, to explore their correlations and to report the successful establishment and validation of a diagnostic model for COVID-19.

What was studied?

Endometriosis (EM) in reproductive females has an incidence of 6-10% and greatly affects female fertility, quality of life, and long-term health. The gut microbiota can affect the physiological and pathological processes of humans through various pathways, such as those involving the nervous and endocrine systems and immunity, and it plays important roles in endocrine and inflammatory diseases. Whether the gut microbiota plays a role in EM has gradually attracted researchers' attention. In the present study, fecal and blood samples were collected from 12 patients with stage 3/4 EM and 12 healthy controls. We performed 16S rRNA high-throughput sequencing to compare the gut microbiota between the EM and control groups. Serum levels of hormones and inflammatory cytokines were measured. We found that compared with the control group, the EM group had a lower α diversity of gut microbiota and a higher Firmicutes/Bacteroidetes ratio. The abundances of various taxa (such as Actinobacteria, Tenericutes, Blautia, Bifidobacterium, Dorea, and Streptococcus) were significantly different between the two groups. The taxon with the highest abundance in the EM group was Prevotella_7, and that in the control group was Coprococcus_2. The serum levels of E2 and IL-8 were significantly higher in the EM group than in the control group (E2: EM group 74.7 ± 22.5 pg/L vs CON group 47.9 ± 12.5 pg/L; IL-8: EM group 6.39 ± 1.59 pg/mL vs CON group 4.14 ± 0.73 pg/mL). Additionally, the gut microbiota of the EM group was enriched for the microbial function categories environmental information processing, endocrine system, and immune system. Correlations were detected between each of Blautia and Dorea abundance and estradiol level and between Subdoligranulum abundance and IL-8 level. This study elucidated the associations between the gut microbiota and both serum hormones and inflammatory factors in EM. However, the findings need to be verified in future studies.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study examined whether gut microbiota composition is associated with fever in patients with moderate COVID-19. Researchers compared clinical features and laboratory results between patients with and without fever, and identified inflammatory markers linked to fever. They then conducted a gut metagenome-wide association study to characterize the microbes and microbial epitopes potentially involved in fever and hyperinflammation.

Who was studied?

The cohort included 187 patients with moderate COVID-19, of whom 127 (67.9 percent) presented with fever and the remainder did not. A subset of 31 individuals from this group underwent gut metagenome-wide association analysis to identify microbial features linked to fever and hyperinflammation. The abstract does not provide further demographic details such as age or sex distribution.

What were the most important findings?

Patients with fever showed significantly reduced lymphocytes, CD3+ T cells, CD4+ T cells, and CD4+ to CD8+ T cell ratios, alongside significantly elevated AST, LDH, CRP, IL-6, and IL-10. Gut microbiome composition differed significantly between patients with fever and those without. Opportunistic pathogens, including Enterococcus faecalis and Saccharomyces cerevisiae, were enriched in patients with fever, and E. faecalis abundance was positively correlated with LDH and D-dimer levels.

What are the greatest implications of this study?

These findings suggest that gut microbiota dysbiosis, particularly enrichment of opportunistic pathogens such as Enterococcus faecalis, may be linked to the abnormal immune responses and inflammation seen in febrile moderate COVID-19 patients. This raises the possibility that gut microbes or their components contribute to fever and hyperinflammation in this population. The results point to gut microbiota as a potential area of interest for understanding COVID-19 severity and prognosis in moderate cases.

What was studied?

Intestinal microbiota seems to play a key role in obesity. The impact of the composition and/or functionality of the obesity-associated microbiota have yet to be fully characterized. This work assessed the significance of the taxonomic composition and/or metabolic activity of obese- microbiota by massive 16S rRNA gene sequencing of the fecal microbiome of obese and normoweight individuals. The obese metabolic activity was also assessed by in vitro incubation of obese and normoweight microbiotas in nutritive mediums with different energy content. We found that the microbiome richness and diversity of the two groups did not differ significantly, except for Chao1 index, significantly higher in normoweight individuals. At phylum level, neither the abundance of Firmicutes or Bacteroidetes nor their ratio was associated with the body mass index. Besides, the relative proportions in Collinsella, Clostridium XIVa, and Catenibacterium were significantly enriched in obese participants, while Alistipes, Clostridium sensu stricto, Romboutsia, and Oscillibacter were significantly diminished. In regard to metabolic activity, short-chain fatty acids content was significant higher in obese individuals, with acetate being the most abundant followed by propionate and butyrate. Acetate and butyrate production was also higher when incubating obese microbiota in mediums mimicking diets with different energy content; interestingly, a reduced capability of propionate production was associated to the obese microbiome. In spite of the large interindividual variability, the obese phenotype seems to be defined more by the abundance and/or the absence of distinct communities of microorganism rather than by the presence of a specific population.

What was studied?

Compelling evidence supports alterations in gut microbial diversity, bacterial composition, and/or relative abundance of several bacterial taxa in attention-deficit/hyperactivity disorder (ADHD). However, findings for ADHD are inconsistent among studies, and specific gut microbiome signatures for the disorder remain unknown. Given that previous studies have mainly focused on the pediatric form of the disorder and involved small sample sizes, we conducted the largest study to date to compare the gastrointestinal microbiome composition in 100 medication-naïve adults with ADHD and 100 sex-matched healthy controls. We found evidence that ADHD subjects have differences in the relative abundance of several microbial taxa. At the family level, our data support a lower relative abundance of Gracilibacteraceae and higher levels of Selenomonadaceae and Veillonellaceae in adults with ADHD. In addition, the ADHD group showed higher levels of Dialister and Megamonas and lower abundance of Anaerotaenia and Gracilibacter at the genus level. All four selected genera explained 15% of the variance of ADHD, and this microbial signature achieved an overall sensitivity of 74% and a specificity of 71% for distinguishing between ADHD patients and healthy controls. We also tested whether the selected genera correlate with age, body mass index (BMI), or scores of the ADHD rating scale but found no evidence of correlation between genera relative abundance and any of the selected traits. These results are in line with recent studies supporting gut microbiome alterations in neurodevelopment disorders, but further studies are needed to elucidate the role of the gut microbiota on the ADHD across the lifespan and its contribution to the persistence of the disorder from childhood to adulthood.

What was studied?

The lack of tools for the precise manipulation of the tick microbiome is currently a major limitation to achieve mechanistic insights into the tick microbiome. Anti-tick microbiota vaccines targeting keystone bacteria of the tick microbiota alter tick feeding, but their impact on the taxonomic and functional profiles of the tick microbiome has not been tested. In this study, we immunized a vertebrate host model (Mus musculus) with live bacteria vaccines targeting keystone (i.e., Escherichia-Shigella) or non-keystone (i.e., Leuconostoc) taxa of tick microbiota and tested the impact of bacterial-specific antibodies (Abs) on the structure and function of tick microbiota. We also investigated the effect of these anti-microbiota vaccines on mice gut microbiota composition. Our results showed that the tick microbiota of ticks fed on Escherichia coli-immunized mice had reduced Escherichia-Shigella abundance and lower species diversity compared to ticks fed on control mice immunized with a mock vaccine. Immunization against keystone bacteria restructured the hierarchy of nodes in co-occurrence networks and reduced the resistance of the bacterial network to taxa removal. High levels of E. coli-specific IgM and IgG were negatively correlated with the abundance of Escherichia-Shigella in tick microbiota. These effects were not observed when Leuconostoc was targeted with vaccination against Leuconostoc mesenteroides. Prediction of functional pathways in the tick microbiome using PICRUSt2 revealed that E. coli vaccination reduced the abundance of lysine degradation pathway in tick microbiome, a result validated by qPCR. In contrast, the gut microbiome of immunized mice showed no significant alterations in the diversity, composition and abundance of bacterial taxa. Our results demonstrated that anti-tick microbiota vaccines are a safe, specific and an easy-to-use tool for manipulation of vector microbiome. These results guide interventions for the control of tick infestations and pathogen infection/transmission.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

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.

Who was studied?

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).

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

The gut microbiota can affect human metabolism, immunity, and other biologic pathways through the complex gut-kidney axis (GKA), and in turn participate in the occurrence and development of kidney disease. In this study, 39 patients with stage 4-5 chronic kidney disease (CKD) and 40 healthy individuals were recruited and 16S rDNA sequencing was performed to analyze the V3-V4 conserved regions of their microbiota. A total of 795 operational taxonomic units (OTUs) shared between groups or specific to each group were obtained, among which 255 OTUs with significant differences between the two groups were identified (P<0.05). Adonis differential analysis showed that the diversity of gut microbiota was highly correlated with CKD stages 4-5. Additionally, 61 genera with differences in the two groups were identified (P<0.05) and 111 species with significant differences in the phyla, classes, orders, families, and genera between the two groups were identified (P<0.05). The differential bacterial genera with the greatest contribution were, in descending order: c_Bacteroidia, o_Bacteroidales, p_Bacteroidetes, c_Clostridia, o_Clostridiales, etc. Those with the greatest contribution in stages 4-5 CKD were, in descending order: p_Proteobacteria, f_Enterobacteriaceae, o_Enterobacteriales, c_Gammaproteobacteria, c_Bacilli, etc. The results suggest that the diversity of the microbiota may affect the occurrence, development, and outcome of the terminal stages of CKD.

What was studied?

High-fat (HF) diet-induced neuroinflammation and cognitive decline in humans and animals have been associated with microbiota dysbiosis via the gut-brain axis. Our previous studies revealed that excretory-secretory products (ESPs) derived from the larval Echinococcus granulosus (E. granulosus) function as immunomodulators to reduce the inflammatory response, while the parasitic infection alleviates metabolic disorders in the host. However, whether ESPs can improve cognitive impairment under obese conditions remain unknown. This study aimed to investigate the effects of E. granulosus-derived ESPs on cognitive function and the microbiota-gut-brain axis in obese mice. We demonstrated that ESPs supplementation prevented HF diet-induced cognitive impairment, which was assessed behaviorally by nest building, object location, novel object recognition, temporal order memory, and Y-maze memory tests. In the hippocampus (HIP) and prefrontal cortex (PFC), ESPs suppressed neuroinflammation and HF diet-induced activation of the microglia and astrocytes. Moreover, ESPs supplementation improved the synaptic ultrastructural impairments and increased both pre- and postsynaptic protein levels in the HIP and PFC compared to the HF diet-treated group. In the colon, ESPs reversed the HF diet-induced gut barrier dysfunction, increased the thickness of colonic mucus, upregulated the expression of zonula occludens-1 (ZO-1), attenuated the translocation of bacterial endotoxins, and decreased the colon inflammation. Notably, ESPs supplementation alleviated the HF diet-induced microbiota dysbiosis. After clarifying the role of antibiotics in obese mice, we found that broad-spectrum antibiotic intervention abrogated the effects of ESPs on improving the gut microbiota dysbiosis and cognitive decline. Overall, the present study revealed for the first time that the parasite-derived ESPs alleviate gut microbiota dysbiosis and improve cognitive impairment induced by a high-fat diet. This finding suggests that parasite-derived molecules may be used to explore novel drug candidates against obesity-associated neurodegenerative diseases.

What was studied?

This study examined the gut microbiome composition of patients with young-onset colorectal cancer (yCRC), a form of sporadic colorectal cancer whose incidence is rising. Researchers used 16S rRNA gene sequencing to identify microbial markers distinguishing yCRC, then validated these findings in an independent cohort. Metagenome sequencing was also performed to characterize species-level and functional differences in bacterial communities associated with yCRC.

Who was studied?

The discovery analysis drew on 728 samples analyzed by 16S rRNA gene sequencing. An independent validation cohort of 310 samples was used to confirm the identified microbial markers. A further subset of 200 samples underwent metagenome sequencing for species-level and functional analysis.

What were the most important findings?

Gut microbial diversity was increased in yCRC compared to other groups studied. Flavonifractor plautii emerged as an important bacterial species associated with yCRC, whereas the genus Streptococcus contained the key phylotype linked to old-onset colorectal cancer. Functional analysis showed that yCRC-associated bacterial communities were distinguished by a dominance of DNA binding and RNA-dependent DNA biosynthetic processes, and a random forest classifier built on these microbial features achieved strong classification performance.

What are the greatest implications of this study?

The findings suggest that gut microbiota biomarkers, particularly Flavonifractor plautii abundance and associated functional signatures, could serve as a non-invasive tool for detecting and distinguishing yCRC. This approach could help address the diagnostic gap for younger patients as sporadic colorectal cancer incidence rises in this age group. The distinct microbial and functional profile of yCRC versus old-onset colorectal cancer also points to potentially different underlying disease biology between the two age groups.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

This study examined the relationship between the gut microbiota and psychiatric symptom severity among inpatients with serious mental illness. Researchers used 16S rRNA gene sequencing and whole genome shotgun sequencing to characterize fecal samples collected early in hospitalization. They then tested whether microbial richness and alpha diversity were associated with depression, anxiety, trauma, and suicide severity measures, and whether these microbial features predicted treatment outcome at discharge.

Who was studied?

The study population consisted of 111 adult inpatients with serious mental illness. Diagnoses, suicide severity, trauma, depression, and anxiety were assessed shortly after admission. Participants self-collected fecal swabs early in the course of their hospital stay for microbiota analysis.

What were the most important findings?

Depression and anxiety severity shortly after admission were negatively associated with bacterial richness and alpha diversity, meaning more severe symptoms corresponded to a less rich and less diverse gut microbiota. Specific bacterial taxa were identified as associated with depression and anxiety severity. Gut microbiota richness and alpha diversity measured early in hospitalization also significantly predicted depression remission by the time of discharge.

What are the greatest implications of this study?

The findings support a link between gut microbial diversity and psychiatric symptom severity in a clinical inpatient population, extending prior evidence from animal models and small human studies. Because early microbiota measures predicted depression remission at discharge, gut microbiota composition may hold value as a marker of treatment response in serious mental illness. This strengthens the rationale for further investigating the brain-gut relationship as a factor in psychiatric care and outcomes.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

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.

Who was studied?

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.

What were the most important findings?

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.

What are the greatest implications of this study?

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.

What was studied?

Very low-carbohydrate, high-fat ketogenic diets (KDs) induce a pronounced shift in metabolic fuel utilization that elevates circulating ketone bodies; however, the consequences of these compounds for host-microbiome interactions remain unknown. Here, we show that KDs alter the human and mouse gut microbiota in a manner distinct from high-fat diets (HFDs). Metagenomic and metabolomic analyses of stool samples from an 8-week inpatient study revealed marked shifts in gut microbial community structure and function during the KD. Gradient diet experiments in mice confirmed the unique impact of KDs relative to HFDs with a reproducible depletion of bifidobacteria. In vitro and in vivo experiments showed that ketone bodies selectively inhibited bifidobacterial growth. Finally, mono-colonizations and human microbiome transplantations into germ-free mice revealed that the KD-associated gut microbiota reduces the levels of intestinal pro-inflammatory Th17 cells. Together, these results highlight the importance of trans-kingdom chemical dialogs for mediating the host response to dietary interventions.

What was studied?

Endometriosis (EMS) is a chronic inflammatory disease with unclear pathogenesis. Three studies have uncovered the influence of gut microbiota on mice with EMS, but no study has investigated the characteristics of fecal metabolomics to determine some important clues on EMS. This research aims to uncover the interaction between fecal metabolomics and gut microbiota in EMS mice.

Who was studied?

Female C57BL/6J mice were used to construct the EMS model. Non-target metabolomics was applied to detect the fecal metabolites of EMS mice. The 16s rRNA sequencing was used for clarifying the composition of the gut microbiota. The functional characteristics of gut microbiota were analyzed using the PICRUSt. The receiver operator characteristic curve (ROC) analysis was utilized for determining the potential important differential metabolites, and the Spearman correlation coefficient was applied for expressing the correlation between the important differential metabolites and gut microbiota.

What were the most important findings?

A total of 156 named differential metabolites were screened. The diversity and the abundance of gut microbiota in EMS mice decreased. Eleven pathways were involved in the differential metabolites and the functional prediction of gut microbiota, among which the second bile acid biosynthesis and alpha-linolenic acid (ALA) metabolism were the significant enrichment pathways. The increased abundance of chenodeoxycholic and ursodeoxycholic acids and the decreased abundance of ALA and 12,13-EOTrE were found in the feces of EMS mice.

What are the greatest implications of this study?

The abnormal fecal metabolites, which are influenced by dysbacteriosis, may be the characteristics of EMS mice and can be the potential important indices to distinguish the disease.

What was studied?

Primary ovarian failure (POF) is defined as follicular failure in women of reproductive age. Although many factors are speculated to contribute to the occurrence of POF, the exact aetiology remains unclear. Moreover, alterations in the microbiome of patients with POF are poorly studied.

What were the most important findings?

This study investigated the vaginal microbiota of 22 patients with POF and 29 healthy individuals. High-throughput Illumina MiSeq sequencing targeting the V3-V4 region of the 16S ribosomal RNA (rRNA) gene was used to evaluate the relationships between the vaginal flora and clinical characteristics of POF. Different from results of previous studies, we found that the diversity and richness of the vaginal flora of patients with POF was significantly different from those of healthy controls. Comparison of the vaginal flora of patients with POF with that of menopausal women revealed that the relative abundance of Lactobacillus was significantly reduced in the latter. A reduced abundance of Lactobacillus was furthermore associated with a lower pregnancy success rate. Of particular interest is that L. gallinarum especially appeared to be beneficially associated with reproductive-related indicators (FSH, E2, AMH, PRL) whilst L. iners appeared to have a detrimental effect. The result of the present study may enable the identification of microbiota associated with POF, however, further investigations of differences in the microbiota in the context of POF will enable a deeper understanding of the disease pathogenesis that involves modification of the vaginal microbiota.

What are the greatest implications of this study?

The present study identified the microbiota associated with POF. Further investigations on the differences in the microbiota in the context of POF will improve our understanding of the pathogenesis of the disease which involves modification of the vaginal microbiota.

What was studied?

Lysine acetylation (Kac), an abundant post-translational modification (PTM) in prokaryotes, regulates various microbial metabolic pathways. However, no studies have examined protein Kac at the microbiome level, and it remains unknown whether Kac level is altered in patient microbiomes. Herein, we use a peptide immuno-affinity enrichment strategy coupled with mass spectrometry to characterize protein Kac in the microbiome, which successfully identifies 35,200 Kac peptides from microbial or human proteins in gut microbiome samples. We demonstrate that Kac is widely distributed in gut microbial metabolic pathways, including anaerobic fermentation to generate short-chain fatty acids. Applying to the analyses of microbiomes of patients with Crohn's disease identifies 52 host and 136 microbial protein Kac sites that are differentially abundant in disease versus controls. This microbiome-wide acetylomic approach aids in advancing functional microbiome research.