Collinsella

What was studied?

This randomized, double-blind, placebo-controlled trial tested whether daily supplementation with two specific probiotic strains, Bifidobacterium animalis subsp. lactis XLTG11 and Lactiplantibacillus plantarum CCFM8661, could reduce recurrent respiratory tract infections (RRTIs) in children. Over 180 days, the study tracked infection frequency and duration alongside changes in gut microbiota composition, functional metabolic pathways, and immune biomarkers. The design allowed the researchers to link clinical respiratory outcomes to underlying shifts in the gut microbial community and immune regulation.

Who was studied?

The study enrolled 120 children who had been diagnosed with recurrent respiratory tract infections. Participants were randomly assigned to receive either the probiotic combination or a matched placebo daily for 180 days. The abstract does not provide further demographic details such as age range or sex distribution.

What were the most important findings?

Children receiving the probiotics had significantly reduced duration and frequency of fever, cough, upper respiratory tract infections, trachea or bronchitis, pneumonia, and overall RRTI recurrence compared with placebo (all p < 0.05). Gut microbiota profiling at day 180 showed clear community differences between groups, with the probiotic group showing greater abundance of beneficial commensal taxa and the placebo group showing more opportunistic genera. Functional pathway analysis pointed to enhanced metabolic stability in the probiotic recipients, and immune biomarker patterns showed comparatively stable IgG, IgM, and complement C3 levels, suggesting a more regulated humoral immune response. Growth trajectories remained normal in both groups.

What are the greatest implications of this study?

These findings support strain-defined probiotic supplementation as a viable adjunct strategy for reducing the burden of recurrent respiratory infections in children. The parallel shifts in gut microbial composition, metabolic function, and humoral immune stability suggest the respiratory benefit may be mediated through gut-immune axis modulation rather than a direct respiratory-tract effect. Because growth remained normal, the intervention appears well tolerated over a six-month period, supporting its potential for longer-term pediatric preventive use pending further confirmatory trials.

What was studied?

Early diagnosis of Parkinson's disease (PD) and distinguishing it from essential tremor (ET) remains a significant challenge. We analyzed fecal samples (gut microbiota via 16S rRNA gene sequencing with DADA2-denoising/OTU-clustering) and short-chain fatty acids (SCFAs) in 104 drug-naïve early PD patients (73 test/31 validation), 69 ET patients (48/21), and 61 healthy controls (HC; 43/18). Differential taxa were identified using ANCOM, ANCOM-BC, ALDEx2, MaAsLin2, and LEfSe; top diagnostic potential was selected by random forest and assessed by ROC curve analysis. Compared to HC, PD showed reduced Citrobacter/Haemophilus, increased Eggerthella, and elevated isovaleric/isobutyric acids (validation AUC = 0.864). PD vs. ET exhibited decreased Bilophila/Bacteroides/Haemophilus with elevated isovaleric/isobutyric/valeric acids (validation AUC = 0.825). Tremor-dominant PD (TD-PD) was distinguished from ET by lower Lachnoclostridium/Haemophilus/Bilophila and higher isovaleric/isobutyric acids (validation AUC = 0.780), while non-TD-PD differed from TD-PD only in decreased Dialister (validation AUC = 0.802). Gut microbiota and SCFAs might serve as specific, non-invasive candidate biomarkers for early PD diagnosis.

What was studied?

This study examined how high exposure to toxic metals and metalloids, specifically arsenic, lead, mercury, and cadmium, relates to gut microbiome composition and metabolic risk. Researchers analyzed associations among gut microbiota taxa, dichotomized (high versus low) metal levels, and clinical measures including BMI, fasting blood glucose, and blood pressure. They also examined diagnoses of hypertension, obesity, and type 2 diabetes (T2DM) alongside metabolic pathway enrichment linked to metal exposure. The goal was to clarify mechanisms by which toxic metal exposure may contribute to obesity and T2DM risk through the gut microbiome.

Who was studied?

The study included 178 adults of African origin drawn from five countries: Ghana, South Africa, Jamaica, Seychelles, and the United States. The cohort was 52% female with a mean age of 43.0 plus or minus 6.4 years. This multi-country design allowed comparison of metal exposure and microbiome relationships across diverse African-origin populations rather than a single national sample.

What were the most important findings?

High versus low lead and arsenic levels significantly affected gut microbiome beta diversity (p less than 0.05). Seventy-one taxa were associated with high lead levels, including 30 linked to elevated BMI, 22 to T2DM, and 23 to elevated fasting blood glucose. Arsenic showed an even broader association, with 115 taxa linked to high exposure, including 32 tied to elevated BMI, 33 to T2DM, and 26 to elevated blood glucose. Porphyrin metabolism emerged as the most enriched metabolic pathway among taxa associated with higher lead and arsenic exposure.

What are the greatest implications of this study?

This is described as the first evidence from African-origin adults linking gut microbiome composition to lead and arsenic exposure alongside cardiometabolic risk markers. The porphyrin metabolism signal suggests a plausible microbial pathway connecting heavy metal exposure to metabolic dysregulation, since porphyrin metabolism is tied to heme synthesis and metal handling. These findings support further investigation of the gut microbiome as a mechanistic link between environmental toxic metal exposure and obesity or diabetes risk in understudied, high-exposure populations.

What was studied?

Modern treatment, a healthy diet, and physical activity routines lower the risk factors for metabolic syndrome; however, this condition is associated with all-cause and cardiovascular mortality worldwide. This investigation involved a randomized controlled trial, double-blind, parallel study. Fifty-eight participants with risk factors of metabolic syndrome according to the inclusion criteria were randomized into two groups and given probiotics (Lacticaseibacillus paracasei MSMC39-1 and Bifidobacterium animalis TA-1) (n = 31) or a placebo (n = 27). The participants had a mean age of 42.29 ± 7.39 and 43.89 ± 7.54 years in the probiotics and placebo groups, respectively. Stool samples, anthropometric data, and blood chemistries were taken at baseline and at 12 weeks. The primary outcome was achieved by the probiotics group as their low-density lipoprotein-cholesterol level dramatically lowered compared to the placebo group (the difference was 39.97 ± 26.83 mg/dl, p-value <0.001). Moreover, significant reductions in body weight, body mass index, waist circumference, systolic blood pressure, and total cholesterol were observed in the volunteers treated with probiotics compared to the placebo. In the gut microbiome analysis, the results showed statistically significant differences in the beta diversity in the post-intervention probiotics group. Blautia, Roseburia, Collinsella, and Ruminococcus were among the gut microbiomes that were more prevalent in the post-intervention probiotics group. In addition, this group exhibited increases in the predicted functional changes in ATP-binding cassette (ABC) transporters, as well as ribonucleic acid transport, the biosynthesis of unsaturated fatty acids, glycerophospholipid metabolism, and pyruvate metabolism. In conclusion, this research demonstrated that the probiotics L. paracasei MSMC39-1 and B. animalis TA-1 have the efficacy to lower risk factors associated with metabolic syndrome.

What was studied?

Attention-deficit/hyperactivity disorder (ADHD), a common neurodevelopmental disorder in children, is associated with alterations in gut microbiota and short-chain fatty acids (SCFAs), which are metabolites influencing the gut-brain axis. Evidence suggests that psychostimulant medications, widely used to manage ADHD symptoms, may also impact gut microbiota composition and SCFA levels. This study explores these potential effects by examining gut microbiota profiles and SCFA concentrations in unmedicated and medicated children with ADHD, compared to healthy controls. Fecal samples from 30 children aged 6-12 years (10 unmedicated ADHD, 10 medicated ADHD, and 10 healthy controls) were analyzed using 16 S rRNA sequencing and targeted metabolomics. Unmedicated ADHD children show distinct gut microbiota profiles, with lower level of Tyzzerella, Prevotellaceae, and Coriobacteriaceae, compared to controls. Notably, propionic acid levels were negatively associated with ADHD symptom severity, suggesting a potential biomarker role. Medicated ADHD children showed lower gut microbial diversity, unique taxa, and lower SCFA levels, compared to unmedicated children with ADHD. These findings suggest that gut microbiota and SCFAs may be linked to ADHD symptomatology, underscoring the importance of gut-brain interactions in ADHD. This study highlights the potential of gut health monitoring as part of future ADHD management strategies.

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?

Wild animals face numerous challenges in less ideal habitats, including the lack of food as well as changes in diet. Understanding how the gut microbiomes of wild animals adapt to changes in food resources within suboptimal habitats is critical for their survival. Therefore, we conducted a longitudinal sampling of three gibbon species living in high-quality (Nomascus hainanus) and suboptimal (Nomascus concolor and Hoolock tianxing) habitats to address the dynamics of gut microbiome assembly over one year. The three gibbon species exhibited significantly different gut microbial diversity and composition. N. hainanus showed the lowest alpha diversity and highest nestedness, suggesting a more specialized and potentially stable microbial community in terms of composition, while H. tianxing displayed high species turnover and low nestedness, reflecting a more dynamic microbial ecosystem, which may indicate greater sensitivity to environmental changes or a flexible response to habitat variability. The gut microbial community of N. concolor was influenced by homogeneous selection in the deterministic process, primarily driven by Prevotellaceae. In contrast, the gut microbial communities of H. tianxing and N. hainanus were influenced by dispersal limitation in the stochastic process, driven by Acholeplasmataceae and Fibrobacterota, respectively. Further, the microbial response patterns to leaf feeding in N. hainanus differed from those of the other two gibbon species. In conclusion, this first cross-species comparative study provides initial insights into the different ecological adaptive strategies of gut microbiomes from a point of community assembly, which could contribute to the long-term conservation of wild primates. In this study, we conducted longitudinal sampling of three gibbon species living in high-quality (Nomascus hainanus) and suboptimal (Nomascus concolor and Hoolock tianxing) habitats to address the dynamics of gut microbiome (composition, alpha diversity, beta diversity and assembly process) over one year.

What was studied?

The relationship between the oral microbiome and oral squamous cell carcinoma (OSCC) has been extensively investigated. Nonetheless, most previous studies were single-center, resulting in the absence of systematic evaluations. To address this gap, we performed a comprehensive meta-analysis on 1,255 samples from OSCC-related 16S rRNA gene data sets, representing a diverse range of OSCC phenotypes. It is recognized that the progression of cancer is related to the alterations in the microbiome among different phenotypes. Our findings revealed distinct microbiome characteristics among different sample types, with Biopsy (Bios) and Swab samples exhibiting significant differences between phenotypes. In Bios samples, the microbiomes of the Cancer group and the normal tissue adjacent to the tumor (NAT) group display a higher similarity, while both differ from the microbiome of the Fibroepithelial polyp (FEP) group. Moreover, the identified differential genera and pathways corresponded with these observations. We developed a diagnostic model using the random forest algorithm on Swab samples, achieving an area under the receiver operating characteristic curve (AUC) of 0.918. Importantly, this model exhibited considerable effectiveness (AUC = 0.849) when applied to another sequencing platform. Taken together, our study provides a comprehensive overview of the oral microbiome during various OSCC progression stages, potentially enhancing early detection and treatment.IMPORTANCEThis study answers key questions regarding the universal microbial characteristics and comprehensive oral microbiome dynamics during oral squamous cell carcinoma (OSCC) progression. By integrating multiple data sets, we examine the following critical aspects: (1) Do different sample types harbor distinct microbial communities within the oral cavity? (2) Which sample types offer greater potential for investigating OSCC progression? (3) How are the oral microbiomes of the Cancer group, normal tissue adjacent to the tumor group, and Fibroepithelial polyp group related, and what is their potential association with OSCC development? (4) Can a diagnostic model based on microbial signatures effectively distinguish between Cancer and Health groups using Swab samples?

What was studied?

The study examined how Zhuyang Tongbian Decoction (ZTD), a treatment for functional constipation (FC), affects the gut microbiome and related inflammatory markers. Researchers used 16S rRNA sequencing, metagenomics, and metabolomics to track changes in intestinal flora composition and microbiota metabolic function. They also measured fecal short-chain fatty acid (SCFA) levels and serum concentrations of TLR4, NF-κB, TNF-α, and IL-6 before and after treatment.

Who was studied?

The study included 40 patients with functional constipation, randomly divided into a control group (20 cases, treated with lactulose) and a treatment group (20 cases, treated with ZTD). Twenty healthy volunteers were also recruited during the same period, presumably for comparison. Sample sizes were small, consistent with the pilot nature of the study.

What were the most important findings?

The ZTD treatment group showed a significant increase in beneficial bacteria, including Bifidobacterium, Lactobacillus, and Faecalibacterium prausnitzii (P < 0.05). Desulfobacterota and Ruminococcus were significantly reduced in the treatment group (P < 0.05). Fecal acetic and propionic acid levels, both short-chain fatty acids linked to anti-inflammatory commensal activity, were also affected by treatment, though the abstract text describing the exact direction and magnitude was cut off.

What are the greatest implications of this study?

The findings suggest ZTD may relieve functional constipation partly by reshaping the gut microbiota toward beneficial, SCFA-producing organisms such as Faecalibacterium prausnitzii while reducing potentially less favorable taxa. This points to a microbiome-mediated mechanism, possibly involving reduced inflammatory signaling through the TLR4/NF-κB pathway, as part of ZTD's therapeutic effect. As a pilot study with a small sample size, these results support further, larger trials to confirm the mechanism and clinical benefit.

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?

The human gut microbiome-endocannabinoidome axis is crucial for several homeostatic processes, including inflammation and energy metabolism, and is influenced by many endogenous and exogenous factors, such as dietary habits. Changes in the gut microbiome in response to seasonal variations were previously reported and tentatively attributed to shifts in dietary patterns. However, there is a need for longitudinal studies in industrialized populations to comprehensively explore seasonal variations independently of lifestyle confounding factors. To investigate the longitudinal effects of seasonal variations on the composition of the gut microbiome and the circulating levels of endocannabinoidome mediators in humans, while elucidating the contributing factors underlying these changes.

Who was studied?

Plasma and fecal samples were collected at the end of both the winter and summer in a longitudinal cohort of 48 individuals living in Québec City (Canada). Dietary habits, medical history, fecal microbiota taxonomic composition and plasma levels of circulating N‑acyl‑ethanolamines (NAEs) and 2‑monoacyl-glycerols (2‑MAGs) were obtained at each time point.

What were the most important findings?

Lower circulating levels of most NAEs were observed at the end of summer. These changes were accompanied by a reduction in the relative abundance of the Bifidobacteriaceae and Lachnospiraceae families, along with an increase in the abundance of the Bacteroidaceae and Ruminococcaceae families. These seasonal variations were not associated with concurrent changes in adiposity parameters, dietary intakes, physical activity habits, or vitamin D status. Importantly, the magnitude of the shift in gut microbiota composition from winter to summer was found to be associated with the seasonal variations in circulating endocannabinoidome (eCBome) mediators.

What are the greatest implications of this study?

This study identified specific seasonal changes in gut microbiota composition and circulating levels of several NAEs, which were not associated with vitamin D status and lifestyle habits. It underscores the importance of the gut microbiota-endocannabinoidome axis in the pathophysiology of seasonal changes, and of considering seasons in clinical trials on these systems.

What was studied?

This study aimed to explore the distinct characteristics of the gut microbiota in tuberculosis (TB) patients who experienced liver injury following anti-TB treatment compared with those who did not.

Who was studied?

We employed a nested case-control study design, recruiting newly diagnosed pulmonary TB patients at Tangshan Infectious Disease Hospital. Participants were categorized into the Antituberculosis Drug-Induced Liver Injury (ADLI) group and the Non-ADLI group based on the occurrence of liver injury after treatment. Both groups received identical anti-TB regimens. Stool samples were collected from patients who developed liver injury within 2-3 weeks of starting treatment, alongside matched controls during the same timeframe. The samples underwent 16S rDNA sequencing, and clinical data and blood samples were also collected for further analysis. At the same time, we constructed mouse models to explore the effects of different anti-tuberculosis drugs on gut microbiota.

What were the most important findings?

Following anti-TB treatment, we observed a decrease in microbial diversity and significant structural changes in the gut microbiota of TB patients (P < 0.05). At T1, the Non_ADLI_T1 group presented relatively high levels of Phascolarctobacterium, Anaerofustis and Mailhella. In contrast, the ADLI_ T1 group presented elevated levels of Bacteroides, Veillonella, Clavibacter, Corynebacterium, Anaerococcus, Gardnerella, Peptostreptococcus and Lautropia. At T2, the ADLI_T2 group presented increased levels of Enterococcus, Faecalibacterium, unclassified_f__Burkholderiaceae, Cardiobacterium, Ruminococcus_gnavus_group and Tyzzerella_4 than did the Non_ADLI_T2 group. Additionally, the ADLI_T2 group presented decreased levels of Prevotella_9, Akkermansia, Erysipelotrichaceae_UCG-003, Rubrobacter and norank_f__Desulfovibrionaceae than did the Non_ADLI_T2 group. In animal experiments, similar changes to those in the human population were observed in the mouse model compared to the control group. Any single anti-tuberculosis drug or two-drug combination or three-drug combination can cause dysbiosis of the mouse gut microbiota. The signature genera between groups are different and related to the type of anti-tuberculosis drug.

What are the greatest implications of this study?

Anti-tuberculosis treatment induces dysbiosis in the gut microbiota of TB patients. Notably, there are significant differences in microbiota characteristics between TB patients with and without liver injury at both onset and during treatment. There are some differences in the characteristics of bacterial flora in liver injury caused by different drugs.

What was studied?

In the diverse landscape of African hominids, the obligate relationship between the host and its microbiome narrates signals of adaptation and co-evolution. Sequencing 546 African hominid metagenomes, including those from indigenous Hadza and wild chimpanzees, identified similar bacterial richness and diversity surpassing those of westernized populations. While hominids share core bacterial communities, they also harbor distinct, population-specific bacterial taxa tailored to specific diets, ecology and lifestyles, differentiating non-indigenous and indigenous humans and chimpanzees. Even amongst shared bacterial communities, several core bacteria have co-diversified to fulfil unique dietary degradation functions within their host populations. These co-evolutionary trends extend to non-bacterial elements, such as mitochondrial DNA, antimicrobial resistance, and parasites. Our findings indicate that microbiome-host co-adaptations have led to both taxonomic and within taxa functional displacements to meet host physiological demands. The microbiome, in turn, transcends its taxonomic interchangeable role, reflecting the lifestyle, ecology and dietary history of its host.

What was studied?

UNLABELLED: This study investigated the longitudinal effects of acute (7-day) and prolonged (3-month) high-altitude exposure on gut microbiota in healthy adult males, addressing the limited data available in human populations. A cohort of 406 healthy adult males was followed, and fecal samples were collected at three time points: baseline at 800 m (406 samples), 7 days after ascending to 4,500 m (406 samples), and 2 weeks post-return to 800 m following 3 months at high altitude (186 samples). High-throughput 16S ribosomal DNA sequencing was employed to analyze microbiota composition and diversity. Results revealed significant changes in alpha- and beta-diversity, with acute high-altitude exposure inducing more pronounced effects compared to prolonged exposure. Specifically, acute exposure increased opportunistic pathogens (Ruminococcus and Oscillibacter) but decreased beneficial short-chain fatty acid producers (Faecalibacterium and Bifidobacterium). Notably, these changes in microbiota persisted even after returning to low altitude, indicating long-term remodeling. Functional analyses revealed substantial changes in metabolic pathways, suggesting microbiota-driven adaptations to energy utilization under high-altitude hypoxic conditions. In summary, acute high-altitude exposure caused dramatic changes in gut microbiota, while prolonged exposure led to structural and functional reshaping. These findings enhance our understanding of how high-altitude environments reshape gut microbiota. IMPORTANCE: This study is the first to investigate the impact of high-altitude exposure on gut microbiota adaptation in a large-scale longitudinal cohort. It seeks to enhance understanding of how high-altitude environments reshape gut microbiota. Acute exposure to high altitude significantly affected both α-diversity and β-diversity of gut microbiota, with acute exposure causing more pronounced changes than prolonged adaptation, indicating temporary disruptions in microbial communities. Notable shifts in microbial abundance were observed, including increased levels of genera linked to hypoxic stress (e.g., Gemmiger, Ruminococcus, and Parabacteroides) and decreased levels of beneficial bacteria (e.g., Faecalibacterium, Roseburia, and Bifidobacterium), suggesting possible adverse health effects. Functional analysis indicated changes in metabolism-related pathways post-exposure, supporting the idea that high-altitude adaptations involve metabolic adjustments for energy management. These findings enhance understanding of high-altitude physiology, illustrating the role of gut microbiota in hypoxic health.

What was studied?

We developed a two-tiered strategy aiming to identify gut bacteria functionally linked to the development of multiple sclerosis (MS). First, we compared gut microbial profiles in a cohort of 81 monozygotic twins discordant for MS. This approach allowed to minimize confounding effects by genetic and early environmental factors and identified over 50 differently abundant taxa with the majority of increased taxa within the Firmicutes. These included taxa previously described to be associated with MS (Anaerotruncus colihominis and Eisenbergiella tayi), along with newly identified taxa, such as Copromonas and Acutalibacter. Second, we interrogated the intestinal habitat and functional impact of individual taxa on the development of MS-like disease. In an exploratory approach, we enteroscopically sampled microbiota from different gut segments of selected twin pairs and compared their compositional profiles. To assess their functional potential, samples were orally transferred into germfree transgenic mice prone to develop spontaneous MS-like experimental autoimmune encephalomyelitis (EAE) upon bacterial colonization. We found that MS-derived ileal microbiota induced EAE at substantially higher rates than analogous material from healthy twin donors. Furthermore, female mice were more susceptible to disease development than males. The likely active organisms were identified as Eisenbergiella tayi and Lachnoclostridium, members of the Lachnospiraceae family. Our results identify potentially disease-facilitating bacteria sampled from the ileum of MS affected twins. The experimental strategy may pave the way to functionally understand the role of gut microbiota in initiation of MS.

What was studied?

Canine atopic dermatitis (cAD) is a chronic inflammatory disease that significantly reduces the quality of life in dogs. Dysbiosis of the gut microbiota affects skin diseases through the gut-skin axis. Therefore, microbiota-targeted therapy may potentially serve as a new management strategy for cAD. The present study aimed to investigate the association between gut microbiota and cAD and to evaluate the effect of probiotics on the clinical symptoms of cAD and gut microbiota in dogs.

What were the most important findings?

Gut microbiota was analyzed at baseline and after 8 and 16 weeks. Baseline analysis revealed significantly lower (p < 0.05) gut microbial diversity in dogs with cAD than in healthy dogs. Differential abundance analysis showed that Fusobacterium, Megamonas, Collinsella, unclassified Clostridiales, Bacillus, Helicobacter, and Caproiciproducens were significantly more abundant in healthy dogs. In contrast, Clostridioides, Erysipelatoclostridium, Clostridium, Terrisporobacter, and unclassified Ruminococcaceae were significantly more abundant in dogs with cAD, In addition, differential abundance analysis showed that the abundance of 46 metabolic pathways were significantly different between healthy dogs and dogs with cAD indicating the dysbiosis of the gut microbiota in cAD. Moreover, the clinical severity of cAD was negatively correlated (p < 0.05) with alpha diversity and the abundance of Fusobacterium and Megamonas. Notably, daily probiotic administration for 16 weeks significantly decreased the clinical severity (p < 0.05). Dogs with good prognoses exhibited significantly increased alpha diversity, whereas those with poor prognoses did not, suggesting that the therapeutic effects of probiotics may be mediated by changes in gut microbial diversity.

What are the greatest implications of this study?

This study highlights the association between gut microbiota dysbiosis and cAD in dogs and demonstrates that probiotic administration can effectively ameliorate cAD by improving gut microbial dysbiosis. These findings provide a basis for novel microbiota-based therapies in cAD treatment.

Who was studied?

Twenty healthy adult dogs were allocated into two groups: the control group (CON) and the yeast probiotic supplementation (YPS). All dogs were initially fed Diet 1 for 4 weeks, followed by an abrupt switch to Diet 2 for another 4 weeks. Throughout the study, the YPS group received 0.1% Actisaf® Sc 50 product in a capsule given with their food, while the control group received a placebo.

What were the most important findings?

Compared to the CON group, the YPS group exhibited lower serum globulin levels and higher albumin-to-globulin ratios on days 28 and 56 (p < 0.05). On day 56, the YPS group showed lower white blood cell counts and lower serum glucose levels (p < 0.05). Fecal IgA concentrations were higher in the YPS group on days 28, 30, 42, and 56 (p < 0.05). In the CON group, the abundance of Firmicutes significantly increased and the abundance of Fusobacteriota and Bacteroidota significantly decreased on days 42 compared to day 28 (q < 0.05). The YPS group showed a more stable gut microbiota transition post-dietary change. In the CON group, no significant changes in metabolite composition were observed 2 days after the dietary transition, but notable changes appeared after 2 weeks. In contrast, the YPS group exhibited substantial changes in metabolite composition 2 days after the diet change. Tyrosine metabolism showed significant changes in both groups of dogs following the dietary transition.

What are the greatest implications of this study?

Saccharomyces cerevisiae supplementation during rapid dietary transition in dogs led to beneficial changes in blood parameters, increased fecal IgA levels, and promoted a more stable gut microbiota. These findings suggest that yeast probiotics may support gut health and immune function during periods of dietary change.

What was studied?

Metabolic syndrome (MS) and type 2 diabetes (T2D) are metabolically related diseases with rising global prevalence and increasingly evident links to the intestinal microbiota. Research suggests that imbalances in microbiota composition may play a crucial role in their pathogenesis. Specific population cohorts, such as the one in Galicia, Spain, offer the opportunity to analyze microbiota patterns within a distinct geographical and genetic context. This study was performed to investigate the relationship between the intestinal microbiota and MS and T2D.

Who was studied?

A cohort of 79 volunteers was analyzed over a 2-year study period. Recruitment posed significant challenges because of strict inclusion criteria (918PTE0540; PCI2018-093284), which required participants to be free from chronic medications and have a moderate to high risk of developing T2D. Volunteers were classified based on their serum glucose levels, body mass index, and the presence or absence of MS. To analyze the microbiota composition, amplicon sequencing of 16S rRNA genes was performed on stool samples. Alpha diversity was assessed using the Chao and Shannon indices, while beta diversity was evaluated using permutational analysis of variance with Bray-Curtis and Chao distances. Differential abundance analysis was conducted using the LinDA method.

What were the most important findings?

In patients with MS, we observed a higher Firmicutes/Bacteroidetes ratio and an increased prevalence of Blautia compared to healthy patients. than in healthy individuals. Other enriched taxa in patients with MS included Tyzerella, Streptococcus, and Ruminococcus callidus. In patients with T2D, we observed a higher Bacteroidetes/Firmicutes ratio and a decrease in the phylum Actinobacteria compared with healthy individuals. Taxa such as Dorea, Prevotella, Dialister invisus, Fusicatenibacter, and Coprococcus were associated with T2D, while beneficial taxa such as Eubacterium, Ligilactobacillus, and Acidaminococcus were more prevalent in healthy or prediabetic individuals.

What are the greatest implications of this study?

This study reveals notable differences in the intestinal microbiota composition among patients with MS and T2D. Changes in microbial composition, particularly the Firmicutes/Bacteroidetes ratio, may serve as indicators of underlying pathology. At more specific taxonomic levels, several enriched taxa were identified in patients with MS, including Blautia, Tyzzerella, Dorea, Streptococcus, and Ruminococcus callidus. Additionally, species such as Dorea longicatena and Dialister invisus were enriched in prediabetic and diabetic patients, whereas beneficial genera (Eubacterium, Acidaminococcus, Bifidobacterium, and Ligilactobacillus) were more prevalent in healthy and prediabetic individuals than in those with T2D.

What was studied?

This study investigated whether gut microbiota composition and plasma metabolic profiles are altered in lymph node tuberculosis (LNTB), a form of tuberculosis whose relationship with gut microbiota had not previously been explored. Researchers used metagenomic sequencing to characterize gut microbial diversity and composition, paired with plasma metabolomics to assess circulating metabolite changes. KEGG pathway analysis was applied to link microbial gene content to metabolic function, focusing especially on short-chain fatty acid (SCFA) biosynthesis. An integrated analysis then examined correlations between specific gut bacteria and plasma metabolites in LNTB.

Who was studied?

The abstract does not report specific participant numbers, ages, or geographic setting. It indicates a comparison between individuals diagnosed with lymph node tuberculosis (the LNTB group) and healthy individuals serving as controls. Samples analyzed included gut microbiota (via metagenomic sequencing) and plasma (via metabolomics) from these two groups.

What were the most important findings?

LNTB patients showed significantly altered gut microbial diversity, with notable reductions in SCFA-producing taxa including Ruminococcus, Faecalibacterium, Roseburia, and Blautia compared to healthy individuals. KEGG pathway analysis indicated that this gut dysbiosis negatively affected SCFA biosynthesis and metabolism. Plasma metabolomics revealed disruptions in metabolites tied to SCFA synthesis and inflammation pathways, and integrated analysis found significant correlations between taxa such as Blautia, Butyricicoccus, Coprococcus, Ruminococcus, Bacteroides, and Clostridium and plasma metabolites including alpha-benzylbutyric acid, acetic acid, and succinic acid.

What are the greatest implications of this study?

The findings suggest that gut microbiota dysbiosis and consequent metabolic dysfunction, particularly reduced SCFA production, may play a role in LNTB pathophysiology. Because SCFAs and related anti-inflammatory commensal bacteria appear diminished in LNTB, restoring these microbial functions could represent a novel therapeutic target for disease management. This work opens a new avenue for considering the gut-immune axis in tuberculosis affecting lymph nodes, beyond the traditional focus on pulmonary disease.

What was studied?

This cross-sectional study examined how westernization affects the gut microbiome by comparing Indians living in India, Indo-Immigrants, and Indo-Canadians against Euro-Canadian and Euro-Immigrant controls. Stool samples underwent 16S rRNA and shotgun sequencing to characterize microbial taxa and functional gene profiles. Dietary and demographic data were also collected to evaluate lifestyle patterns alongside the microbiome data.

Who was studied?

The study population consisted of Indians residing in India, Indo-Immigrants, and Indo-Canadians, compared against Euro-Canadian and Euro-Immigrant control groups. The abstract does not report specific sample sizes or detailed demographic breakdowns for these groups. The comparison design was built around migration status and country of residence rather than clinical diagnosis.

What were the most important findings?

Indians and Indo-Immigrants harbored gut microbiotas distinct from Euro-Canadian and Euro-Immigrant controls, marked by high abundances of Prevotella species and carbohydrate-active enzymes (CAZymes) reflecting a diet rich in complex carbohydrates. Indo-Canadians showed a transitional microbiome profile that moved toward the westernized pattern seen in controls. This shift paralleled increasing dietary acculturation among Indo-Canadians rather than a fixed, heritable microbial signature.

What are the greatest implications of this study?

Because 44% of Canadians are first- or second-generation immigrants, and westernized dietary practices are spreading globally, microbiome transitions like this one may be widespread and consequential. Since Indian immigration to westernized countries has surged and post-migration IBD risk rises accordingly, this dietary-driven microbiome shift may help explain that increased disease susceptibility. The authors call for future research into the health implications of such microbiome transitions in immigrant populations and in newly industrialized nations.

What was studied?

The exploration of how dysbiosis relates to lung masses is still nascent, with few studies focusing on the microbial characteristics across various sites. Therefore, we categorized the microbiota into feces and bronchoalveolar fluid (BALF) groups to compare microbial characteristics between benign and malignant masses, analyze their clinical correlations, and develop predictive models for lung cancer.

Who was studied?

A total of 238 fecal samples and 34 BALF samples were collected from patients with benign and malignant masses and then analyzed by 16 SrRNA. We explored the distinct composition of the gut and lung microbiota and their associations with clinical features. The diagnostic models were constructed using microbial features identified through two approaches: random forest algorithm with five-fold cross-validation and comparative analysis of significantly differential taxa. The performance evaluation was subsequently conducted using receiver operating characteristic (ROC) analysis.

What were the most important findings?

There was no significant difference in α-and β-diversity between feces and BALF groups. The relative abundance of Lachnospiraceae_NK4A136_group (P = 0.003232) and Erysipelotrichaceae_UCG-003 (P = 0.01316) in feces group and Proteobacteria (P = 0.03654) in BALF group were significantly increased in lung cancer patients. We also found Bacteroides (P = 0.01458) was abundant in NSCLC than those of SCLC in feces group, while the BALF group was dominated by norank_c_Cyanobacteria (P = 0.03384). Smoking history appeared to be related to the distribution of microbiota, with enrichment of Parabacteroides (P = 0.02054) in feces and Prevotella_1 (P = 0.03286) in BALF. Furthermore, the patients with Sellimonas (P = 0.04148) in feces and Alloprevotella (P = 0.04283) in BALF seemed to have better response to chemotherapy combined with immunotherapy. For differentiating benign and malignant masses, the combination of Megasphaera and norank_p__Saccharibacteria in BALF demonstrated superior predictive performance, with an AUC reaching 0.8 (95% CI 0.59-1).

What are the greatest implications of this study?

The microbiota composition significantly differed between benign and malignant masses in both fecal and BALF groups, with minimal evidence supporting microbial migration between these two sites. Our findings suggest that BALF microbiota may serve as a more reliable biomarker for lung masses classification, offering valuable insights for early diagnosis and clinical decision-making.

What was studied?

This study examined how obesity affects the gut microbiome and biomarkers of microbial translocation (MT) and inflammation during simian immunodeficiency virus (SIV) infection and subsequent antiretroviral therapy (ART). Researchers tracked changes in gut bacterial community composition alongside circulating markers of gut barrier breakdown and immune activation. The work was motivated by the rising rate of obesity among people living with HIV and the shared role of dysbiosis and impaired gut barrier integrity in driving chronic immune activation in both conditions.

Who was studied?

The study used lean and obese rhesus macaques that were experimentally infected with SIV and then treated with ART. This is an animal model of HIV infection rather than a human cohort, allowing controlled comparison of body-weight status on gut and immune outcomes over the course of infection and treatment. The abstract does not give an exact number of animals per group.

What were the most important findings?

Obese animals had higher MT and inflammation biomarkers from the start, and these levels stayed constant throughout the study, whereas lean animals showed significant increases in these same markers that eventually approached the levels seen in obese animals. At baseline, lean and obese animals had similar numbers of observed amplicon sequence variants (ASVs), but obese animals lost ASV diversity during acute SIV infection before rebounding after 39 weeks of ART. Beta diversity differed between the two groups and continued to shift over time in the obese animals, which also showed significant changes in about four times as many bacterial genera as the lean animals. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism specifically.

What are the greatest implications of this study?

The findings suggest that obesity establishes a baseline state of elevated gut barrier disruption and inflammation that changes little with SIV infection or ART, while lean animals start healthier but converge toward similarly elevated inflammatory states as infection progresses. This implies that obesity may reshape how the gut microbiome and immune activation respond to HIV infection and treatment, with broader and more sustained microbial community disruption in obese hosts. These results support considering body weight status when evaluating gut health and inflammation in people living with HIV on ART.

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?

Thirty participants undergoing health checkups were classified into three groups-normal weight (BMI 18.5-22.9), overweight (BMI 23.0-24.9), and obese (BMI ≥25.0)-with ten individuals per group. Those with H. pylori infection, atrophic gastritis, or intestinal metaplasia were excluded. Gastric microbiota from four antral biopsies per subject were analyzed using 16S rRNA sequencing and functional profiling by metagenomic prediction.

What were the most important findings?

Alpha diversity (Gini-Simpson index) was significantly lower in the combined overweight/obese group than that in the normal group (P=0.049). Beta diversity analysis revealed clear group separation (Bray-Curtis, P=0.005; unweighted UniFrac, P=0.004). Significant species differences between the groups were observed; specifically, the abundances of Muribaculum gordoncarteri, Turicibacter bilis, and Duncaniella dubosii, were significantly reduced in the overweight/obese group. Functional predictions showed differential enrichment of pathways related to fatty acid, amino acid, vitamin, and carbohydrate metabolism across BMI categories. These findings suggest that alterations in the gastric microbiota may be linked to obesity and metabolic dysregulation.

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?

This cross-sectional study examined how vitamin K status relates to gut microbiota composition and inflammation in patients undergoing hemodialysis. Vitamin K status was determined using plasma dephosphorylated-uncarboxylated matrix gla-protein (dp-ucMGP) levels, with adequate status defined as 500 pmol/L or below and inadequate status as above 500 pmol/L. Plasma cytokines were measured with a multiplex assay and uremic toxins by reverse-phase HPLC, while gut microbiota was profiled in a subgroup using fecal DNA extraction and 16S rRNA gene sequencing on the Illumina NovaSeq PE250 platform. The premise was that vitamin K insufficiency in chronic kidney disease may stem from gut dysbiosis that reduces vitamin K-producing bacteria, in turn worsening inflammation, vascular calcification, and oxidative stress.

Who was studied?

The cohort consisted of 107 hemodialysis patients who completed the study, with a median age of 53 years and a median of 36 months on hemodialysis. Of these, 70 patients had inadequate vitamin K status (median age 53 years, BMI 24.2 kg/m2), and 37 patients had adequate vitamin K status (median age 52.5 years, BMI 25.6 kg/m2). Gut microbiota composition was assessed in a subgroup of these patients rather than the full cohort.

What were the most important findings?

The majority of hemodialysis patients in this cohort, 70 of 107, had inadequate vitamin K status based on elevated dp-ucMGP levels. This grouping allowed comparison of plasma cytokines, uremic toxins, and gut microbiota composition between patients with adequate and inadequate vitamin K status. The abstract text provided is truncated before the specific comparative results are given, so the precise microbiota or cytokine differences between groups cannot be stated here. No mention of Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism appears in the portion of the abstract provided.

What are the greatest implications of this study?

The findings support the premise that vitamin K insufficiency is common among hemodialysis patients and may be intertwined with gut microbiota changes and systemic inflammation in chronic kidney disease. This suggests that monitoring vitamin K status, for example via dp-ucMGP, could help identify hemodialysis patients at greater risk of inflammation-related complications such as vascular calcification. It also points to gut microbiota composition as a potential factor connecting vitamin K metabolism to inflammatory processes in this population, warranting further investigation into microbiota-targeted or vitamin K-directed interventions.

What was studied?

This study examined whether the gut microbiome is related to brain structure in apparently healthy adults. The researchers used 16S ribosomal RNA gene sequencing of stool samples to characterize gut microbiome composition and diversity. They paired this with brain magnetic resonance imaging and automated voxel-based morphometry to measure brain volumes, including gray matter and white matter. Statistical methods included principal coordinate analysis, linear discriminant analysis, and multivariable linear regression to test associations between microbiome measures and brain volume.

Who was studied?

The study population was 623 Japanese men drawn from the Shiga Epidemiological Study on Subclinical Atherosclerosis (SESSA), a population-based cross-sectional cohort. Stool samples were collected during the study's follow-up stage, and participants had a mean age of 68.0 years (SD 8.0), ranging from 46 to 83 years. All participants underwent brain MRI as part of the same assessment.

What were the most important findings?

After adjusting for age and total intracranial volume, gray matter volume showed a positive association with alpha diversity, specifically the Shannon index richness, at a q-value below 0.01. However, this association was no longer significant once the analysis further adjusted for body mass index, physical activity, smoking, drinking, and hypertension. Beta diversity, measured using weighted UniFrac distances via principal coordinate analysis, showed differences related to white matter volume, though the abstract text describing this result is incomplete. This pattern of the abstract is not about Christensenellaceae, Christensenella, leanness, BMI-associated taxa, or heritability; the study centers instead on gut microbiome diversity and brain morphometry.

What are the greatest implications of this study?

The findings suggest that in generally healthy older men, any apparent link between gut microbial diversity and gray matter volume may largely reflect shared lifestyle and metabolic factors such as body mass index, physical activity, smoking, drinking, and hypertension rather than a direct, independent relationship. This underscores the importance of adjusting for lifestyle and cardiometabolic confounders when studying gut-brain associations in human populations. The results also support continued investigation of beta diversity and white matter relationships as a potentially distinct avenue linking the gut microbiome to brain structure. Overall, the study adds population-based human evidence to a field previously dominated by animal models and specific patient populations.

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?

Clonorchiasis, a foodborne parasitic disease caused by Clonorchis sinensis (C. sinensis), is prevalent in certain regions of Asia and can result in severe hepatobiliary complications, including cholangiocarcinoma, peribiliary fibrosis, and hepatic fibrosis. In certain regions of China, the concurrent consumption of raw freshwater fish and alcohol, which are components of the local dietary culture, has contributed to the high prevalence of this disease. Infected individuals often endure the dual burden of clonorchiasis and alcoholic liver disease (ALD). While both C. sinensis infection and alcohol abuse can disrupt the gut microbiota, the synergistic mechanisms of these two factors in patients with alcoholic cirrhosis (ALC) remain poorly understood. This study aims to elucidate the impact of C. sinensis infection on the gut microbiota of patients with ALC, with the objective of identifying potential diagnostic or therapeutic targets. A total of 64 patients diagnosed with ALC were recruited for this study, with half of the participants infected with C. sinensis and the other half remaining uninfected. Fresh fecal samples were collected from all participants. Alterations in the gut microbiota were analyzed using high-throughput sequencing of the 16S ribosomal RNA gene derived from the fecal samples. Our results showed that analysis of β-diversity revealed significant differences in gut microbial communities between C. sinensis-infected and non-infected groups (P < 0.05). The Linear discriminant analysis effect size (LEfSe) identified the phylum Firmicutes (highest LDA score at the phylum level) and the genus Prevotella (dominant at the genus level) as key taxa driving gut microbial composition differences in patients with ALC and C. sinensis infection (P < 0.05). Correlation analysis at the genus level demonstrated significant negative associations between Enterococcus and multiple bacterial genera in the C. sinensis-infected group. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis further highlighted divergent metabolic pathways between groups, with the vancomycin resistance pathway showing the most pronounced disparity. In conclusion, patients with ALC and C. sinensis infection show alterations in gut microbiota compared to non-infected counterparts. Notably, specific bacteria such as Prevotella and Enterococcus may represent potential targets for the development of novel diagnostic and therapeutic strategies for ALC patients afflicted by C. sinensis infection.

What was studied?

Fecal microbiota transplantation (FMT) has emerged as a widely used treatment for various diseases. While previous efforts have focused on selecting "super donors", the precise modulation of donor microbiota to enhance FMT efficacy remains a critical challenge. This study aimed to develop strategies to modify donor microbiota to promote gastrointestinal development and maturation in germ-free mice. Probiotic Pediococcus pentosaceus Li05 (Li05) was used as gut microbiota modulator to establish a healthier donor fecal microbiota, and a microencapsulation method was applied to ensure high bacterial viability during gastrointestinal tract transition.

What were the most important findings?

Probiotic intervention initially altered the stability of the gut microbiota but eventually fostered a more complex bacterial interaction network and established a new equilibrium within 14 days. Transplantation of encapsulated Li05-modulated fecal microbiota significantly promoted epithelial development, improved barrier function, and altered the colonic transcriptome profile. These effects were found to be more dependent on the abundance of some bacterial genera instead of their co-occurrence network, and the key functional bacterial genera associated with these benefits were believed to be Parabacteroides, Parasutterella, Lachnoclostridium, Muribaculum and Desulfovibrio. Notably, both encapsulation and probiotic modulation played critical roles in enhancing the functional efficacy of these key bacterial genera, and the community composed of key functional bacteria demonstrated an antagonistic relationship with other bacterial communities. Moreover, encapsulated Li05-modulated fecal microbiota induced dramatical changes in host lipid metabolism, especially the bile acids and their derives. Sporobiota gained the function of promoting epithelium development gene expression only after Li05-modulation since high abundance of Lachnoclostridium was introduced.

What are the greatest implications of this study?

These findings underscore the importance of encapsulation and donor microbiota modulation in FMT and provide valuable strategies for improving transplantation precision and outcomes.

What was studied?

This study examined how the gut microbiome changes across a rural-to-urban lifestyle transition in Indonesia. The researchers assembled metagenome-assembled genomes to characterize species and subspecies diversity within these communities. They also investigated how bacterial physiology, specifically sporulation capacity, relates to how widespread or restricted a given microbial taxon is across villages. Finally, they assessed whether diet variation between communities versus within communities better predicts overall microbiome composition.

Who was studied?

The dataset comes from 116 Indonesians whose lifestyles span transitional hunter-gatherer, rural agricultural, and urban populations. This sampling directly addresses a gap in microbiome research, since existing datasets are heavily biased toward Western urban cohorts and Southeast Asia has been especially under-represented. From these 116 individuals, the team assembled 11,070 metagenome-assembled genomes for analysis.

What were the most important findings?

The researchers identified 1,304 species and 3,258 subspecies, revealing substantial novelty at both the species level (15%) and the subspecies level (50%). Novel taxa tended to be rare, often specific to a single village, and depleted in sporulation genes, linking bacterial physiology to transmission patterns, prevalence, and the likelihood of prior discovery. Clear rural-to-urban clines emerged across multiple levels of biological organization, from individual species abundance to overall microbiome composition and diversity. Diet variation between communities, but not variation within a community, strongly predicted microbiome composition.

What are the greatest implications of this study?

The findings suggest that microbiome divergence across lifestyles is shaped primarily by community-level factors rather than individual-level differences in diet. The link between sporulation genes and village-specific, rarely detected taxa highlights how bacterial physiology influences transmission and the chances a species has been previously characterized. This work underscores the need to expand microbiome sampling beyond Western urban populations to capture the full scope of human microbiome diversity and biogeography. It also demonstrates that lifestyle transition, population structure, and bacterial physiology jointly shape microbiome variation at the scale of human communities.

What was studied?

Background People living with HIV (PLWH) with chronic inflammation may have an increasing risk for coronavirus disease 2019 (COVID-19) severity; however, the impact of their gut microbiota on COVID-19 is not fully elucidated. Here, we analyzed the temporal changes in the gut microbiota composition of hospitalized severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected PLWH (PLWH-CoV) and their correlation with COVID-19 severity. Result The 16S rRNA analysis results using stool samples (along the timeline from disease onset) from 12 hospitalized PLWH-CoV, whose median CD4 + T cell count was 671 cells/µl, were compared to those of 19 healthy people and 25 PLWH. Bacterial diversity in PLWH-CoV is not significantly different from that of healthy people and SARS-CoV-2 non-infected PLWH, but a significant difference in the microbiota diversity was observed in the classification according to the disease severity. Immediately after the disease onset, remarkable changes were observed in the gut microbiota of PLWH-CoV, and the changing with a decrease in some short-chain fatty acid-producing bacteria and an increase in colitis-related pathobiont. In the second week after disease onset, relative amounts of specific bacteria distinguished between disease severity. One month after the disease onset, dysbiosis of the gut microbiota persisted, and the number of Enterobacteriaceae, mainly Escherichia-Shigella, which is potentially pathogenic, increased and were enriched in patients who developed post-acute sequelae of COVID-19 (PASC). Conclusion The changes in the gut microbiota associated with SARS-CoV-2 infection observed in PLWH in this study indicated a persistent decrease in SCFA-producing bacteria and an intestinal environment with an increase in opportunistic pathogens associated with enteritis. This report demonstrates that the intestinal environment in PLWH tends to show delayed improvement even after COVID-19 recovery, and highlights the importance of the dysbiosis associated with SARS-CoV-2 infection as a potential factor in the COVID-19 severity and the PASC in PLWH.

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 examined whether the gut and pharyngeal microbiome is associated with tuberculosis (TB) disease stages. Researchers used full-length 16S rDNA amplicon sequencing performed with Oxford Nanopore Technologies to profile bacterial communities. The comparison spanned TB-negative controls, latent TB, and active TB groups. The goal was to identify microbial differences that track with TB progression from latent to active disease.

Who was studied?

The subjects were 71 cynomolgus macaques, an animal model used to study TB pathogenesis. The macaques were divided into three groups: TB (-) control, TB (+) latent, and TB (+) active. No human cohort was involved, so findings reflect a non-human primate model rather than a human population.

What were the most important findings?

In the pharyngeal microbiome, Haemophilus hemolyticus was decreased and Prevotella species were increased in TB (+) macaques compared to controls. In the gut microbiome, Eubacterium coprostanoligenes was enriched in TB (+) macaques. These shifts distinguished infected animals from TB-negative controls, suggesting that specific taxa track with TB status in both the pharynx and the gut.

What are the greatest implications of this study?

The findings suggest that alterations in gut and pharyngeal bacteria may influence host immune regulation and TB severity, though the underlying mechanisms still need to be explored and validated. This work points to potential host-microbe interactions relevant to TB progression that could inform future understanding of disease biology. It also raises the possibility that microbiome-based markers or targets could eventually contribute to TB therapeutics, pending further mechanistic and translational research.

What was studied?

People living with HIV (PLWH), even when viral replication is controlled through antiretroviral therapy (ART), experience persistent inflammation. This inflammation is partly attributed to intestinal microbial dysbiosis and translocation, which may lead to non-AIDS-related aging-associated comorbidities. The extent to which living with HIV - influenced by the infection itself, ART usage, sexual orientation, or other associated factors - affects the biological age of the intestines is unclear. Furthermore, the role of microbial dysbiosis and translocation in the biological aging of PLWH remains to be elucidated. To investigate these uncertainties, we used a systems biology approach, analyzing colon and ileal biopsies, blood samples, and stool specimens from PLWH on ART and people living without HIV (PLWoH) as controls.

What were the most important findings?

PLWH exhibit accelerated biological aging in the colon, ileum, and blood, as measured by various epigenetic aging clocks, compared to PLWoH. Investigating the relationship between microbial translocation and biological aging, PLWH had decreased levels of tight junction proteins in the intestines, along with increased microbial translocation. This intestinal permeability correlated with faster biological aging and increased inflammation. When investigating the relationship between microbial dysbiosis and biological aging, the intestines of PLWH had higher abundance of specific pro-inflammatory bacteria, such as Catenibacterium and Prevotella. These bacteria correlated with accelerated biological aging. Conversely, the intestines of PLWH had lower abundance of bacteria known for producing the anti-inflammatory short-chain fatty acids, such as Subdoligranulum and Erysipelotrichaceae, and these bacteria were associated with slower biological aging. Correlation networks revealed significant links between specific microbial genera in the colon and ileum (but not in feces), increased aging, a rise in pro-inflammatory microbe-related metabolites (e.g., those in the tryptophan metabolism pathway), and a decrease in anti-inflammatory metabolites like hippuric acid.

What are the greatest implications of this study?

We identified specific microbial compositions and microbiota-related metabolic pathways that are intertwined with intestinal and systemic biological aging. This microbial signature of biological aging is likely reflecting various factors including the HIV infection itself, ART usage, sexual orientation, and other aspects associated with living with HIV. A deeper understanding of the mechanisms underlying these connections could offer potential strategies to mitigate accelerated aging and its associated health complications. Video Abstract.

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?

This study tested whether Parkinson's disease alters the periodontitis-associated oral microbiome. Researchers collected unstimulated saliva samples and stool samples and profiled microbial communities using next-generation sequencing of the 16S ribosomal RNA gene (V1-V3 regions). Clinical, periodontal, and neurological parameters were recorded, including the severity of Parkinson's disease motor dysfunction.

Who was studied?

Three groups were enrolled: patients with periodontitis and Parkinson's disease (PA+P), patients with periodontitis but without Parkinson's disease (P), and systemically and periodontally healthy individuals used as controls (HC). The abstract does not give exact group sizes. The PA+P group had mild to moderate motor dysfunction, and plaque scores were comparable between the PA+P and P groups, indicating similarly effective oral hygiene.

What were the most important findings?

Beta diversity in saliva differed significantly between HC and PA+P, between HC and P, and between P and PA+P groups, showing that both periodontitis and the presence of Parkinson's disease reshape the oral microbial community. Saliva and fecal microbial profiles were distinct from each other. Mycoplasma faucium, Tannerella forsythia, Parvimonas micra, and Saccharibacteria (TM7) were increased in the P group, while Prevotella pallens, Prevotella melaninogenica, and Neisseria multispecies were more abundant in the PA+P group. In fecal samples from the P group, Ruthenibacterium lactatiformans, Dialister succinatiphilus, Butyrivibrio crossotus, and Alloprevotella tannerae were detected.

What are the greatest implications of this study?

The findings support the hypothesis that Parkinson's disease is associated with a distinct periodontitis-related oral microbial signature, separate from periodontitis alone. Because oral and gut microbial profiles diverged between groups despite similar oral hygiene, the results suggest disease-associated shifts rather than simple hygiene differences drive these community changes. This points to the oral-gut microbiome axis as a potential area for further investigation in Parkinson's disease and periodontitis.

What was studied?

Graves' disease (GD), characterized by immune aberration, is associated with gut dysbiosis. Despite the growing interest, substantial evidence detailing the precise impact of gut microbiota on GD's autoimmune processes remains exceedingly rare. This study was designed to investigate the influence of gut microbiota on immune dysregulation in GD.

Who was studied?

It encompassed 52 GD patients and 45 healthy controls (HCs), employing flow cytometry and enzyme-linked immunosorbent assay to examine lymphocyte and cytokine profiles, alongside lipopolysaccharide (LPS) levels. Gut microbiota profiles and metabolic features were assessed using 16S rRNA gene sequencing and targeted metabolomics.

What were the most important findings?

Our observations revealed a disturbed B-cell distribution and elevated LPS and pro-inflammatory cytokines in GD patients compared to HCs. Significant differences in gut microbiota composition and a marked deficit in short-chain fatty acid (SCFA)-producing bacteria, including ASV263(Bacteroides), ASV1451(Dialister), and ASV503(Coprococcus), were observed in GD patients. These specific bacteria and SCFAs showed correlations with thyroid autoantibodies, B-cell subsets, and cytokine levels. In vitro studies further showed that LPS notably caused B-cell subsets imbalance, reducing conventional memory B cells while increasing naïve B cells. Additionally, acetate combined with propionate and butyrate showcased immunoregulatory functions, diminishing cytokine production in LPS-stimulated cells.

What are the greatest implications of this study?

Overall, our results highlight the role of gut dysbiosis in contributing to immune dysregulation in GD by affecting lymphocyte status and cytokine production.

What was studied?

Recent studies have suggested that periodontal disease and alterations in the oral microbiome may be associated with cognitive decline and Alzheimer's disease (AD) development. Here, we report a case-control study of oral microbiota diversity in AD patients compared to healthy seniors from Central Asia. We have characterized the bacterial taxonomic composition of the oral microbiome from AD patients (n = 64) compared to the healthy group (n = 71) using 16S ribosomal RNA sequencing. According to our results, the oral microbiome of AD has a higher microbial diversity, with an increase in Firmicutes and a decrease in Bacteroidetes in the AD group. LEfSe analysis showed specific differences at the genus level in both study groups. A region-based analysis of the oral microbiome compartment in AD was also performed, and specific differences were identified, along with the absence of differences in bacterial richness and on the functional side. Noteworthy findings demonstrated the decrease in periodontitis-associated bacteria in the AD group. Distinct differences were revealed in the distribution of metabolic pathways between the two study groups. Our study confirms that the oral microbiome is altered in AD. However, a comprehensive picture of the complete composition of the oral microbiome in patients with AD requires further investigation.

What was studied?

Schizophrenia (SCZ), as a neurodevelopmental disorder and devastating disease, affects approximately 1% of the world population. Although numerous studies have attempted to elucidate the causes of SCZ occurrence, it is not clearly understood. Recently, the emerging roles of the gut microbiota in a range of brain disorders, including SCZ, have attracted much attention. While the molecular mechanism of gut microbiota in regulating the pathogenesis of SCZ is still lacking. Here, we first confirmed the difference of gut microbiome between SCZ patients and healthy controls, and then, we performed fecal microbiota transplantation (FMT) to clarify the roles of SCZ patients-derived microbiota in a specific pathogen free (SPF) mice model. 16 S rDNA sequencing confirmed that a significant difference of gut microbiome was present between two groups of FMT mice, which has a similar trend with the above human gut microbiome. Furthermore, we found that transplantation of fecal microbiota from SCZ patients into SPF mice was sufficient to induce schizophrenia-like (SCZ-like) symptoms, such as deficits in sociability and hyperactivity. Furthermore, the brains of mice colonized with SCZ microbiota displayed dysregulated transcript response and alternative splicing of SCZ-relevant genes. Moreover, 10 key genes were identified to be correlated with SCZ by an integrative transcriptome data analysis. Finally, 4 key genes were identified to be correlated with the 12 differential genera between two groups of FMT mice. Our results thus demonstrated that the gut microbiome might modify the transcriptomic profile in the brain, thereby modulating social behavior, and our present study can help better understand the link between gut microbiota and SCZ pathogenesis through the gut-brain axis.

What was studied?

The study examined whether gut microbial composition differs between colorectal cancer (CRC) patients who developed liver metastasis (LM) and those who did not (NLM). Researchers used high-throughput 16S rRNA sequencing to characterize microbial richness, diversity, and taxonomic composition in stool and tumor tissue samples. The goal was to identify microbial features associated with LM and poor prognosis in CRC, since liver metastasis is a major driver of mortality in advanced disease and gut microbiota has been linked to liver disease progression.

Who was studied?

The study drew on colorectal cancer patients grouped by metastasis status across three cohorts. A supplementary discovery cohort (cohort 1) analyzed primary carcinoma tissue from 8 LM and 10 NLM patients. A discovery cohort (cohort 2) used fresh feces from 18 LM and 36 NLM patients, and a validation cohort (cohort 3) used fresh feces from 13 LM and 41 NLM patients.

What were the most important findings?

Intestinal microbiota richness and diversity were higher in the LM group compared to the NLM group. Species composition differed significantly between the two groups. Across the two discovery cohorts, which used different sample types, the dominant bacterial phyla were consistent, though composition varied at lower taxonomic levels. The phylum Fusobacteria showed consistent alterations associated with liver metastasis across these analyses.

What are the greatest implications of this study?

The consistent association between Fusobacteria alterations and liver metastasis across independent discovery and validation cohorts suggests gut and tumor-associated microbiota could serve as a biomarker for metastatic risk and prognosis in colorectal cancer. This raises the possibility of using microbial profiling to help identify CRC patients at higher risk of liver metastasis. It also points toward the gut microbiota, and Fusobacteria specifically, as a potential target for future diagnostic or therapeutic strategies in advanced CRC.

What was studied?

Transition from traditional high-fiber to Western diets in urbanizing communities of Sub-Saharan Africa is associated with increased risk of non-communicable diseases (NCD), exemplified by colorectal cancer (CRC) risk. To investigate how urbanization gives rise to microbial patterns that may be amenable by dietary intervention, we analyzed diet intake, fecal 16 S bacteriome, virome, and metabolome in a cross-sectional study in healthy rural and urban Xhosa people (South Africa). Urban Xhosa individuals had higher intakes of energy (urban: 3,578 ± 455; rural: 2,185 ± 179 kcal/d), fat and animal protein. This was associated with lower fecal bacteriome diversity and a shift from genera favoring degradation of complex carbohydrates (e.g., Prevotella) to taxa previously shown to be associated with bile acid metabolism and CRC. Urban Xhosa individuals had higher fecal levels of deoxycholic acid, shown to be associated with higher CRC risk, but similar short-chain fatty acid concentrations compared with rural individuals. Fecal virome composition was associated with distinct gut bacterial communities across urbanization, characterized by different dominant host bacteria (urban: Bacteriodota; rural: unassigned taxa) and variable correlation with fecal metabolites and dietary nutrients. Food and skin microbiota samples showed compositional differences along the urbanization gradient. Rural-urban dietary transition in South Africa is linked to major changes in the gut microbiome and metabolome. Further studies are needed to prove cause and identify whether restoration of specific components of the traditional diet will arrest the accelerating rise in NCDs in Sub-Saharan Africa.

Who was studied?

According to QIIME2, we analyzed 16SrDNA sequencing of the gut microbiome on the Illumina MiSeq. Enzyme-linked immunosorbent assay was used to measure the concentrations of cytokines.

What were the most important findings?

We showed the presence of 26 identifiable differential microbiomes in the gut and 44 metabolic pathways between healthy controls and the different time points in the development of TB in patients. Five bacterial genera (Bacteroides, Bifidobacterium, Faecalibacterium, Collinsella, and Clostridium) were most closely associated with CD4/CD8, whereas three bacterial taxa (Faecalibacterium, Collinsella, and Clostridium) were most closely associated with CD4. Three bacterial taxa (Faecalibacterium, Ruminococcus, and Dorea) were most closely associated with IL-4. Ruminococcus was most closely associated with IL-2 and IL-10.

What are the greatest implications of this study?

Diverse microorganisms, subsets of T cells, and cytokines, exhibiting varying relative abundances and structural compositions, were observed in both healthy controls and patients throughout distinct phases of tuberculosis. Gaining insight into the function of the gut microbiome, T cell subsets, and cytokines may help modulate therapeutic strategies for TB.

What was studied?

Gastric cancer is one of the global health concerns. A series of studies on the stomach have confirmed the role of the microbiome in shaping gastrointestinal diseases. Delineation of microbiome signatures to distinguish chronic gastritis from gastric cancer will provide a non-invasive preventative and treatment strategy. In this study, we performed whole metagenome shotgun sequencing of fecal samples to enhance the detection of rare bacterial species and increase genome sequence coverage. Additionally, we employed multiple bioinformatics approaches to investigate the potential targets of the microbiome as an indicator of differentiating gastric cancer from chronic gastritis.

What were the most important findings?

A total of 65 patients were enrolled, comprising 33 individuals with chronic gastritis and 32 with gastric cancer. Within each group, the chronic gastritis group was sub-grouped into intestinal metaplasia (n = 15) and non-intestinal metaplasia (n = 18); the gastric cancer group, early stage (stages 1 and 2, n = 13) and late stage (stages 3 and 4, n = 19) cancer. No significant differences in alpha and beta diversities were detected among the patient groups. However, in a two-group univariate comparison, higher Fusobacteria abundance was identified in phylum; Fusobacteria presented higher abundance in gastric cancer (LDA scored 4.27, q = 0.041 in LEfSe). Age and sex-adjusted MaAsLin and Random Forest variable of importance (VIMP) analysis in species provided meaningful features; Bacteria_caccae was the most contributing species toward gastric cancer and late-stage cancer (beta:2.43, se:0.891, p:0.008, VIMP score:2.543). In contrast, Bifidobacterium_longum significantly contributed to chronic gastritis (beta:-1.8, se:0.699, p:0.009, VIMP score:1.988). Age, sex, and BMI-adjusted MasAsLin on metabolic pathway analysis showed that GLCMANNANAUT-PWY degradation was higher in gastric cancer and one of the contributing species was Fusobacterium_varium.

What are the greatest implications of this study?

Microbiomes belonging to the pathogenic phylum Fusobacteria and species Bacteroides_caccae and Streptococcus_anginosus can be significant targets for monitoring the progression of gastric cancer. Whereas Bifidobacterium_longum and Lachnospiraceae_bacterium_5_1_63FAA might be protection biomarkers against gastric cancer.

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?

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?

Gut dysbiosis has been established as a characteristic of schizophrenia (SCH). However, the signatures regarding SCH patients with prominent negative symptoms (SCH-N) in young adults have been poorly elucidated.

Who was studied?

Stool samples were obtained from 30 young adults with SCH-N, 32 SCH patients with prominent positive symptoms (SCH-P) along with 36 healthy controls (HCs). Microbial diversity and composition were analyzed by 16S rRNA gene sequencing. Meanwhile, psychiatric symptoms were assessed by the positive and negative syndrome scale (PANSS).

What were the most important findings?

There is a significant difference in β-diversity but not α-diversity indexes among the three groups. Moreover, we found a higher abundance of Fusobacteria and Proteobacteria phyla and a lower abundance of Firmicutes phyla in SCH-N when compared with HC. Besides, we identified a diagnostic potential panel comprising six genera (Coprococcus, Monoglobus, Prevotellaceae_NK3B31_group, Escherichia-Shigella, Dorea, and Butyricicoccus) that can distinguish SCH-N from HC (area under the curve = 0.939). However, the difference in microbial composition between the SCH-N and SCH-P is much less than that between SCH-N and the HC, and SCH-N and SCH-P cannot be effectively distinguished by gut microbiota.

What are the greatest implications of this study?

The composition of gut microbiota was changed in the patients with SCH-N, which may help in further understanding of pathogenesis in young adults with SCH-N.

What was studied?

This study examined how gut microbiota composition differs in children with diarrhea versus children with constipation, compared to healthy children. The researchers used 16S rRNA sequencing on stool samples to profile bacterial communities and looked for microbial diversity changes and specific taxa shifts. They also ran pathway analysis to identify functional mechanisms that might link the two opposite digestive conditions through a shared microbial driver.

Who was studied?

The study included 618 Chinese children aged 0 to 3 years, drawn from a cross-sectional case-control design. Of these, 66 children had diarrhea, 138 had constipation, and 414 were healthy controls. Stool samples were collected from each child for gut microbiota analysis.

What were the most important findings?

Children with diarrhea showed significantly lower gut microbial diversity than healthy controls, while children with constipation showed significantly higher diversity (p < 0.05). Ruminococcus was identified as a key differentiator: it increased in constipation (p = 0.03) and decreased in diarrhea (p < 0.01) relative to healthy children. Pathway analysis linked Ruminococcus to five shared pathways (membrane transport, nervous system, energy metabolism, signal transduction, and endocrine system), suggesting one underlying regulatory mechanism connects both conditions.

What are the greatest implications of this study?

The findings point to Ruminococcus as a core microorganism whose imbalance may disrupt gut steady-state in opposite directions, contributing to either diarrhea or constipation in young children. Because the same genus and overlapping metabolic pathways appear to regulate both conditions, it may serve as a useful reference point for diagnosis. The authors suggest this shared mechanism could inform future treatment approaches that target gut microbial balance rather than treating diarrhea and constipation as unrelated conditions.

What was studied?

This study used shotgun metagenomics to compare the microbial composition and function of normal rectal mucosa against matched fecal samples. The researchers analyzed both microbial taxonomic classification and KEGG Orthology (KO) functional annotations for each sample type. They then examined how the mucosal microbiota related to host factors including age, gender, BMI, and colonic polyp risk level.

Who was studied?

The study included 20 patients with colonic polyps, each contributing a paired sample of normal rectal mucosa and feces. This matched within-person design let the researchers directly compare the two sample types from the same individuals. No further demographic breakdown is given in the abstract beyond age, gender, and BMI being used as variables of interest.

What were the most important findings?

The mucosal and fecal microbiomes were clearly distinct from one another, with the mucosal microbiome containing fewer genera overall. Burkholderia was identified as the single most discriminating genus separating feces from mucosa, indicating a notably strong mucosal presence. The team also identified novel taxonomic biomarkers linked to host factors, such as Clostridium ramosum and Enterobacter cloacae in association with age. Functionally, the mucosal microbiota was enriched for KO pathways involved in sugar transport and short-chain fatty acid metabolism.

What are the greatest implications of this study?

The findings show that fecal samples alone do not capture the distinct microbial community living at the rectal mucosal surface, a gap most gut microbiome research has overlooked. Because the mucosal niche appears compositionally and functionally distinct, with its own host-associated biomarkers and short-chain fatty acid-related activity, mucosal sampling may add diagnostic or mechanistic information that feces cannot provide. This supports incorporating mucosal microbiome analysis alongside fecal analysis in future studies of colonic polyps and related conditions.

What was studied?

This study examined the composition and function of the gut microbiota in people with schizophrenia. Researchers used both 16S rRNA gene sequencing and whole-genome shotgun metagenomic sequencing to characterize microbial diversity, taxonomic composition, and functional gene content. The aim was to explore how gut microbes, acting through the gut-brain axis, might relate to this severe and complex psychiatric disorder.

Who was studied?

The study included 29 patients diagnosed with schizophrenia and 30 age-matched normal controls. This is a relatively small clinical cohort, and the abstract does not specify additional demographic details such as sex distribution, geographic location, or illness duration. Both 16S rRNA and metagenomic sequencing were performed on samples from these same participants.

What were the most important findings?

Patients with schizophrenia had higher abundances of the bacterial genera Clostridium and Megasphaera compared to controls. Functional analysis linked schizophrenia to alterations in sphingolipid metabolism, phosphonate and phosphinate metabolism, and glutamine metabolism. These findings were consistent across both the 16S rRNA and metagenomic sequencing approaches. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.

What are the greatest implications of this study?

The findings support the idea that the gut microbiota has a measurable effect on schizophrenia, reinforcing the relevance of the gut-brain axis to this disorder. Specific taxa such as Clostridium and Megasphaera, along with the identified metabolic pathways, may serve as leads for future mechanistic or biomarker research. These results provide a foundation for further investigation into microbiome-based understanding or management of schizophrenia.

What was studied?

This study examined whether a history of repeated, but not recent, antibiotic use has lasting effects on the gut microbiota and on microbiota-mediated intestinal mucus barrier function. Researchers used human-to-mouse fecal microbiota transplantation to transfer gut microbial communities from previously antibiotic-exposed and healthy individuals into mice. They then measured mucus growth rate and mucus penetrability using ex vivo analyses of viable colonic tissue explants, and characterized the transplanted microbiota using shotgun metagenomic sequencing and metabolite profiling.

Who was studied?

The human source population was drawn from the deeply phenotyped Estonian Microbiome Cohort (EstMB), from which individuals with a history of repeated antibiotic use and healthy controls were selected for fecal sampling. The functional experiments were then carried out in mice that received fecal microbiota transplants from these human donors, so the mucus and microbiota outcomes reported reflect this humanized mouse model rather than direct measurements in the human donors themselves.

What were the most important findings?

Mice transplanted with microbiota from humans with a history of repeated antibiotic use showed a reduced mucus growth rate and increased mucus penetrability compared to mice given microbiota from healthy controls. Shotgun metagenomic sequencing showed the antibiotic-shaped microbial community had a significantly altered composition, with mucus-utilizing bacteria, including Akkermansia muciniphila and Bacteroides fragilis, dominating the gut. This altered microbiota was also marked by a distinct metabolite profile.

What are the greatest implications of this study?

The findings suggest that repeated antibiotic use can leave a lasting, microbiota-encoded imprint on the gut that impairs the mucus barrier long after the antibiotics themselves are gone. Because a healthy mucus layer normally protects the intestinal epithelium against infection and inflammation, this microbiota-driven thinning and increased penetrability could plausibly raise vulnerability to gut infection or inflammatory conditions. The dominance of mucus-utilizing organisms such as Akkermansia muciniphila and Bacteroides fragilis points to microbial mucus consumption as a candidate mechanism linking antibiotic history to barrier dysfunction, warranting further mechanistic study.

What was studied?

Person with human immunodeficiency virus type-1 (PWH) are prone to chronic inflammation due to residual viral production, even with antiretroviral therapy (ART), which increases the risk of age-related diseases. There is also limited information on changes in the intestinal environment of PWH during ART. In this longitudinal study, we investigated changes in the gut microbiota, persistence of chronic inflammation, interactions between the gut environment and inflammation, and metabolic changes in PWH using long-term ART.

What were the most important findings?

We analyzed changes in clinical parameters and gut microbiota in 46 PWH over a mean period of 4 years to understand the influence of gut dysbiosis on inflammation. Overall, changes in the gut microbiota included a decrease in some bacteria, mainly involved in short-chain fatty acid (SCFA) production, and an increase in certain opportunistic bacteria. Throughout the study period, an increase in bacterial-specific metabolic activity was observed in the intestinal environment. Continued decline in certain bacteria belonging to the Clostridia class and metabolic changes in gut bacteria involved in glucose metabolism. Additionally, patients with a low abundance of Parabacteroides exhibited low bacterial alpha diversity and a significant increase in body mass index (BMI) during the study period. Monocyte chemoattractant protein 1, a marker of macrophage activation in the plasma, continued to increase from baseline (first stool collection timepoint) to follow-up (second stool collection timepoint), demonstrating a mild correlation with BMI. Elevated BMI was mild to moderately correlated with elevated levels of plasma interleukin 16 and chemokine ligand 13, both of which may play a role in intestinal inflammation and bacterial translocation within the gut microbiota. The rate of BMI increase correlated with the rate of decrease in certain SCFA-producing bacteria, such as Anaerostipes and Coprococcus 3.

What are the greatest implications of this study?

Our data suggest that despite effective ART, PWH with chronic inflammation exhibit persistent dysbiosis associated with gut inflammation, resulting in a transition to an intestinal environment with metabolic consequences. Moreover, the loss of certain bacteria such as Parabacteroides in PWH correlates with weight gain and may contribute to the development of metabolic diseases.

What was studied?

Scavenging indigenous village chickens play a vital role in sub-Saharan Africa, sustaining the livelihood of millions of farmers. These chickens are exposed to vastly different environments and feeds compared to commercial chickens. In this study, we analysed the caecal microbiota of 243 Ethiopian village chickens living in different altitude-dependent agro-ecologies.

What were the most important findings?

Differences in bacterial diversity were significantly correlated with differences in specific climate factors, topsoil characteristics, and supplemental diets provided by farmers. Microbiota clustered into three enterotypes, with one particularly enriched at high altitudes. We assembled 9977 taxonomically and functionally diverse metagenome-assembled genomes. The vast majority of these were not found in a dataset of previously published chicken microbes or in the Genome Taxonomy Database.

What are the greatest implications of this study?

The wide functional and taxonomic diversity of these microbes highlights their importance in the local adaptation of indigenous poultry, and the significant impacts of environmental factors on the microbiota argue for further discoveries in other agro-ecologies. Video Abstract.

What was studied?

This study investigated gut microbiota composition and systemic immune function in patients with schizophrenia comorbid with metabolic syndrome (SZ-MetS). Researchers used 16S rRNA gene sequencing (V3-V4 hypervariable regions) to profile fecal bacterial communities. They paired this with a 27-plex cytokine assay to characterize host immune responses. The goal was to clarify how gut dysbiosis and immune dysfunction relate to one another in this comorbid condition.

Who was studied?

The study enrolled 114 Chinese patients with schizophrenia comorbid with metabolic syndrome and 111 age-matched healthy controls, all recruited from Zhejiang, China. Fecal samples from these participants were sequenced to assess gut bacterial diversity and composition. Blood-based cytokine profiling was performed using the same cohort to link microbial and immune findings.

What were the most important findings?

Patients with SZ-MetS showed decreased bacterial alpha-diversity and significant shifts in beta-diversity compared to healthy controls. LEfSe analysis identified enrichment of acetate-producing genera, specifically Megamonas and Lactobacillus, alongside depletion of butyrate-producing bacteria, including Subdoligranulum and Faecalibacterium. These altered bacterial genera correlated with body mass index and with the severity of clinical measures, linking microbial shifts to metabolic and disease-related parameters. The abstract did not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.

What are the greatest implications of this study?

The findings suggest that gut dysbiosis, marked by loss of butyrate producers and gain of acetate producers, may contribute to the pathogenesis of metabolic syndrome in people with schizophrenia. This supports a role for the gut microbiota as a potential mechanistic link between psychiatric illness and metabolic dysfunction. It also raises the possibility that microbiome-targeted approaches could be explored as adjunctive strategies for this high-risk comorbid population.

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?

The respiratory microbiota plays a crucial role in the development of tuberculosis (TB). While existing research has underscored imbalances in the respiratory microbiota of adult patients with TB, information regarding the lower respiratory tract (LRT) microbiota in pediatric patients with TB remains scarce.

Who was studied?

We employed 16S rRNA gene sequencing technology to investigate the LRT microbial communities of 85 children of different ages with active TB of different severities, 33 children with infectious diseases other than TB, and 48 sex- and age-matched healthy children.

What were the most important findings?

A marked imbalance in the respiratory microbiota was observed in children with TB, highlighted by reduced alpha diversity and a distinct microbial community structure. Comparative analysis indicated that patients with severe TB exhibited lower Neisseria levels than those with non-severe TB (1.01% vs. 3.93%, respectively; p = .02). Streptococcus and Gemella levels were lower in bacteriologically confirmed TB cases compared with clinically diagnosed cases, and higher in healthy children younger than 10 years old than in the older group. Spearman correlation analysis demonstrated significant associations between the microbiota of the LRT and cytokine concentrations in the sputum of children with TB (e.g., an inverse correlation between Veillonella and interleukin-17A).

What are the greatest implications of this study?

TB induced significant dysbiosis in the LRT microbiota of children that was associated with disease severity and the immunological response in the respiratory tract. Our findings may offer a deeper understanding of the role of the respiratory microbiome in TB pathogenesis and progression.

What was studied?

This study examined how the gut microbiome and serum metabolome differ between people with lactose intolerance (LI) and those without it. The researchers combined a paired-sample analysis of American Gut Project (AGP) data with metagenomic and untargeted metabolomic analyses in a separate cohort. They also performed fecal microbiota transplantation (FMT) experiments to test whether the LI-associated gut microbiome could influence inflammatory outcomes. The goal was to characterize the interaction between gut microbiota and circulating metabolites in LI.

Who was studied?

The study drew on two data sources: paired samples from the American Gut Project (AGP), a large public microbiome dataset, and a Chinese cohort in which metagenomic and metabolomic profiling was performed. The abstract does not give exact sample sizes for either group. FMT experiments were also conducted, implying an animal model component, though further details are not specified in the abstract.

What were the most important findings?

Fourteen microbial genera differed significantly between LI and control individuals in the AGP data. In the Chinese cohort, a machine learning approach identified seven bacterial species and nine metabolites that could distinguish the two groups. Notably, increased Escherichia coli in the LI group was negatively correlated with several metabolites, including PC (22:6/0:0), indole, and Lyso PC, while reduced levels of Faecalibacterium prausnitzii and Eubacterium rectale were positively associated with other metabolic changes.

What are the greatest implications of this study?

The findings suggest that lactose intolerance is accompanied by a distinct gut microbial and metabolic signature, not just a lactase enzyme deficiency. The rise in Escherichia coli alongside depletion of beneficial short-chain-fatty-acid producers like Faecalibacterium prausnitzii and Eubacterium rectale points to a shift toward a more pro-inflammatory microbial community. This raises the possibility that microbiome-targeted interventions could help manage LI-related gastrointestinal symptoms, and the FMT experiments support a causal link between this altered microbiome and inflammatory outcomes.

What was studied?

This study examined how laparoscopic sleeve gastrectomy (LSG), a form of bariatric surgery, affects cognitive function through the microbiota-gut-brain axis (MGBA). Researchers integrated fecal 16S microbiota profiling, serum metabolomics, cognitive assessment scales, and resting-state functional connectivity MRI (rs-fMRI) to capture changes across the gut, blood, and brain simultaneously. Correlation-based statistical methods, including Spearman correlation and Co-inertia analysis, were used to link microbiota shifts and metabolite changes to changes in brain connectivity and cognitive scores.

Who was studied?

The cohort consisted of 39 obese patients who underwent laparoscopic sleeve gastrectomy. Each patient was assessed at two time points, before surgery and six months after, using demographic data, serum samples, fecal samples, cognitive testing, and rs-fMRI scans. The abstract does not specify age, sex distribution, or geographic location of the cohort.

What were the most important findings?

LSG produced substantial weight loss, with reductions of up to 28% of body weight at six months. The surgery was accompanied by measurable changes in gut microbiota composition, serum metabolite profiles, and brain functional connectivity networks identified through rs-fMRI. The abstract indicates that these multi-omics changes were statistically correlated with alterations in cognitive assessment scores, suggesting coordinated shifts across the gut-brain axis, though the specific taxa, metabolites, and brain regions most strongly implicated are not detailed in the available text.

What are the greatest implications of this study?

The findings support the idea that bariatric surgery's cognitive benefits may be mediated in part by changes in gut microbiota and their downstream metabolic effects on the brain, rather than weight loss alone. This multi-omics approach, linking microbiota, serum metabolomics, and neuroimaging, offers a framework for identifying specific microbial and metabolic targets that could explain or potentially enhance post-surgical cognitive improvement. Further work identifying the exact bacterial taxa and metabolites involved could inform future non-surgical interventions aimed at the same gut-brain pathways.

What was studied?

This prospective cohort pilot study investigated whether oral, vaginal, and stool microbial communities could serve as non-invasive diagnostic biomarkers for endometriosis. Researchers self-collected samples from each of the three body sites at a single time point, then performed 16S rRNA amplicon sequencing followed by bioinformatics analysis. Diversity analyses and LEfSe were used to compare microbial composition and identify differentially abundant taxa across groups.

Who was studied?

The study enrolled sixty-four age- and sex-matched subjects recruited at Nepean Hospital and the UNSW Microbiome Research Centre in Australia. Participants were divided into three cohorts: 19 healthy controls, 24 non-endometriosis patients, and 21 patients with confirmed endometriosis. All participants other than healthy controls underwent laparoscopic surgical assessment, with histology performed on excised lesions to confirm diagnosis.

What were the most important findings?

Oral microbiota composition differed significantly between the three cohorts, as did stool microbiota composition. LEfSe analysis identified differentially abundant taxa distinguishing each group. Notably, Fusobacterium was enriched in the oral samples of patients with moderate or severe disease.

What are the greatest implications of this study?

These findings suggest that oral and stool microbial signatures, rather than vaginal samples alone, may carry diagnostic signal for distinguishing endometriosis from non-endometriosis and healthy states. The enrichment of Fusobacterium in more severe disease raises the possibility that microbial shifts track with disease severity. If validated in larger cohorts, this approach could support development of a non-invasive diagnostic test that reduces reliance on laparoscopic surgery for endometriosis diagnosis.

What was studied?

This study examined how exclusive enteral nutrition (EEN), a first-line therapy for pediatric Crohn's disease, produces its protective effects on the gut. The researchers used integrated multi-omics analysis of fecal microbiota and metabolites to identify functional network clusters associated with treatment response. They further validated these diet-driven microbiome changes using gut chemostat cultures and by transferring microbiota into germ-free Il10-deficient mice.

Who was studied?

The abstract describes a prospective pediatric cohort of treatment-naive Crohn's disease patients, registered as German Clinical Trials DRKS00013306, who were followed as they began EEN therapy. Exact patient numbers are not given in the abstract. Findings from this human cohort were then extended experimentally using gnotobiotic (germ-free) Il10-deficient mice colonized with patient-derived microbiota.

What were the most important findings?

Multi-omics analysis identified individually variable microbiome network clusters, with Lachnospiraceae and medium-chain fatty acids emerging as protective features associated with EEN response. Bioorthogonal non-canonical amino acid tagging pinpointed specific bacterial species that responded to medium-chain fatty acids, and metagenomic analysis revealed high strain-level dynamics during EEN therapy. When patient-derived microbiota were transferred into gnotobiotic Il10-deficient mice, individual patient-specific strain signatures could either prevent or cause inflammatory bowel disease-like inflammation.

What are the greatest implications of this study?

The findings show that EEN operates through explicit, functional, and highly individualized changes in the fecal microbiome rather than a single uniform mechanism. Because protective effects were tied to specific strains and metabolites such as medium-chain fatty acids, this suggests that microbiome and metabolite profiling could help predict or enhance EEN response in pediatric Crohn's disease. The demonstration that individual strain signatures can causally prevent or induce inflammation in a gnotobiotic model also supports strain-level and metabolite-targeted approaches as a path toward more precise dietary or microbial therapies for Crohn's disease.

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?

Many human-targeted drugs alter the gut microbiome, leading to implications for host health. However, the mechanisms underlying these effects are not well known. Here we combined quantitative microbiome profiling, long-read metagenomics, stable isotope probing and single-cell chemical imaging to investigate the impact of two widely prescribed drugs on the gut microbiome. Physiologically relevant concentrations of entacapone, a treatment for Parkinson's disease, or loxapine succinate, used to treat schizophrenia, were incubated ex vivo with human faecal samples. Both drugs significantly impact microbial activity, more so than microbial abundance. Mechanistically, entacapone can complex and deplete available iron resulting in gut microbiome composition and function changes. Microbial growth can be rescued by replenishing levels of microbiota-accessible iron. Further, entacapone-induced iron starvation selected for iron-scavenging gut microbiome members encoding antimicrobial resistance and virulence genes. These findings reveal the impact of two under-investigated drugs on whole microbiomes and identify metal sequestration as a mechanism of drug-induced microbiome disturbance.

What was studied?

Background/Objectives: The prevalence of food allergy (FA) in children is increasing. Dysbiosis of the microbiome has been linked to FA but needs to be better understood. We aimed to characterize the gut and skin microbiome of young food-allergic children over time and within different types of immunoglobulin E (IgE)-mediated FA. Methods: We studied 23 patients, as a pilot study of an ongoing prospective multicenter cohort study including children < 2y with newly diagnosed IgE-mediated FA. Samples (feces/skin swabs) were collected at enrollment and at 1-year follow-up and sequenced for the bacterial 16S rRNA gene (hypervariable v1–v2 region). Results: Gut and skin bacterial diversity was significantly higher in patients compared with controls and increased over time (beta test, Shannon diversity, p < 0.01). Within different types of IgE-mediated FA, bacterial diversity was similar. Community composition differed significantly over time and within IgE-mediated FA types (PERMANOVA: p < 0.01). Several significantly different genus abundances were revealed. We observed a positive correlation between high total IgE and a high abundance of the genus Collinsella in patients with a higher number of allergies/sensitizations (≥3), and patients with tree nut and/or peanut allergy. Conclusions: This study revealed an increased bacterial diversity in children with FA compared with non-atopic children. Importantly, the gut and skin microbiome differed in their composition over time and within different types of IgE-mediated FA. These findings contribute to the understanding of microbiome changes in children with FA and indicate the potential of the genus Collinsella as a biomarker for tree nut and/or peanut allergy and possibly for allergy persistence.

What was studied?

Developing microbiome-based markers for pediatric inflammatory bowel disease (PIBD) is challenging. Here, we evaluated the diagnostic and prognostic potential of the gut microbiome in PIBD through a case-control study and cross-cohort analyses. In a Korean PIBD cohort (24 patients with PIBD, 43 controls), we observed that microbial diversity and composition shifted in patients with active PIBD versus controls and recovered at remission. We employed a differential abundance meta-analysis approach to identify microbial markers consistently associated with active inflammation and remission across seven PIBD cohorts from six countries (n = 1,670) including our dataset. Finally, we trained and tested various machine learning models for their ability to predict a patient's future remission based on baseline bacterial composition. An ensemble model trained with the amplicon sequence variants effectively predicted future remission of PIBD. This research highlights the gut microbiome's potential to guide precision therapy for PIBD.