Helicobacter

What was studied?

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

Who was studied?

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

What were the most important findings?

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

What are the greatest implications of this study?

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

What was studied?

Noma is a rapidly progressive orofacial gangrene that predominantly affects children living in extreme poverty. Despite its documentation since antiquity and its designation as a World Health Organisation Neglected Tropical Disease in 2023, the microbiological cause of noma remains poorly understood, with no specific organisms confidently identified as definitive aetiological agents. Here, we present the first deep shotgun metagenomic profiling of oral saliva microbiomes from 19 Nigerian children with acute noma. Our analyses of this preliminary study reveal marked microbial dysbiosis in noma microbiomes, with machine learning and multivariate statistical analyses indicating significant enrichment of Treponema, Porphyromonas, and Bacteroides, alongside depletion of Streptococcus and Rothia, as key microbial signatures of noma disease. From the dataset we recovered 40 high-quality Treponema metagenome assembled genomes (MAGs) spanning 19 species, 14 of which were novel. Notably, a novel species designated Treponema sp. A was detected in 15 of the 19 noma participants and was entirely absent from an internationally representative set of healthy saliva metagenomes. Re-analysis of previously published 16S rRNA datasets from children with noma in Niger also revealed Treponema sp. A to be highly prevalent in noma cases but extremely rare in controls. While these findings highlight Treponema, particularly Treponema sp. A, as an organism of interest and a potential contributor to noma pathogenesis, further comprehensive studies will be required to confirm this association and to clarify whether it reflects a causal role and/or is a genuine marker of noma dysbiosis. Additionally, analysis of antimicrobial resistance determinants detected in noma metagenomes revealed concerning levels of resistance to antibiotics commonly used in noma treatment, particularly β-lactams and metronidazole, especially among Prevotella spp. These findings provide the first high-resolution microbial framework for noma and offer a foundation for future research into its pathogenesis and the development of novel diagnostics, therapeutics, and preventive strategies in endemic settings.

What was studied?

UNLABELLED: Metabolic dysfunction-associated steatotic liver disease (MASLD) has become one of the most prevalent chronic liver conditions worldwide, with its incidence steadily rising. However, the underlying mechanisms linking MASLD to colorectal adenoma remain unclear, and the role of gut microbiota and metabolites in this association requires further investigation. This study aims to characterise the gut microbiota and metabolites in patients with MASLD and colorectal adenoma. A cohort of 58 MASLD patients was enrolled and stratified into two groups based on colorectal adenoma status: the MASLD with colorectal adenoma group (M-CA group, n = 30) and the MASLD without colorectal adenoma group (M-NCA group, n = 28). The gut microbial ecosystem in the M-CA group showed significant dysregulation, evidenced by a decreased Gut Microbiome Health Index (GMHI) and significantly increased Microbiome Dysbiosis Index (MDI). Linear Discriminant Analysis Effect Size (LEfSe) identified 75 differentially abundant microbial taxa between groups, with Bacteroides vulgatus, Bacteroides ovatus, uncultured bacterium of norank genus of Muribaculaceae family, Muribaculaceae, and norank of Muribaculaceae family being significantly enriched in the M-CA group, representing potential microbial biomarkers for this cohort. Partial Least Squares Discriminant Analysis (PLS-DA) screened 116 differential metabolites. When combined with Random Forest (RF), Support Vector Machine (SVM) and Least Absolute Shrinkage and Selection Operator (LASSO) machine learning algorithms, 16 significantly identified biomarkers were discovered. The joint analysis of both omics revealed that variations in differential metabolite levels were associated with changes in specific microbiota abundances. Kyoto encyclopedia of genes and genomes (KEGG) functional prediction analysis indicated that the coordinated alterations in metabolites and microbiota may collectively influence multiple metabolic pathways, including lipid metabolism, xenobiotics biodegradation and metabolism, amino acid metabolism, carbohydrate metabolism, biosynthesis of other secondary metabolites and nucleotide metabolism. This study revealed that patients with MASLD and colorectal adenoma exhibited significant alterations in the gut microbiota composition and metabolic profile, indicating potential impacts on associated metabolic pathways. These findings provided novel insights and a foundation for future research into potential intervention strategies for this clinical complication. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-45782-w.

What was studied?

This study investigated whether high-fat-diet (HFD) induced disruption of the gut microbiota contributes to erectile dysfunction (ED) in rats. Researchers compared erectile function and stool-based 16S rRNA sequencing profiles between rats fed a normal diet (ND) and rats fed an HFD for 24 weeks. To test whether the microbiota itself was responsible for this effect, they performed fecal microbiota transplantation (FMT), transplanting stool from ND-group and HFD-group rats into new groups of rats and again assessing erectile function, microbiota composition, and serum metabolomics after another 24 weeks.

Who was studied?

The subjects were male Sprague-Dawley rats, aged 8 weeks at the start of the experiment. They were randomly divided into a normal diet group and a high-fat diet group for the initial phase, then two additional groups of rats received fecal microbiota transplants from those donor groups. No human subjects were studied; the findings come entirely from this rat model.

What were the most important findings?

Erectile function and intestinal microbiota species diversity were both significantly lower in the HFD group compared to the ND group, and overall microbiota community structure differed markedly between the two groups. Critically, rats that received fecal microbiota transplants from HFD-diet donors (HFD-FMT group) also developed significantly lower erectile function than rats transplanted with normal-diet microbiota (ND-FMT group). The microbiota community characteristics in the FMT recipient groups mirrored those of their respective donor groups, and serum metabolomic differences were also detected between groups.

What are the greatest implications of this study?

These findings suggest that HFD-induced gut microbiota dysbiosis is not merely associated with erectile dysfunction but can causally transmit impaired erectile function, since transplanting dysbiotic microbiota alone reproduced the deficit in previously unexposed rats. This supports a gut-microbiota-to-erectile-function axis, potentially mediated through microbial metabolites detectable in serum. The results point to the gut microbiome as a possible target for future diagnostic or therapeutic strategies in diet-related erectile dysfunction, though this remains to be tested in humans.

What was studied?

This study examined whether the probiotic Bifidobacterium longum subsp. longum BL21 could mitigate symptoms of polycystic ovary syndrome (PCOS) in a DHT-induced (prenatal androgen-induced) mouse model. The researchers focused on BL21's effects on metabolic dysregulation, inflammation, and neuroprotection, framed through the gut-brain-ovary axis. Mice received a daily oral dose of 1 x 10^9 CFU of BL21 for a continuous 8-week treatment period. Outcomes assessed included body weight, glucose tolerance, serum BDNF, inflammatory markers, sex hormone levels, and gut microbiota composition via 16S rRNA gene sequencing.

Who was studied?

The subjects were twenty-four ICR mice with prenatal androgen (DHT)-induced PCOS, an established animal model rather than human patients. The abstract does not specify how the 24 mice were divided among treatment and control groups. All findings therefore come from a controlled mouse model of PCOS, not from a human cohort.

What were the most important findings?

BL21 significantly increased sex hormone levels, particularly follicle-stimulating hormone (FSH) and estradiol (E2), suggesting improved ovarian function (P < 0.05). The probiotic also curbed weight gain and improved glucose tolerance in the PCOS mice (P < 0.05). Additionally, BL21 reduced inflammatory markers, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and lipopolysaccharides (LPS), while increasing the anti-inflammatory marker IL-10. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so this study is summarized on its own terms.

What are the greatest implications of this study?

These results position Bifidobacterium longum subsp. longum BL21 as a novel candidate approach for addressing hormonal, metabolic, and inflammatory disturbances in PCOS. The findings support the concept of a gut-brain-ovary axis, in which a targeted probiotic can influence ovarian hormone output and systemic inflammation together. Because this work was conducted in a mouse model, further research would be needed to establish whether similar effects occur in humans with PCOS.

What was studied?

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

What was studied?

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

What was studied?

This study investigated whether alterations in the gut microbiome are associated with allograft rejection in kidney transplant (KT) recipients. Researchers used 16S rRNA gene amplicon sequencing to characterize gut microbiome composition and function over time. They tracked how the microbiome changed from the pre-transplant, chronic kidney disease (CKD) state through recovery, and examined shifts occurring before and after rejection events. Functional analysis focused on the microbiome's capacity to produce short-chain fatty acids, including propionate and butyrate.

Who was studied?

The study analyzed 562 samples collected from 245 individuals as part of a multicenter prospective study. Of these participants, 217 had received a kidney transplant. This design allowed comparison of microbiome trajectories across the CKD-to-post-transplant recovery period and around the time of graft rejection events.

What were the most important findings?

Overall, gut microbiome composition gradually recovered after transplantation, mirroring the CKD-to-health transition, as shown by increasing Shannon diversity. However, prior to graft rejection, microbial diversity decreased along with a reduction in short-chain fatty acid-producing taxa. Functional analysis confirmed a decreased potential for short-chain fatty acid production before rejection, and this was validated using quantitative PCR targeting propionate and butyrate production potential. After rejection, these microbiome features normalized again, and the alterations preceding rejection partially overlapped with microbiome signatures previously reported in CKD patients.

What are the greatest implications of this study?

The findings suggest that gut microbiome changes, particularly loss of diversity and short-chain fatty acid-producing taxa, may precede and potentially help predict graft rejection in kidney transplant recipients. This raises the possibility that monitoring microbiome composition and short-chain fatty acid production capacity could serve as an early warning signal for clinicians. Because these pre-rejection alterations partially resemble CKD-associated microbiome signatures, they may reflect a shared pathway of microbial dysfunction linked to immune dysregulation. This work supports further exploration of the gut microbiome as a noninvasive biomarker source and a potential target for interventions to support graft survival.

What was studied?

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.

What was studied?

Lifestyle factors, particularly physical exercise, significantly influence brain structure and cognitive function through a hormetic effect -a phenomenon where low to moderate doses of a stimulus (in this case, exercise) induce beneficial adaptations, while excessive doses could lead to detrimental effects. This effect depends on exercise intensity and duration, though the underlying mechanisms remain largely unexplored. Recently, the gut microbiota has emerged as potent modulator of lifestyle-induced changes in brain and behaviour.

Who was studied?

We used a 40-min, 1200 cm/min exercise protocol. We measured cognition through several tests and analysed microbiota composition comparing adult exercised animals to sedentary controls. Finally, we performed fecal microbiota transplantation from exercised to sedentary mice.

What were the most important findings?

Exercise enhances cognitive abilities related to object recognition and object location memory, as well as increases hippocampal neurogenesis. However, these cognitive and neurogenic benefits vanish when the exercise intensity or duration is increased. Furthermore, we identified significant changes in alpha and beta diversity and distinct bacteria composition profiles in the gut microbiota associated with different exercise regimens. Specific bacterial families showed altered relative abundances depending on exercise intensity and duration, with certain families' quantities significantly correlating with cognitive performance (Angelakisella, Acetatifactor, Erysipelatoclostridium, and Coriobacteriaceae UCG-002.). To explore causal mechanisms, we performed fecal microbiota transplantation from exercised to sedentary mice, which replicated the cognitive and neurogenic changes observed in the donor animals.

What are the greatest implications of this study?

These findings suggest that the hormetic effects of physical exercise on cognitive function and neurogenesis are mediated by corresponding changes in the gut microbiota, highlighting a novel mechanistic link between exercise, brain function, and gut microbiota composition.

What was studied?

This study examined cocoa (Theobroma cacao L.) bean fermentation, the spontaneous process that shapes the final flavour of chocolate. The researchers investigated how abiotic factors (pH and temperature) and biotic factors (bacterial and fungal microbiota) interact to produce key flavour attributes in premium chocolate. They used genome-resolved metagenomics to identify the metabolic traits within the fermentation microbial community responsible for flavour development. They then tested whether a defined microbial consortium could reproduce those fine flavour attributes under controlled conditions.

Who was studied?

The study drew on cocoa bean fermentation samples collected from farms in Colombia. From these samples, the researchers characterized the natural bacterial and fungal community and used genome-resolved metagenomics to build a picture of the metabolic capacities present. They then assembled a separate, defined and metabolically competent microbial consortium, rather than studying a human or animal cohort, to test controlled fermentation. A trained tasting panel was also used to evaluate the resulting chocolate.

What were the most important findings?

The pH, temperature, and combined bacterial and fungal microbiota composition of the fermentation samples all influenced key flavour attributes of the resulting premium chocolate. Genome-resolved metagenomics showed that the metabolic traits needed for flavour development were redundantly encoded across multiple members of the fermentation community, not confined to a single organism. Using a defined microbial consortium built from this information, the researchers replicated fine flavour attributes of chocolate under controlled conditions. This was confirmed through omics analyses, metabolic network modeling, and evaluation by a trained tasting panel.

What are the greatest implications of this study?

These findings show that the flavour-relevant functions of spontaneous cocoa fermentation can be captured in a defined, reproducible microbial consortium rather than relying on uncontrolled natural fermentation. This provides a basis for designing standardized fermentation starters that can reliably reproduce fine chocolate flavour characteristics. Such starters could help cocoa producers achieve consistent premium quality across batches and locations. The approach also demonstrates a model for linking metagenomic and metabolic data to sensory outcomes in food fermentation more broadly.

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 seasonal changes in gut microbiota composition and function across four bear species: giant pandas, Asian black bears, brown bears, and polar bears. Researchers combined comparative seasonal microbiome analysis with fecal microbiota transplantation (FMT) experiments in mice to test whether bear gut microbiota actively drives host energy metabolism. The core question was whether giant pandas, long considered metabolically unique due to their specialized herbivorous diet and low metabolic rate, actually rely on a distinct microbial regulatory mechanism compared to other bears.

Who was studied?

The subjects were four Ursidae species: giant pandas (Ailuropoda melanoleuca), Asian black bears (Ursus thibetanus), brown bears (Ursus arctos), and polar bears (Ursus maritimus), sampled across seasons to capture gut microbiota dynamics. The abstract does not specify exact animal counts or sampling sites. Recipient mice were also used as a secondary population in the fecal microbiota transplantation experiments to test the functional effects of bear gut microbiota on host metabolism and appetite.

What were the most important findings?

The gut microbial composition was similar across all four bear species, with Firmicutes and Proteobacteria as the dominant phyla. Firmicutes became enriched in winter, which enhanced lipid metabolism and helped the bears adapt to seasonal dietary differences, pointing to a convergent microbial functional strategy shared across the Ursidae family rather than a panda-specific mechanism. In FMT experiments, winter bear gut microbiota transferred stronger capacity to regulate host energy metabolism and appetite in mice, increasing energy intake, demonstrating that these microbial shifts causally promote seasonal metabolic adaptation.

What are the greatest implications of this study?

By showing convergent, shared microbial functional strategies across giant pandas, black bears, brown bears, and polar bears, the findings challenge the long-standing view that giant panda gut microbiota is metabolically unique among bears. This reframes seasonal energy adaptation in Ursidae as a family-wide, diet-responsive microbiome trait rather than an evolutionary novelty confined to pandas. The FMT results also suggest that bear-derived winter microbiota could serve as a model system for studying microbiome-driven regulation of energy intake and appetite in mammals more broadly.

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 chronic intermittent hypoxia (CIH), the hallmark feature of obstructive sleep apnoea syndrome (OSAS), affects the gut microbiota. Researchers used a mouse model of OSAS to test whether repeated cycles of low oxygen exposure alter gut microbial community structure over time. They assessed both microbiota composition, via 16S rRNA gene sequencing, and predicted functional pathways using PICRUSt2. The goal was to fill a gap in understanding how CIH-driven metabolic and gastrointestinal complications might be mediated by the gut microbiome.

Who was studied?

The subjects were male C57BL/6 mice, not human patients, exposed either to normoxia (NM) or chronic intermittent hypoxia (CIH) conditions for six weeks. Faecal samples were collected via stress defecation at baseline (NM0 and CIH0 groups) and again after six weeks (NM6 and CIH6 groups). In total, 40 faecal samples were analyzed, with 10 mice per group across the four conditions.

What were the most important findings?

The abstract provided does not include the specific results section detailing which taxa changed or which functional pathways were predicted to shift. It confirms only that a full dataset of 40 faecal samples across four groups was generated and analyzed using 16S rRNA sequencing and PICRUSt2 functional prediction. No mention of Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism appears in the abstract text supplied. Without the omitted results, specific compositional or functional outcomes cannot be reported here.

What are the greatest implications of this study?

By establishing a controlled mouse model comparing gut microbiota before and after chronic intermittent hypoxia exposure, this work lays groundwork for identifying microbiota-mediated mechanisms behind OSAS-associated metabolic and gastrointestinal complications. Such a model could help pinpoint specific microbial or functional changes that contribute to systemic disease in sleep apnoea. This approach may eventually support the identification of therapeutic targets aimed at the gut microbiome for patients with OSAS. Further reporting of the study's actual results would be needed to draw more specific conclusions.

What was studied?

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

What were the most important findings?

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

What are the greatest implications of this study?

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

What was studied?

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

Who was studied?

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

What were the most important findings?

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

What are the greatest implications of this study?

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

What was studied?

The gut microbiota and Short-chain fatty acids (SCFAs) can influence the progression of diseases, yet the role of these factors on gastric cancer (GC) remains uncertain. In this work, the analysis of the gut microbiota composition and SCFA content in the blood and feces of both healthy individuals and GC patients indicated that significant reductions in the abundance of intestinal bacteria involved in SCFA production were observed in GC patients compared with the controls. ABX mice transplanted with fecal microbiota from GC patients developed more tumors during the induction of GC and had lower levels of butyric acid. Supplementation of butyrate during the induction of gastric cancer along with H. pylori and N-methyl-N-nitrosourea (MNU) in WT in GPR109A-/-mice resulted in fewer tumors and more IFN-γ+ CD8+ T cells, but this effect was significantly weakened after knockout of GPR109A. Furthermore, In vitro GC cells and co-cultured CD8+ T cells or CAR-Claudin 18.2+ CD8+ T cells, as well as in vivo tumor-bearing studies, have indicated that butyrate enhanced the killing function of CD8+ T cells or CAR-Claudin 18.2+ CD8+ T cells against GC cells through G protein-coupled receptor 109A (GPR109A) and homologous domain protein homologous box (HOPX). Together, these data highlighted that the restoration of gut microbial butyrate enhanced CD8+ T cell cytotoxicity via GPR109A/HOPX, thus inhibiting GC carcinogenesis, which suggests a novel theoretical foundation for GC management against GC.

What was studied?

Remodeling eubiosis of the gut microenvironment may contribute to preventing the occurrence and development of depression. Mounting experimental evidence has shown that complement C3 signaling is associated with the pathogenesis of depression, and disruption of the gut microbiota may be an underlying cause of complement system activation. However, the mechanism by which complement C3 participates in gut-brain crosstalk in the pathogenesis of depression remains unknown.

What were the most important findings?

In the present study, we found that chronic unpredictable mild stress (CUMS)-induced mice exhibited obvious depression-like behavior as well as cognitive impairment, which was associated with significant gut dysbiosis, especially enrichment of Proteobacteria and elevation of microbiota-derived lipopolysaccharides (LPS). In addition, peripheral and central complement C3 activation and central C3/CR3-mediated aberrant synaptic pruning in microglia have also been observed. Transplantation of gut microbiota from CUMS-induced depression model mice into specific pathogen-free and germ-free mice induced depression-like behavior and concomitant cognitive impairment in the recipient mice, accompanied by increased activation of the complement C3/CR3 pathway in the prefrontal cortex and abnormalities in microglia-mediated synaptic pruning. Conversely, antidepressants and fecal microbiota transplantation from antidepressant-treated donors improved depression-like behaviors and restored gut microbiome disturbances in depressed mice. Concurrently, inhibition of the complement C3/CR3 pathway, amelioration of abnormal microglia-mediated synaptic pruning, and increased expression of the synapsin and postsynaptic density protein 95 were observed. Collectively, our results revealed that gut dysbiosis induces the development of depression-like behaviors through abnormal synapse pruning in microglia-mediated by complement C3, and the inhibition of abnormal synaptic pruning is the key to targeting microbes to treat depression.

What are the greatest implications of this study?

Our findings provide novel insights into the involvement of complement C3/CR3 signaling and aberrant synaptic pruning of chemotactic microglia in gut-brain crosstalk in the pathogenesis of depression. Video Abstract.

What was studied?

Polycystic ovary syndrome (PCOS) is a frequent cause of infertility in reproductive-age women. Our work aims to evaluate the effects of glucagon-like peptide-1 receptor agonists (GLP-1RAs) on gut microbiota, with metabolic parameters including body weight and the hormone profile in PCOS.

Who was studied?

Dehydroepiandrosterone (DHEA)-induced PCOS mice were established and then treated with two GLP-1RAs: liraglutide and novel form semaglutide for four weeks. Changes in body weight and metabolic parameters were measured. Fecal samples were collected and analyzed using metagenomic sequencing.

What were the most important findings?

Liraglutide and semaglutide modulated both alpha and beta diversity of the gut microbiota in PCOS. Liraglutide increased the Bacillota-to-Bacteroidota ratio through up-regulating the abundance of butyrate-producing members of Bacillota like Lachnospiraceae. Moreover, liraglutide showed the ability to reverse the altered microbial composition and the disrupted microbiota functions caused by PCOS. Semaglutide increased the abundance of Helicobacter in PCOS mice (p < 0.01) which was the only bacteria found negatively correlated with body weight. Moreover, pathways involving porphyrin and flavonoids were increased after semaglutide intervention.

What are the greatest implications of this study?

Liraglutide and semaglutide improved reproductive and metabolic disorders by modulating the whole structure of gut microbiota in PCOS. The greater efficacy in weight loss compared with liraglutide observed after semaglutide intervention was positively related with Helicobacter. The study may provide new ideas in the treatment and the underlying mechanisms of GLP-1RAs to improve PCOS.

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?

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

Who was studied?

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

What were the most important findings?

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

What are the greatest implications of this study?

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

What was studied?

This study investigated whether the oral microbiome, independent of the gut microbiome, contributes to depression through a proposed microbiota-oral-brain axis. The researchers combined clinical comparisons of oral microbial composition and metabolomics with an animal model using chronic restraint stress (CRS) and saliva transplantation into germ-free mice. The goal was to determine whether oral microbial dysbiosis could causally drive depression-like behavior and altered host metabolism.

Who was studied?

The clinical portion compared 87 patients with depressive symptoms to 70 healthy controls, analyzing their oral microbial and metabolic profiles. The animal portion used germ-free mice that received saliva transplants from mice exposed to chronic restraint stress. This paired human cohort with a controlled mouse model allowed the researchers to move from association in people to causal testing in animals.

What were the most important findings?

Oral microbial and metabolic signatures differed significantly between depressed patients and healthy controls. Germ-free mice given saliva from chronically stressed mice developed depression-like behaviors along with oral microbial dysbiosis, marked by enrichment of Pseudomonas, Pasteurellaceae, and Muribacter and depletion of Streptococcus. Metabolomic analysis also showed altered plasma metabolites accompanying these behavioral and microbial changes, though the abstract does not describe sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism as part of these findings.

What are the greatest implications of this study?

The findings suggest the oral microbiome can influence depression-like behavior independent of the gut, supporting a microbiota-oral-brain axis alongside the gut-brain axis. Saliva-based microbial transfer inducing behavioral changes in germ-free mice points to a potentially causal, transmissible mechanism linking oral dysbiosis to mood-related metabolism. This raises the possibility that oral microbial and metabolic signatures could serve as biomarkers or intervention targets for depression.

What was studied?

Bats are a diverse and ecologically important group of mammals that exhibit remarkable diversity in their feeding habits. These diverse feeding habits are thought to be reflected in the composition and function of their gut microbiota, which plays important roles in nutrient acquisition, immune function, and overall health. Despite the rich biodiversity of bat species in South America, there is a lack of microbiome studies focusing on bats from this region. Such studies could offer major insights into conservation efforts and the preservation of biodiversity in South America. In this work, we aimed to compare the gut microbiota of four bat species with different feeding habits from Southern Brazil, including nectarivorous, frugivorous, insectivorous, and hematophagous bats. Our findings demonstrate that feeding habits can have a significant impact on the diversity and composition of bat gut microbiotas, with each species exhibiting unique metabolic potentials related to their dietary niches. In addition, the identification of potentially pathogenic bacteria suggests that the carriage of microbial pathogens by bats may vary, depending on feeding habits and host-specific factors. These findings provide novel insights into the relationship between bat feeding habits and gut microbiota composition, highlighting the need to promote diverse habitats and food sources to support these ecologically important species.

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 investigated the relationship between periodontitis and the oral-gut axis in first-trimester pregnant women using integrative microbiome and metabolome profiling. Researchers combined 16S rRNA sequencing of subgingival plaque, saliva, and stool with untargeted metabolomics of serum and other sample types, alongside clinical traits. The goal was to characterize how oral dysbiosis linked to periodontitis translates into distal gut microbial and metabolic changes during early pregnancy.

Who was studied?

The cohort consisted of 54 Chinese pregnant women sampled at the first trimester. Of these, 31 women had maternal periodontitis (the Perio group) and 23 women served as Non-Perio controls. Subgingival plaque, saliva, serum, and stool samples were collected from each participant for multi-omics analysis.

What were the most important findings?

The study identified a novel bacterial distinguisher, Coprococcus, in the feces of women with periodontitis, and this genus was associated with subgingival periodontopathogens. Notably, Coprococcus behaved differently from other fecal genera within the Lachnospiraceae family. The ratio of fecal Coprococcus to Lachnoclostridium was able to discriminate between the Perio and Non-Perio groups, indicating a measurable gut-level signature tied to oral disease status.

What are the greatest implications of this study?

The findings support the existence of a functional oral-gut axis through which periodontitis in early pregnancy is reflected in distinct gut microbial and metabolic alterations. Identifying the fecal Coprococcus to Lachnoclostridium ratio as a discriminating feature suggests potential translational value as a biomarker linking oral and gut health in pregnant women. This integrative multi-omics approach may help clarify how periodontitis contributes to adverse pregnancy outcomes via systemic, gut-mediated pathways.

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?

This study examined how changes in social living conditions affect the composition of the gut microbiota (GM), independent of diet. The researchers designed a longitudinal experiment that sequentially manipulated housing arrangements (single versus paired) and diet (variable versus controlled) so that the effects of each factor on GM composition could be separated. This approach directly addressed a limitation of prior human and non-human primate research, in which social effects on the GM were often confounded by shared diet.

Who was studied?

The study population was a captive cohort of 13 male cynomolgus macaques followed over 15 months. Animals began in single housing on a variable diet for the first three months, then were switched to a controlled diet, moved to paired housing for six months, and finally returned to single housing. The abstract does not report ages, weights, or other demographic details beyond sex, species, and group size.

What were the most important findings?

The abstract text provided is truncated before the results are described in detail, so specific findings on how housing and diet shifts altered GM composition are not available here. What can be stated is that the structured sequencing of diet and housing changes was designed specifically to let the researchers distinguish diet-driven from social-environment-driven shifts in the gut microbiota. No mention of Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism appears in the provided text.

What are the greatest implications of this study?

By experimentally separating diet from social housing, this design offers a clearer causal framework for understanding how social environment shapes the primate gut microbiota. Such findings could inform how captive animal management, and by extension human social and living arrangements, might be adjusted to support a healthier microbiome. The approach also provides a methodological template for future studies aiming to disentangle correlated environmental influences on host-associated microbial communities.

What was studied?

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

Who was studied?

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

What were the most important findings?

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

What are the greatest implications of this study?

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

What was studied?

Gut microecosystem has been shown to play an important role in human health. In recent years, the concept of the gut-kidney axis has been proposed to explain the potential association between gut microbiota and chronic kidney disease (CKD). Here, a cohort of fecal samples collected from patients with CKD (n = 13) were involved. The composition of gut microbial communities and clinical features in CKD and end-stage renal disease (ESRD) were characterized. Our study focused on the changes in gut microbiome and the correlation with clinical features in patients with CKD and ESRD by analyzing high-throughput sequencing results of collected feces. We elucidated the alterations of gut microbiota in CKD patients at different stages of disease and initially identified the gut microbiota associated with CKD progression. We also combined correlation analysis to identify clinical features closely related to the gut microbiome. Our results offered the possibility of using non-invasive gut microbiome in the early diagnosis of course from CKD to ESRD and provide new insights into the association between clinical features and gut microbiota in CKD.

What was studied?

This study examined whether the timing of offspring exposure to maternal glucocorticoids (GCs), stress-related hormones, during early gestation, late gestation, or lactation was associated with differences in the gut bacterial community of a wild primate. The researchers looked at bacterial diversity, composition, and function, and tracked whether any associations changed or persisted as offspring aged. The work addresses a gap in understanding how maternal hormonal exposure during development shapes long-term gut microbiome outcomes in long-lived species living in their natural habitat.

Who was studied?

The study used a cross-sectional sample of wild Assamese macaques spanning infant, juvenile, and adult age classes. Naturally varying maternal glucocorticoid levels during early gestation, late gestation, and lactation were assessed in relation to each offspring's gut bacterial community. The abstract does not give an exact sample size, but the design draws on a natural, free-ranging primate population rather than a laboratory cohort.

What were the most important findings?

Naturally elevated maternal glucocorticoids during early gestation, but not during late gestation or lactation, were associated with reduced gut bacterial richness in offspring. The association between early gestational maternal glucocorticoids and offspring gut bacterial composition and function grew stronger, not weaker, as the offspring aged. This early-gestation effect was about 10 times stronger than the effect linked to glucocorticoid exposure during the late prenatal or postnatal period, which showed a comparatively smaller association with the gut bacterial community. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.

What are the greatest implications of this study?

The findings suggest that the timing of prenatal maternal hormonal exposure can programmatically shape offspring gut bacterial communities for the long term, rather than producing only transient effects. Because the early-gestation effect intensified with age instead of fading, this points to a durable, developmentally timed maternal influence on the gut microbiome rather than a short-lived one. This work extends maternal-effects and developmental-programming research from morphology and behavior into the gut microbiome domain in a wild, long-lived primate model. It also underscores that studying only late pregnancy or postnatal exposures could miss the most consequential window for maternal glucocorticoid effects on offspring gut bacteria.

What was studied?

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

What was studied?

This study examined how surgery-induced gut microbial dysbiosis contributes to perioperative neurocognitive disorders (PND), a common but poorly treated postoperative complication. The researchers investigated the mechanisms linking postoperative changes in the gut microbiota to disruptions in intestinal barrier function, serum metabolism, and cognitive outcomes. Behavioral testing, 16S rRNA gene sequencing, non-target metabolomics, intestinal permeability assays, protein analysis, and immunofluorescence staining were used to trace this gut-brain pathway. The metabolite palmitic amide was identified as a specific link between microbial changes and cognitive effects.

Who was studied?

The study was conducted in mice, comparing aged and young animals subjected to surgery. Aged mice were the primary focus, since surgery-induced cognitive impairment occurred predominantly in this group. Interventions including fecal microbiota transplantation from young donors, dexamethasone, Lactobacillus supplementation, indole propionic acid, and palmitic amide administration were tested in these mouse models.

What were the most important findings?

Surgery altered gut microbiota composition and worsened intestinal barrier disruption specifically in aged mice, which corresponded with the cognitive impairment seen mainly in this group. These adverse effects could be reduced by transferring microbiota from young donors or by strengthening intestinal barrier function with dexamethasone, Lactobacillus, or indole propionic acid. The abstract also points to microbiota-linked changes in metabolism, including the metabolite palmitic amide, as part of the mechanism connecting gut dysbiosis to cognitive outcomes.

What are the greatest implications of this study?

The findings suggest that age-related vulnerability to postoperative cognitive decline may be driven in part by how surgery disrupts the gut microbiota and intestinal barrier. Because microbiota transfer, probiotic supplementation, and metabolite-targeted interventions each improved outcomes in this model, gut-directed strategies could represent a therapeutic avenue for PND. This supports viewing perioperative cognitive complications through a gut-brain axis lens rather than treating them as purely neurological events.

What was studied?

This study examined the uterine microbiome of post-partum dairy cows using deep shotgun metagenomic sequencing. Researchers compared microbial ecology and diversity in cows with metritis, purulent vaginal discharge, and no disease. The goal was to characterize taxonomic composition and identify differences in community structure associated with metritis.

Who was studied?

The study drew on intrauterine swab samples from post-partum dairy cows across 24 commercial California dairy farms. A subset of 95 samples was analyzed out of a larger collection of 307 individual cow samples. Cows within 21 days post-partum were classified into three clinical groups: control (n = 32), metritis (n = 33), and purulent discharge (n = 31), based on the appearance and odor of vaginal discharge.

What were the most important findings?

All three clinical groups showed highly diverse uterine microbial communities, with the top 12 most abundant genera accounting for only about 8.8 to 10.3 percent of mean relative abundance across groups. Alpha diversity was lower in samples from cows with metritis and purulent discharge compared to control cows. PERMANOVA testing showed a statistically significant difference in overall microbial community composition (beta diversity) between groups.

What are the greatest implications of this study?

The findings suggest that uterine disease states in post-partum dairy cows are associated with reduced microbial diversity rather than dominance by a single pathogen, reflecting a broader ecological shift in the uterine environment. Deep shotgun sequencing offers a more complete picture of this community than earlier culture-based or amplicon-based approaches. These results could inform future work on diagnosing and managing metritis through microbiome-based markers rather than single-organism detection.

What was studied?

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

What was studied?

This study examined whether Parkinson's disease (PD) medications themselves, rather than the disease process alone, alter gastrointestinal motility and microbiota composition in the small intestine. The small intestine is the primary site of drug absorption, yet it had not previously been studied in this context. Researchers treated healthy, non-PD rats with dopamine, pramipexole (combined with levodopa-carbidopa), or ropinirole (combined with levodopa-carbidopa) for 14 sequential days. The aim was to determine whether the medications alone could reproduce microbiota changes resembling those reported in human PD patients.

Who was studied?

The subjects were healthy, non-PD, wild-type Groningen rats, not human patients or a public dataset. The rats were divided into treatment groups receiving dopamine, pramipexole with levodopa-carbidopa, or ropinirole with levodopa-carbidopa, alongside a vehicle (control) group. The abstract does not specify the exact number of animals per group. Using healthy animals allowed the researchers to isolate the effects of the medications from any confounding effects of PD itself.

What were the most important findings?

Rats treated with dopamine agonists showed significantly reduced small intestinal motility and increased bacterial overgrowth in the distal small intestine. Treated animals also showed significant microbial taxa shifts compared to vehicle controls, including increases in Lactobacillus and Bifidobacterium and decreases in Lachnospiraceae and Prevotellaceae. These shifts closely resembled differences previously reported between human PD patients and healthy controls. Notably, certain Lactobacillus species correlated negatively with systemic levodopa levels, suggesting these bacteria may affect the drug's bioavailability.

What are the greatest implications of this study?

The findings suggest that PD medications themselves, not just the underlying disease, can drive gastrointestinal motility changes and microbiota alterations previously attributed to PD pathology. This represents an important confounder that should be accounted for when interpreting microbiome studies in PD patients taking dopaminergic therapy. The negative correlation between certain Lactobacillus species and levodopa levels also raises the possibility that drug-induced microbiota shifts could feed back to affect medication bioavailability. Future PD microbiome research and drug-microbiome interaction studies should account for medication effects independent of disease status.

What was studied?

People with COPD have been reported to bear a distinct airway microbiota from healthy individuals based on bronchoalveolar lavage (BAL) and sputum samples. Unfortunately, the collection of these samples involves relatively invasive procedures and is resource-demanding, limiting its regular use. Non-invasive samples from the upper airways could constitute an interesting alternative, but its relationship with COPD is still underexplored. We examined the merits of saliva to identify the typical profile of COPD oral bacteria and test its association with the disease.

Who was studied?

Outpatients with COPD and age-sex matched healthy controls were recruited and characterised based on clinical parameters and 16S rRNA profiling of oral bacteria. A clustering analysis based on patients' oral bacteria beta-diversity and logistic regressions were performed to evaluate the association between oral bacteria composition and COPD.

What were the most important findings?

128 individuals participated (70 patients and 58 controls). Differential abundance analyses showed differences in patients comparable to the ones previously observed in samples from the lower respiratory tract, i.e., an increase in Proteobacteria (particularly Haemophilus) and loss of microbiota diversity. An unsupervised clustering analysis separated patients in two groups based on microbiota composition differing significantly in the frequency of patients hospitalized due to severe acute exacerbation of COPD (AECOPD) and in the frequency of GOLD D patients. Furthermore, a low frequency of Prevotella was associated with a significantly higher risk of recent severe AECOPD and of being GOLD D.

What are the greatest implications of this study?

Salivary bacteria showed an association with COPD, particularly with severe exacerbations, supporting the use of this non-invasive specimen for future studies of heterogeneous respiratory diseases like COPD.

What was studied?

The objective of this study was to describe and compare the dynamic microbiota characteristics in the gastrointestinal (GI) tract in Chinese participants via high-throughput sequencing techniques. The study collected saliva, esophageal swab, cardia biopsy, noncardia biopsy, gastric juice, and fecal specimens from 40 participants who underwent upper GI tract cancer screening in Linzhou (Henan, China) in August 2019. The V4 region of 16S rRNA genes was amplified and sequenced using the Illumina MiniSeq platform. The observed amplicon sequence variants (ASVs) gradually decreased from saliva to esophageal swab, cardia biopsy, noncardia biopsy, and gastric juice specimens and then increased from gastric juice to fecal specimens (P < 0.05). Each GI site had its own microbial characteristics that overlapped those of adjacent sites. Characteristic genera for each site were as follows: Neisseria and Prevotella in saliva, Streptococcus and Haemophilus in the esophagus, Helicobacter in the noncardia, Pseudomonas in gastric juice, Faecalibacterium, Roseburia, and Blautia in feces, and Weissella in the cardia. Helicobacter pylori-positive participants had decreased observed ASVs (cardia, P < 0.01; noncardia, P < 0.001) and Shannon index values (cardia, P < 0.001; noncardia, P < 0.001) compared with H. pylori-negative participants both in cardia and noncardia specimens. H. pylori infection played a more important role in the microbial composition of noncardia than of cardia specimens. In gastric juice, the gastric pH and H. pylori infection had similar additive effects on the microbial diversity and composition. These results show that each GI site has its own microbial characteristics that overlap those of adjacent sites and that differences and commonalities between and within microbial compositions coexist, providing essential foundations for the continuing exploration of disease-associated microbiota. IMPORTANCE Upper gastrointestinal (UGI) tract cancer is one of the most common cancers worldwide, while limited attention has been paid to the UGI microbiota. Microbial biomarkers, such as Fusobacteria nucleatum and Helicobacter pylori, bring new ideas for early detection of UGI tract cancer, which may be a highly feasible method to reduce its disease burden. This study revealed that each gastrointestinal site had its own microbial characteristics that overlapped those of adjacent sites. There were significant differences between the microbial compositions of the UGI sites and feces. Helicobacter pylori played a more significant role in the microbial composition of the noncardia stomach than in that of the cardia. Gastric pH and Helicobacter pylori had similar additive effects on the microbial diversity of gastric juice. These findings played a key role in delineating the microbiology spectrum of the gastrointestinal tract and provided baseline information for future microbial exploration covering etiology, primary screening, treatment, outcome, and health care products.

What was studied?

This study investigated atherosclerosis co-occurring with depression through the lens of the microbiota-gut-brain axis. Researchers examined changes in lipid metabolites in the prefrontal cortex and hippocampus, alongside characteristics of the gut microbiota, in ApoE-/- mice. The animal model combined a high-fat diet with binding stimulation for 16 weeks to induce both atherosclerotic damage and depression-like behavior. Non-targeted lipidomics using LC-MS/MS profiled brain lipid metabolites, while 16S rDNA amplicon sequencing characterized the gut microbiota, with association analysis linking the two.

Who was studied?

The subjects were male ApoE-/- mice, a genetic knockout strain prone to atherosclerosis, assigned to a hyperlipid feeding combined with binding (HFB) group of 14 animals. This group was compared against a normal control (NC) group of mice not subjected to the high-fat diet and binding stimulation. The study is therefore a controlled animal model investigation rather than a human cohort study.

What were the most important findings?

Compared with the normal control group, the HFB group showed depression-like behaviors, assessed through body weight changes, the sucrose preference test, open field test, and tail suspension test. Oil-red O staining, HE staining, and biochemical parameters confirmed atherosclerotic damage in the HFB mice. The abstract indicates that differential lipid metabolites were identified in the prefrontal cortex and hippocampus, and that differential gut microbial taxa were identified via 16S rDNA sequencing and linked to these lipid changes through association analysis. The abstract text provided does not specify which particular bacterial taxa or lipid species were altered.

What are the greatest implications of this study?

The findings support the microbiota-gut-brain axis as a plausible mechanistic link between atherosclerosis and co-occurring depression, connecting peripheral gut microbial changes to lipid alterations in brain regions governing mood and cognition. This suggests that gut microbiota and brain lipid metabolism could represent new targets for understanding and potentially treating atherosclerosis co-depression. Because diagnosis, treatment, and prevention of this comorbid condition are currently poor, identifying such targets addresses an urgent clinical need. Further work would be needed to translate these animal-model associations into human-relevant mechanisms or interventions.

What was studied?

In this study, three different microencapsulation methods were used to embed Bifidobacterium to explore the alleviating effects of embedding methods on constipated mice. By measuring the defecation-related parameters, it was found that the Bifidobacteria treated by electrostatic spray drying had the best ability to relieved constipation. Furthermore, by detecting constipation-related gastrointestinal regulatory peptides, inflammatory factors, intestinal microbiota, and SCFAs, it was discovered that Bifidobacteria treated by electrostatic spray drying changed the composition of intestinal microbiota, especially the relative abundance of bacteria that were positively correlated with AQP3, but negatively correlated with ET-1 and SS, then increased the level of AQP3 in the intestine, and finally relieved constipation by increasing the fecal water content and small intestinal propulsion rate. In conclusion, the electrostatic spray drying method was superior to the other two methods in maintaining the activity of Bifidobacteria and relieved constipation by changing the relative abundance of bacteria that were correlated with gastrointestinal regulatory peptides and increasing the content of fecal water and small intestinal propulsion rate.

What was studied?

This study performed a meta-analysis of gastric mucosal microbiome data across multiple published studies to determine whether microbial associations with gastric cancer are consistent across different patient populations. The researchers examined compositional and ecological shifts in gastric microbial communities across the stages of gastric carcinogenesis. They also assessed how bacterial co-occurrence patterns and microbial diversity change as the disease progresses from a healthy state toward cancer.

Who was studied?

The abstract does not specify a single original cohort, since this was a meta-analysis pooling gastric mucosal microbiome data from multiple prior studies. The comparisons were made between samples representing gastric cancer (GC) and samples representing superficial gastritis (SG), spanning different stages of gastric carcinogenesis. Helicobacter pylori infection status was also used to stratify samples within this pooled dataset.

What were the most important findings?

Opportunistic pathobionts including Fusobacterium, Parvimonas, Veillonella, Prevotella, and Peptostreptococcus were enriched in gastric cancer, while commensals such as Bifidobacterium, Bacillus, and Blautia were depleted compared to superficial gastritis. Co-occurrence correlation strength among GC-enriched bacteria increased with disease progression, while correlations among GC-depleted bacteria weakened. The study newly identified eight bacterial taxa, Veillonella, Dialister, Granulicatella, Herbaspirillum, Comamonas, Chryseobacterium, Shewanella, and Helicobacter, as universal biomarkers that discriminated gastric cancer from superficial gastritis with an area under the curve of 0.85. H. pylori-positive samples showed reduced microbial diversity, altered community composition, and weaker interactions among gastric microbes.

What are the greatest implications of this study?

By pooling data across multiple independent studies, this meta-analysis establishes a set of universal, reproducible microbial signatures associated with gastric carcinogenesis rather than findings specific to one cohort. The eight-taxa biomarker panel, with an AUC of 0.85, suggests potential value as a non-invasive or biopsy-based tool for distinguishing gastric cancer from superficial gastritis. The finding that H. pylori infection reshapes microbial diversity and community interactions reinforces its role as a driver of dysbiosis during gastric cancer development, highlighting the broader gastric microbiome as a target for risk stratification.

What was studied?

This study examined how a high-fat diet (HFD) influences colorectal cancer (CRC) tumorigenesis and liver metastasis through changes in gut microbiota. The researchers assessed gut barrier function and inflammation in the colorectum and liver following HFD exposure. They used 16S rRNA sequencing to characterize microbiota shifts and tested whether a specific bacterial genus could reproduce the observed barrier and inflammatory effects.

Who was studied?

The study drew on faecal samples from HFD-fed rats as well as from CRC patients with liver metastasis. Beyond this, the abstract does not provide details on sample size, age, or sex of the subjects. The rat model was used alongside human patient samples to compare microbiota changes across species.

What were the most important findings?

A high-fat diet promoted gut barrier dysfunction and inflammation in both the colorectum and liver. 16S rRNA sequencing revealed an abundance of Desulfovibrio (DSV) in both HFD-fed rats and CRC patients with hepatic metastasis. DSV itself was shown to induce colorectal barrier dysfunction and inflammation in the colorectum and liver, indicating it can independently generate a tumor-permissive microenvironment.

What are the greatest implications of this study?

These findings suggest that Desulfovibrio abundance driven by high-fat diet consumption may be a mechanistic contributor to CRC initiation and progression to liver metastasis. This positions gut microbiota composition, and DSV specifically, as a potential target for reducing metastatic risk in CRC. The results also support diet as a modifiable factor influencing the gut microenvironment relevant to cancer spread.

What was studied?

This study examined whether alterations in the gut microbiota and their metabolic byproducts are linked to glaucoma, a neurodegenerative eye disease marked by progressive loss of retinal ganglion cells (RGCs). Researchers used 16S rRNA (V1-V9 region) sequencing to profile cecal bacterial communities and untargeted metabolomics to characterize circulating metabolites. They then examined how microbial composition and metabolite levels related to RGC status. The overall aim was to determine whether gut-derived signals interact with the neurodegenerative process occurring in glaucoma.

Who was studied?

The study population was a glaucomatous rat model compared against a control group of rats, rather than a human cohort. Cecal bacterial samples and metabolomic profiles were obtained from these two groups of animals. Specific numbers of animals per group are not stated in the abstract, so no sample size can be reported beyond the two-group comparison.

What were the most important findings?

Glaucomatous rats showed markedly reduced diversity of cecal bacteria compared with controls, along with a significantly different overall microbial composition. The Firmicutes/Bacteroidetes ratio, the phylum Verrucomicrobia, and the genera Romboutsia, Akkermansia, and Bacteroides were all substantially elevated in glaucomatous animals, and each of these showed a negative correlation with RGC measures. Untargeted metabolomic analysis identified 284 differentially expressed metabolites, with pathway enrichment analysis pointing strongly to alterations in bile secretion pathways.

What are the greatest implications of this study?

The findings suggest that gut microbial dysbiosis and disrupted bile-acid-related metabolism may be mechanistically connected to retinal ganglion cell loss in glaucoma. Because several dysbiosis markers correlated negatively with RGC status, the gut-retina axis may represent a contributing factor in glaucoma progression rather than a bystander phenomenon. These results position the gut microbiota and its bile secretion-related metabolites as potential targets for further mechanistic investigation in neurodegenerative eye disease.

What was studied?

This study examined the early-life gut microbiota of term small for gestational age (SGA) infants compared with appropriate for gestational age (AGA) infants. Fecal samples were collected on days 1, 3, 5, and 7 of life and analyzed using 16S ribosomal DNA amplicon sequencing. The researchers then followed the SGA infants for 6 months to assess whether early gut microbiota characteristics related to neurodevelopmental outcomes. The work was motivated by prior evidence that gut microbiota in early life can influence later neurodevelopment, a relationship that had been little studied in SGA populations specifically.

Who was studied?

A total of 162 term neonates born at Peking University First Hospital between June 2020 and June 2021 were enrolled. Of these, 41 infants (25.3%) were classified as SGA and made up the study group, while 121 infants (74.7%) were classified as AGA and served as the control group. Neurodevelopmental outcomes at 6 months were assessed among the SGA infants using the Ages and Stages Questionnaires-3 (ASQ-3).

What were the most important findings?

Gut microbial diversity was consistently lower in the SGA group than in the AGA group on days 1, 3, 5, and 7 after birth. Non-metric multidimensional scaling and analysis of similarities showed significant differences in the overall composition of the gut microbiota between the two groups. These findings indicate that being born small for gestational age is associated with a distinct and less diverse early gut microbial community from the first days of life.

What are the greatest implications of this study?

The findings support the idea that SGA status shapes the gut microbiota from the earliest days of life, in a pattern distinguishable from AGA infants. Because the study also tracked neurodevelopment at 6 months using the ASQ-3, it points toward the gut microbiota as a possible early biological marker linked to the neurodevelopmental risks already known to affect SGA infants. This underscores the value of monitoring gut microbiota composition in SGA newborns as a potential avenue for identifying infants who may benefit from closer developmental follow-up.

What was studied?

Sickle cell disease (SCD) is one of the most common genetic conditions worldwide. It can contribute up to 90% of under-5 mortality in sub-Saharan Africa. Clinical manifestations are very heterogeneous, and the intestinal microbiome appears to be crucial in the modulation of inflammation, cell adhesion and induction of aged neutrophils, the main interveners of recurrent vaso-occlusive crisis. Enterocyte injury, increased permeability, altered microbial composition and bacterial overgrowth have all been documented as microbial and pathophysiologic changes in the gut microbiome of SCD patients in recent studies. Our aim was to sequence the bacterial 16S rRNA gene in order to characterize the gut microbiome of Angolan children with SCA and healthy siblings as a control. A total of 72 stool samples were obtained from children between 3 and 14 years old. Our data showed that the two groups exhibit some notable differences in microbiota relative abundance at different classification levels. Children with SCA have a higher number of the phylum Actinobacteria. As for the genus level, Clostridium cluster XI bacteria was more prevalent in the SCA children, whereas the siblings had a higher abundance of Blautia, Aestuariispira, Campylobacter, Helicobacter, Polaribacter and Anaerorhabdus. In this study, we have presented the first microbiota analysis in an Angolan paediatric population with SCD and provided a detailed view of the microbial differences between patients and healthy controls. There is still much to learn before fully relying on the therapeutic approaches for gut modulation, which is why more research in this field is crucial to making this a reality.

What was studied?

This study examined how maternal dietary deficiencies affect reproduction, body growth, and gut microbiota in greater long-tailed hamsters (Tscherskia triton). Researchers compared low-protein diets and niacin-deficient diets under controlled laboratory conditions. They measured maternal reproductive performance, body weight of mothers and their offspring, and the composition and function of the offspring gut microbial community.

Who was studied?

The subjects were female greater long-tailed hamsters (Tscherskia triton) and their offspring, studied under laboratory conditions. The abstract does not give an exact sample size or number of litters, so no specific cohort figure can be stated. The comparison groups were animals fed low-protein diets versus niacin-deficient diets relative to normal controls.

What were the most important findings?

A maternal low-protein diet, but not niacin deficiency, significantly harmed reproduction, producing longer mating latency and smaller litter sizes, and reduced body weight in both mothers and offspring. Both protein- and niacin-deficient diets produced significant maternal effects on the offspring gut microbial community. The low-protein diet specifically reduced the abundance of major short-chain-fatty-acid-producing bacterial taxa, increased probiotic taxa abundance, and altered microbial function in offspring. Negative effects on gut microbiota were more pronounced in the protein-deficient group than the niacin-deficient group.

What are the greatest implications of this study?

The findings suggest that maternal protein intake, more than niacin intake, is a critical driver of offspring reproductive fitness, growth, and gut microbial health in this rodent species. Because low-protein diets depleted short-chain-fatty-acid producers while favoring probiotic taxa, maternal nutrition appears to reshape the functional capacity of the offspring microbiome, not just its composition. This supports the broader concept that maternal diet can programmatically transfer microbiota-mediated metabolic consequences to offspring across generations.

What was studied?

Gut microbes were closely related to women's health. Previous studies reported that the gut microbes of premenopausal women were different from those of postmenopausal women. However, little was known about the relationship between gut microbiota dysbiosis and menopausal syndrome (MPS). The aim of this study was to explore the relationship between MPS and gut microbes.

Who was studied?

Patients with MPS (P group, n = 77) and healthy women (H group, n = 24) at menopause were recruited in this study. The stool specimen and clinical parameters (demographic data, follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), et al) of participants' were collected. We evaluated the differences in gut microbes by 16S ribosomal RNA gene sequencing. We used LEfSe to identify gut microbes with varying abundances in different groups. The Spearman correlation coefficients of clinical parameters and gut microbes were calculated. PICRUSt was used to predict the potential KEGG Ortholog functional profiles of microbial communities.

What were the most important findings?

The abundance of 14 species differed substantially between the MPS and menopausal healthy women (LDA significance threshold > 2.0) according to LEfSe analysis. Using Spearman's correlation analysis, it was discovered that E2 had a positive correlation with Aggregatibacter segnis, Bifidobacterium animalis, Acinetobacter guillouiae (p < 0.05, these three species were enriched in menopausal healthy women), while FSH and LH had a negative correlation with them (p < 0.05). KEGG level3 metabolic pathways relevant to cardiovascular disease and carbohydrate metabolism were enriched in the MPS (p < 0.05), according to functional prediction by PICRUST and analyzed by Dunn test.

What are the greatest implications of this study?

There was gut microbiota dysbiosis in MPS, which is reflected in the deficiency of the abundance of Aggregatibacter segnis, Bifidobacterium animalis and Acinetobacter guillouiae related to the level of sex hormones. In MPS individuals, species with altered abundances and unique functional pathways were found.

What was studied?

How gastric cancer (GC) incidence is associated with changes in the gastric microbiome has not been firmly established. The present study therefore aims to investigate the microbial communities present within the gastric mucosa of patients with superficial gastritis (SG) or GC.

Who was studied?

Paired tumor and paracancerous samples of the gastric mucosa were collected from 18 patients being surgically treated for GC and from 32 patients with SG being treated via gastroscopy. The gastric microbiome in these samples was then profiled via 16S rRNA sequencing, with a linear discriminant analysis effect size (LEfSe) approach used to identify and compare different bacteria, and with PICRUSt used for predictive functional analyses.

What were the most important findings?

GC patients exhibited a distinct gastric microbiota profile from that observed in SG patients. These changes were evident in both tumor and paracancerous tissues from GC patients. Specifically, we found that 6 bacterial genera were specifically enriched in GC tissue samples relative to SG samples, while 18 genera were depleted in these same samples. Based on the differential abundance of these bacteria, we were able to calculate microbial dysbiosis index (MDI) values, which were significantly higher in GC patients than in SG patients. In addition, MDI values were negatively correlated with gastric Shannon index and were positively correlated with relative Helicobacter spp. abundance. Importantly, these MDI values were readily able to discriminate between GC and SG patient samples. Functional analysis suggested that GC patients were more likely to harbor a nitrosating microbial community.

What are the greatest implications of this study?

GC patients exhibited a gastric microbiome profile distinct from that observed in SG patients, with these differences being evident in both tumor and paracancerous tissues. Differences in the relative abundance of Helicobacter spp. may be the primary driver of gastric dysbiosis in GC patients.

What was studied?

This study examined the environmental drivers of gut microbiome composition and function in wild Ethiopian geladas. Researchers focused on how food availability, tracked using rainfall, and thermoregulatory stress, tracked using temperature, predicted shifts in gut microbial diversity. Geladas were chosen because they live in a cold, high-altitude environment and eat a low-quality, grass-based diet, creating both energetic and thermoregulatory pressures. The study looked beyond diet alone to ask whether other environmental factors also shape the gut microbiome in a natural setting.

Who was studied?

The subjects were wild Ethiopian geladas (Theropithecus gelada), a nonhuman primate species living at high altitude in a cold climate. The dataset comprised 758 gut microbiome samples collected from these wild animals, making it the largest wild nonhuman primate gut microbiome dataset generated to date. The abstract does not specify the number of individual animals sampled or their sex or age distribution.

What were the most important findings?

Gut microbiome composition in geladas covaried with both rainfall and temperature, but in patterns suggesting distinct responses to dietary versus thermoregulatory challenges. Seasonal microbial shifts tracked changes in the dominant components of the diet. During rainier periods, the gut was dominated by cellulolytic and fermentative bacteria specialized in digesting grass, while dry-period communities differed accordingly. This indicates that the gelada gut microbiome adjusts compositionally in step with seasonal food quality and availability.

What are the greatest implications of this study?

The findings suggest that gut microbiome plasticity helps wild primates cope with seasonal swings in diet quality and possibly with thermoregulatory demands, not diet changes alone. By generating the largest wild nonhuman primate gut microbiome dataset to date, this work provides a foundation for studying how environmental variables beyond diet shape host-microbe relationships in natural settings. It also underscores the value of long-term, in-situ sampling for understanding adaptive microbiome responses to seasonal environmental stress.

What was studied?

This study investigated gut dysbiosis and abnormal bile acid metabolism in colitis-associated cancer (CAC), a form of colorectal cancer that can arise from prolonged inflammatory bowel disease. Researchers used an azoxymethane/dextran sodium sulfate (AOM/DSS) model to induce CAC and examined intestinal inflammation, mucosal barrier integrity, and bile acid receptor expression. They profiled the fecal microbiome with 16S rRNA sequencing and measured bile acids using liquid chromatography-mass spectrometry. The goal was to characterize how microbial and bile acid changes relate to inflammation and tumor development.

Who was studied?

The study used C57BL/6 mice, randomly allocated into an AOM/DSS group and a control group. The AOM/DSS group received an azoxymethane injection followed by dextran sodium sulfate in their drinking water to induce colitis-associated cancer. The abstract does not report a human cohort; this was an animal model study.

What were the most important findings?

The AOM/DSS group developed severe mucosal barrier impairment, an inflammatory response, and tumor formation in the colon. Gut microbiota richness and biodiversity decreased, with a significant shift in overall community composition. Pathogen abundance increased while short-chain fatty acid producing bacteria declined. Clostridium XlV and Lactobacillus, bacteria potentially involved in bile acid deconjugation, transformation, and desulfation, were significantly reduced in the CAC model.

What are the greatest implications of this study?

The findings support a link between gut dysbiosis, disrupted bile acid metabolism, and the inflammatory processes that drive progression from colitis to cancer. Loss of bacteria capable of transforming and desulfating bile acids may allow abnormal bile acid profiles to accumulate and worsen mucosal injury. This suggests that restoring specific bile acid-metabolizing bacteria or correcting bile acid imbalance could be explored as strategies to reduce cancer risk in chronic IBD. The results also highlight the fecal microbiome and bile acid profile as potential markers to monitor colitis-associated cancer progression.

What was studied?

Background: Gut microbiome has recently been identified as a new potential risk factor in addition to well-known diabetes risk factors. The aim of this study was to analyze the differences in the composition of gut microbiome in prediabetes(PreDM), type 2 diabetes mellitus (T2DM) and non-diabetic controls. Methods: A total of 180 participants were recruited for this study: 60 with T2DM, 60 with PreDM and 60 non-diabetics (control group). Fecal samples were collected from the participants and genomic DNA was extracted. The composition and diversity of gut microbiome were investigated in fecal DNA samples using Illumina sequencing of the V3∼V4 regions of 16sRNA. Results: There were significant differences in the number of bacteria among patients with PreDM and T2DM and the control group. Compared with the control group, Proteobacteria bacteria were significantly higher in the PreDM group (P = 0.006). On the genus level, Compared with the control group, the relative abundance of Prevotella and Alloprevotella was significantly higher in the T2DM group (P = 0.016, P = 0.018), and the relative abundance of Paraprevotella in T2DM and PreDM groups was lower than that in the control group (P = 0.011, P = 0.045). Compared with the PreDM group and the control group, the relative abundance of Bacteroides in the T2DM group was significantly lower (P = 0.019, P = 0.002). Conclusions: The present study found significant differences in the gut microbiome between PreDM, T2DM and non-diabetic individuals, specifically at the genus level, suggesting that early intervention in PreDM patients could have implications for gut flora transitioning to T2DM. In addition, these results may be valuable for developing strategies to control T2DM by modifying the gut microbiome.

What was studied?

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

What was studied?

This study examined how the gut microbial community changes along different regions of the gastrointestinal tract, comparing the small intestine, cecum, colon, and rectum. It also compared these gut regions across three closely related, co-occurring wild rodent species. The goal was to determine how much of the variation in gut microbiota is explained by gut region versus host species.

Who was studied?

The study sampled three sympatric species of wild rodents: Apodemus speciosus, Apodemus argenteus, and Myodes rufocanus. These animals were presumably collected from the wild and sampled at multiple gastrointestinal sites (small intestine, cecum, colon, and rectum) per individual. The abstract does not give an exact number of animals sampled.

What were the most important findings?

The small intestine harbored a microbial community that was distinct from that of the lower gastrointestinal tract (cecum, colon, and rectum) in all three rodent species. The genus Lactobacillus was notably more abundant in the small intestine than in lower gut regions across all three species. This pattern held consistently regardless of host species, suggesting gut region has a strong and generalizable effect on microbiome composition.

What are the greatest implications of this study?

The findings indicate that gut region is an important driver of microbiome variation, meaning fecal or colon samples alone may not represent the full gastrointestinal microbial community. This has implications for how wild animal microbiome studies are designed, since relying only on fecal samples could miss important small-intestinal features like Lactobacillus enrichment. Comparative host-microbiome research may need to sample multiple gut regions to draw accurate conclusions about host-microbe interactions.

What was studied?

This case-control study characterized the cervical microbiota of women undergoing in vitro fertilization (IVF) with embryo transfer (ET). Researchers collected cervical swabs on the day of embryo transfer and sequenced the V3-V4 regions of the 16S rRNA gene using Illumina MiSeq. The goal was to determine whether cervical microbial composition was associated with subsequent pregnancy outcomes, and to explore factors that might underlie any such association.

Who was studied?

The study enrolled 100 subfertile patients undergoing IVF who received two fresh or frozen-thawed cleavage-stage embryos per cycle. Patients were divided into four groups based on clinical pregnancy outcome after embryo transfer. In the fresh IVF-ET cycles, the clinical pregnancy group comprised 25 women (FP) and the non-pregnancy group comprised 26 women (FN); in frozen-thawed cycles, the clinical pregnancy group comprised 27 women (TP).

What were the most important findings?

In fresh IVF-ET cycles, women who achieved clinical pregnancy (FP group) showed significantly higher cervical microbiota alpha diversity than those who did not (FN group). Beta diversity analysis (ANOSIM) confirmed a significant difference in overall community composition between the pregnant and non-pregnant groups. In frozen-thawed ET cycles, a similar trend toward higher alpha diversity in the pregnant group (TP) was observed, though this difference did not reach statistical significance. The abstract as provided does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.

What are the greatest implications of this study?

These findings suggest that the composition and diversity of the cervical microbiota at the time of embryo transfer may influence the likelihood of achieving clinical pregnancy in IVF. Higher microbial diversity in the cervix could serve as a biomarker for reproductive outcome or reflect a favorable local environment for implantation. This raises the possibility that cervical microbiota profiling could eventually help individualize IVF protocols or identify patients who might benefit from microbiome-targeted interventions before embryo transfer.

What was studied?

Periodontitis is an inflammatory disease of microbial etiology caused primarily by dysbiosis of the oral microbiota. Our aim was to compare variations in the composition of the oral microbiomes of youths with severe periodontitis according to gender.

Who was studied?

Subgingival plaque samples collected from 17 patients with severe periodontitis (11 males and 6 females) were split for 16S rRNA gene sequencing. The composition, α-diversity, and β-diversity of the patients' oral microbiomes were compared between the males and the females. Linear discriminant analysis effect size (LEfSe) was used to analyze the specific taxa enriched in the two groups. Functional profiles (KEGG pathways) were obtained using PICRUSt based on 16S rRNA gene sequencing data.

What were the most important findings?

The Chao1 index and phylogenetic diversity whole tree were significantly higher in males than in females. The Simpson and Shannon indices were not significantly different between the two groups. β-Diversity suggested that the samples were reasonably divided into groups. The Kruskal-Wallis test based on the relative abundance of species, combined with the LEfSe analysis showed that the dominant bacteria in males were Pseudomonas and Papillibacter, whereas the dominant bacteria in women were Fusobacteriales and Tannerella. KEGG analysis predicted that the variation in the oral microbiome may be related to the immune system in women, whereas immune system diseases were the dominant pathway in men.

What are the greatest implications of this study?

We found sex-specific differences in the oral microbiome in a sample of youths with severe periodontitis. The differences may be related to changes in immune homeostasis and lead to a better understanding of periodontitis.

What was studied?

This study examined whether jasmine tea can ease depressive-like behavior through the brain-gut-microbiome axis. Researchers built a chronic unpredictable mild stress (CUMS) rat model to induce depression-like symptoms and then treated the animals with jasmine tea. They tracked depression-related behavioral indicators alongside changes in the gut microbiota using 16S rRNA sequencing. The goal was to connect microbial shifts to neurochemical changes in the brain.

Who was studied?

The subjects were rats subjected to a chronic unpredictable mild stress protocol designed to produce depressive-like symptoms. The abstract does not report a specific number of animals, strain, sex, or age. This was an animal (rodent) model study rather than a human cohort, and no human population was involved.

What were the most important findings?

Jasmine tea treatment improved depressive-like behaviors and normalized neurotransmitter levels in the CUMS rats. It also increased gut microbiota diversity and richness compared to untreated depressed rats. Spearman correlation analysis linked differential bacterial taxa, including Patescibacteria, Firmicutes, Bacteroidetes, Spirochaetes, Elusimicrobia, and Proteobacteria, to depression-related markers such as BDNF, GLP-1, and 5-HT in the hippocampus and cerebral cortex. The abstract does not mention Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism, so this study did not address that angle.

What are the greatest implications of this study?

The findings support the idea that jasmine tea's antidepressant-like effects operate at least partly through modulation of the gut microbiome, not solely through direct brain effects. This strengthens the broader case for the brain-gut-microbiome axis as a target for managing depression. It also suggests dietary or beverage-based interventions could complement other approaches to mood disorders. Because this is a rat model, further work would be needed before drawing conclusions about human depression treatment.

What was studied?

Evidence of the gut microbiota influencing neurodegenerative diseases has been reported for several neural diseases. However, there is little insight regarding the relationship between the gut microbiota and prion disease. Here, using fecal samples of 12 prion-infected mice and 25 healthy controls, we analyzed the structure of the gut microbiota and metabolic changes by 16S rRNA sequencing and LC-MS-based metabolomics respectively as multi-omic analyses. Additionally, SCFAs and common amino acids were detected by GC-MS and UPLC respectively. Enteric changes induced by prion disease affected both structure and abundances of the gut microbiota. The gut microbiota of infected mice displayed greater numbers of Proteobacteria and less Saccharibacteria at the phylum level and more Lactobacillaceae and Helicobacteraceae and less Prevotellaceae and Ruminococcaceae at the family level. A total of 145 fecal metabolites were found to be significantly different in prion infection, and most (114) of these were lipid metabolites. Using KEGG pathway enrichment analysis, we found that 3 phosphatidylcholine (PC) compounds significantly decreased and 4 hydrophobic bile acids significantly increased. Decreases of 8 types of short-chain acids (SCFAs) and increases of Cys and Tyr and decreases of His, Trp, and Arg were observed in prion infection. Correlation analysis indicated that the gut microbiota changes observed in our study may have been the shared outcome of prion disease. These findings suggest that prion disease can cause significant shifts in the gut microbiota. Certain bacterial taxa can then respond to the resulting change to the enteric environment by causing dramatic shifts in metabolite levels. Our data highlight the health impact of the gut microbiota and related metabolites in prion disease.

What was studied?

General chronic periodontitis (GCP) is a bacterial inflammatory disease with complex pathology. Despite extensive studies published on the variation in the oral microbiota and metabolic profiles of GCP patients, information is lacking regarding the correlation between host-bacterial interactions and biochemical metabolism. This study aimed to analyze the oral microbiome, the oral metabolome, and the link between them and to identify potential molecules as useful biomarkers for predictive, preventive, and personalized medicine (PPPM) in GCP.

Who was studied?

In this study, gingival crevicular fluid (GCF) samples were collected from patients with GCP (n = 30) and healthy controls (n = 28). The abundance of oral microbiota constituents was obtained by Illumina sequencing, and the relative level of metabolites was measured by gas chromatography-mass spectrometry. Full-mouth probing depth, clinical attachment loss, and bleeding on probing were recorded as indices of periodontal disease.

What were the most important findings?

The relative abundances of 7 phyla and 82 genera differed significantly between the GCP and healthy groups. Seventeen differential metabolites involved in different metabolism pathways were selected based on variable influence on projection values (VIP > 1) and P values (P < 0.05). Through Spearman's correlation analysis, microorganisms, metabolites in GCF, and clinical data together showed a clear trend, and clinical data regarding periodontitis can be reflected in the shift of the oral microbial community and the change in metabolites in GCF. A combination of citramalic acid and N-carbamylglutamate yielded satisfactory accuracy (AUC = 0.876) for the predictive diagnosis of GCP.

What are the greatest implications of this study?

Dysbiosis in the polymicrobial community structure and changes in metabolism could be mechanisms underlying periodontitis. The differential microorganisms and metabolites in GCF between periodontitis patients and healthy individuals are possibly biomarkers, pointing to a potential strategy for the prediction, diagnosis, prognosis, and management of personalized periodontal therapy.

What was studied?

Dry eye affects millions of individuals. In experimental models, dry eye disease is associated with T helper cell 17-mediated inflammation of the ocular surface that may cause persistent damage to the corneal epithelium. However, the initiating and perpetuating factors associated with chronic inflammation of the ocular surface remain unclear. The ocular microbiota alters ocular surface inflammation and may influence dry eye disease development and progression. Here, we collected serial samples of tears on awakening from sleep, closed eye tears, during a randomized clinical trial of a non-pharmaceutical dry eye therapy and used 16S rRNA metabarcoding to characterize the microbiome. We show the closed dry eye microbiome is distinct from the healthy closed eye microbiome, and that the microbiome remains distinct despite daily saline eye wash upon awakening. The ocular microbiome was described only recently, and this report implicates a distinct microbiome in ocular disease development. Our findings suggest an interplay between microbial commensals and inflammation on the ocular surface. This information may inform future studies of the pathophysiological mechanisms of dry eye disease.

What was studied?

The characterization of the microbial population of many niches of the organism, as the gastrointestinal tract, is now possible thanks to the use of high-throughput DNA sequencing technique. Several studies in the companion animals field already investigated faecal microbiome in healthy or affected subjects, although the methodologies used in the different laboratories and the limited number of animals recruited in each experiment does not allow a straight comparison among published results. In the present study, we report data collected from several in house researches carried out in healthy dogs, with the aim to seek for a variability of microbial taxa in the faeces, caused by factors such as diet and sex. The database contains 340 samples from 132 dogs, collected serially during dietary intervention studies. The procedure of samples collection, storage, DNA extraction and sequencing, bioinformatic and statistical analysis followed a standardized pipeline. Microbial profiles of faecal samples have been analyzed applying dimensional reduction discriminant analysis followed by random forest analysis to the relative abundances of genera in the feces as variables. The results supported the responsiveness of microbiota at a genera taxonomic level to dietary factor and allowed to cluster dogs according this factor with high accuracy. Also sex factor clustered dogs, with castrated males and spayed females forming a separated group in comparison to intact dogs, strengthening the hypothesis of a bidirectional interaction between microbiota and endocrine status of the host. The findings of the present analysis are promising for a better comprehension of the mechanisms that regulate the connection of the microorganisms living the gastrointestinal tract with the diet and the host. This preliminary study deserves further investigation for the identification of the factors affecting faecal microbiome in dogs.

What was studied?

This study investigated whether BDB, a natural bromophenol isolated from the marine red alga Rhodomela confervoides, could alleviate type 2 diabetes mellitus (T2DM) by modulating the gut microbiota. Researchers used 16S rRNA gene pyrosequencing of the V3-V4 regions along with metagenomic analysis to characterize microbial community changes during BDB treatment. The study compared BDB against metformin, a standard antidiabetic drug, and a vehicle control to assess effects on fasting blood glucose and gut microbial composition.

Who was studied?

The study used 24 diabetic BKS db mice, randomly assigned in a blinded manner to receive BDB (n = 6), metformin (n = 6), or vehicle (n = 6) for seven weeks. Non-diabetic BKS mice (n = 6) served as a normal control group. This was an animal model study, not a human cohort.

What were the most important findings?

Diabetic mice treated with BDB or metformin showed significant reductions in fasting blood glucose by the seventh week compared with vehicle-treated diabetic mice. Gut microbiota analysis revealed that short-chain fatty acid (SCFA) producing bacteria, including Lachnospiraceae and Bacteroides, were significantly more abundant in the BDB and metformin groups than in the vehicle group. Notably, Akkermansia was significantly elevated at the genus level in the BDB-treatment group specifically. No sulfate-reducing bacteria, Desulfovibrio, hydrogen sulfide, or sulfur metabolism findings were reported in this abstract.

What are the greatest implications of this study?

These findings suggest that BDB's antidiabetic effects in this mouse model may be linked to favorable shifts in gut microbiota composition, particularly increases in SCFA-producing bacteria and Akkermansia. This positions BDB as a candidate natural compound worth further investigation for T2DM management through a gut-microbiota-mediated mechanism. The metagenomic data point toward specific microbial pathways that could be explored in future mechanistic and translational studies.

What was studied?

This study characterized the gut and genital microbial ecosystems of wild vervet monkeys naturally infected with simian immunodeficiency virus (SIV). Researchers profiled fecal, rectal, vaginal, and penile microbiomes to examine shifts in microbial diversity, composition, and functionality during natural SIV infection. Unlike HIV-infected humans, SIV-infected vervet monkeys do not experience gut dysfunction, microbial translocation, or chronic immune activation, so the study aimed to describe this nonprogressing host-pathogen relationship at the microbiome level for the first time.

Who was studied?

The subjects were wild vervet monkeys from populations across diverse locations in South Africa that were heavily infected with SIV. Fecal, rectal, vaginal, and penile samples were collected from these free-ranging animals rather than from a laboratory cohort. The abstract indicates the population varied by geographic site, age, and sex, all of which were examined as factors affecting the microbiome.

What were the most important findings?

Geographic site, age, and sex all affected the vervet microbiome across different body sites. The fecal microbiome showed marked stratification into three enterotypes, and the vaginal microbiome stratified into two vagitypes, each predicted to be functionally distinct within its respective body site. External bioclimatic factors, biome type, and environmental temperature also influenced the microbiome locally, indicating that environment plays a substantial role alongside host factors in shaping microbial community structure.

What are the greatest implications of this study?

By characterizing the gut and genital microbiome of a natural, nonprogressing SIV host, this study provides a comparative framework for understanding why vervet monkeys avoid the gut dysfunction, microbial translocation, and immune activation seen in HIV-infected humans. The identification of distinct, functionally stratified enterotypes and vagitypes suggests that microbiome composition and function, not just viral dynamics, may contribute to disease outcome in lentivirus infection. These findings support further investigation into host, environmental, and microbial factors that distinguish nonpathogenic SIV infection from progressive HIV disease in humans.

What was studied?

Intestinal microbial dysbiosis is evident in chronic HIV-infected individuals and may underlie inflammation that persists even during antiretroviral therapy (ART). It remains unclear, however, how early after HIV infection gut dysbiosis emerges and how it is affected by early ART.

Who was studied?

Fecal microbiota were studied by 16s rDNA sequencing in 52 Thai men who have sex with men (MSM), at diagnosis of acute HIV infection (AHI), Fiebig Stages 1-5 (F1-5), and after 6 months of ART initiation, and in 7 Thai MSM HIV-uninfected controls. Dysbiotic bacterial taxa were associated with relevant inflammatory markers.

What were the most important findings?

Fecal microbiota profiling of AHI pre-ART vs HIV-uninfected controls showed a mild dysbiosis. Transition from F1-3 of acute infection was characterized by enrichment in pro-inflammatory bacteria. Lower proportions of Bacteroidetes and higher frequencies of Proteobacteria and Fusobacteria members were observed post-ART compared with pre-ART. Fusobacteria members were positively correlated with levels of soluble CD14 in AHI post-ART.

What are the greatest implications of this study?

Evidence of gut dysbiosis was observed during early acute HIV infection and was partially restored upon early ART initiation. The association of dysbiotic bacterial taxa with inflammatory markers suggests that a potential relationship between altered gut microbiota and systemic inflammation may also be established during AHI.

What was studied?

Generalist species able to exploit anthropogenic food sources are becoming increasingly common in urban environments. Coyotes (Canis latrans) are one such urban generalist that now resides in cities across North America, where diseased or unhealthy coyotes are frequently reported in cases of human-wildlife conflict. Coyote health and fitness may be related to habitat use and diet via the gut microbiome, which has far-reaching effects on animal nutrition and physiology. In this study, we used stomach contents, stable isotope analysis, 16S rRNA gene amplicon sequencing, and measures of body condition to identify relationships among habitat use, diet, fecal microbiome composition, and health in urban and rural coyotes. Three distinct relationships emerged: (1) Urban coyotes consumed more anthropogenic food, which was associated with increased microbiome diversity, higher abundances of Streptococcus and Enterococcus, and poorer average body condition. (2) Conversely, rural coyotes harbored microbiomes rich in Fusobacteria, Sutterella, and Anaerobiospirillum, which were associated with protein-rich diets and improved body condition. (3) Diets rich in anthropogenic food were associated with increased abundances of Erysipelotrichiaceae, Lachnospiraceae, and Coriobacteriaceae, which correlated with larger spleens in urban coyotes. Urban coyotes also had an increased prevalence of the zoonotic parasite Echinococcus multilocularis, but there were no detectable connections between parasite infection and microbiome composition. Our results demonstrate how the consumption of carbohydrate-rich anthropogenic food by urban coyotes alters the microbiome to negatively affect body condition, with potential relationships to parasite susceptibility and conflict-prone behavior.

What was studied?

The ongoing global pandemic of COVID-19 disease, which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), mainly infect lung epithelial cells, and spread mainly through respiratory droplets. However, recent studies showed potential intestinal infection of SARS-CoV-2, implicated the possibility that the intestinal infection of SARS-CoV-2 may correlate with the dysbiosis of gut microbiota, as well as the severity of COVID-19 symptoms. Here, we investigated the alteration of the gut microbiota in COVID-19 patients, as well as analyzed the correlation between the altered microbes and the levels of intestinal inflammatory cytokine IL-18, which was reported to be elevated in the serum of in COVID-19 patients. Comparing with healthy controls or seasonal flu patients, the gut microbiota showed significantly reduced diversity, with increased opportunistic pathogens in COVID-19 patients. Also, IL-18 level was higher in the fecal samples of COVID-19 patients than in those of either healthy controls or seasonal flu patients. Moreover, the IL-18 levels were even higher in the fecal supernatants obtained from COVID-19 patients that tested positive for SARS-CoV-2 RNA than those that tested negative in fecal samples. These results indicate that changes in gut microbiota composition might contribute to SARS-CoV-2-induced production of inflammatory cytokines in the intestine and potentially also to the onset of a cytokine storm.

What was studied?

This study examined how the gastric mucosal microbiota differs across distinct microhabitats within the stomach in the context of gastric cancer (GC). Researchers compared microbial diversity, composition, bacterial co-occurrence networks, and predicted functional profiles across normal, peritumoral, and tumoral tissue. The goal was to determine whether GC-associated stomach microhabitats, rather than cancer stage or type, shape the gastric microbiota.

Who was studied?

The cohort consisted of 276 patients with gastric cancer who had not received preoperative chemotherapy and were enrolled retrospectively. Tissue samples were collected from three microhabitats: 230 normal, 247 peritumoral, and 229 tumoral samples. Microbial community composition was assessed using 16S rRNA gene sequencing on the MiSeq platform.

What were the most important findings?

The composition and diversity of the gastric microbiota were determined by the specific stomach microhabitat rather than by GC stage or type. Bacterial richness was decreased in both peritumoral and tumoral microhabitats compared to normal tissue, and the co-occurrence network of abundant bacteria was simplified in the tumoral microhabitat. Helicobacter pylori, Prevotella copri, and Bacteroides uniformis were significantly decreased in tumoral tissue, while Prevotella melaninogenica, Streptococcus anginosus, and Propionibacterium acnes were increased there.

What are the greatest implications of this study?

These findings indicate that the tumor microenvironment reshapes the local microbiota in a site-specific manner, with reduced diversity and simplified microbial networks marking the transition from normal to tumoral tissue. The consistent shifts in specific taxa across microhabitats suggest the gastric microbiota could serve as a biomarker of tissue state within the same stomach. This microhabitat-based framework highlights the importance of sampling location when characterizing microbiota changes associated with gastric cancer.

What was studied?

Recent studies on celiac disease (CeD) have reported alterations in the gut microbiome. Whether this alteration in the microbial community is the cause or effect of the disease is not well understood, especially in adult onset of disease. The first-degree relatives (FDRs) of CeD patients may provide an opportunity to study gut microbiome in pre-disease state as FDRs are genetically susceptible to CeD. By using 16S rRNA gene sequencing, we observed that ecosystem level diversity measures were not significantly different between the disease condition (CeD), pre-disease (FDR) and control subjects. However, differences were observed at the level of amplicon sequence variant (ASV), suggesting alterations in specific ASVs between pre-disease and diseased condition. Duodenal biopsies showed higher differences in ASVs compared to fecal samples indicating larger disruption of the microbiota at the disease site. The duodenal microbiota of FDR was characterized by significant abundance of ASVs belonging to Parvimonas, Granulicatella, Gemella, Bifidobacterium, Anaerostipes, and Actinomyces genera. The duodenal microbiota of CeD was characterized by higher abundance of ASVs from genera Megasphaera and Helicobacter compared to the FDR microbiota. The CeD and FDR fecal microbiota had reduced abundance of ASVs classified as Akkermansia and Dorea when compared to control group microbiota. In addition, predicted functional metagenome showed reduced ability of gluten degradation by CeD fecal microbiota in comparison to FDRs and controls. The findings of the present study demonstrate differences in ASVs and predicts reduced ability of CeD fecal microbiota to degrade gluten compared to the FDR fecal microbiota. Further research is required to investigate the strain level and active functional profiles of FDR and CeD microbiota to better understand the role of gut microbiome in pathophysiology of CeD.

What was studied?

This study compared the mucosa-associated bacterial community of gastric cancer tissue with each patient's own adjacent non-cancer tissue, using paired samples to control for host genetics and environment, and profiled composition, co-occurrence networks, and predicted functions by 16S rRNA (V4 to V5) sequencing.

Who was studied?

124 gastric mucosa samples (cancer plus paired adjacent non-cancer) from 62 gastric adenocarcinoma patients who underwent subtotal gastrectomy at the First Hospital of China Medical University (2012 to 2014), median age 60, excluding anyone recently treated with antibiotics, proton-pump inhibitors, probiotics, chemotherapy, or radiotherapy.

What were the most important findings?

Tumor tissue showed higher microbial richness and diversity than non-cancer tissue, with a denser co-occurrence network. Proteobacteria dominated both groups but were relatively lower in cancer, while Firmicutes, Bacteroidetes, Actinobacteria, and Fusobacteria rose. LEfSe flagged 49 differentially abundant taxa (LDA above 3): 33 enriched in cancer, largely oral bacteria such as Peptostreptococcus, Streptococcus, and Fusobacterium, and 16 enriched in non-cancer tissue, largely lactic-acid bacteria. Predicted purine-metabolism and denitrification functions were enriched in the cancer community.

What are the greatest implications of this study?

The results point to translocated oral bacteria, rather than Helicobacter pylori alone, as a feature of the gastric-cancer microenvironment and a possible contributor to or marker of carcinogenesis. As a cross-sectional tissue study, it establishes association rather than causation.

What was studied?

This study examined whether alterations in the gut microbiota are linked to systemic inflammation in chronic kidney disease (CKD). The researchers used 16S ribosomal DNA pyrosequencing on fecal samples to characterize microbial composition. They also measured serum inflammatory factors to explore possible correlations between gut dysbiosis and inflammation in CKD.

Who was studied?

The study included 50 patients with chronic kidney disease and 22 healthy control subjects. Fecal microbiota samples and serum inflammatory markers were collected from both groups for comparison. The abstract does not provide further demographic details such as age, sex distribution, or CKD stage.

What were the most important findings?

Patients with CKD had significantly reduced richness and altered structure of their fecal microbiota compared to healthy controls. At the phylum level, CKD patients showed reduced Actinobacteria but increased Verrucomicrobia. At the genus level, Lactobacillus, Clostridium IV, Paraprevotella, Clostridium sensu stricto, Desulfovibrio, and Alloprevotella were enriched in CKD patients, while Akkermansia and Parasutterella were enriched in healthy controls, with Akkermansia notably lower in the CKD group.

What are the greatest implications of this study?

These findings support the idea that gut dysbiosis, including enrichment of taxa such as Desulfovibrio, may be tied to the chronic systemic inflammation seen in CKD. The depletion of Akkermansia in CKD patients suggests a potential loss of a genus often associated with gut barrier health. This work points toward the gut microbiota as a possible target for understanding or addressing inflammatory processes that contribute to CKD progression.

What was studied?

This study used next-generation 16S ribosomal RNA gene sequencing to characterize the salivary (oral) microbiota associated with throat cancer. Researchers compared microbial community diversity and composition among throat cancer patients, vocal cord polyp patients, and healthy controls. They also built a diagnostic model based on constituent bacteria and verified select findings with real-time quantitative PCR.

Who was studied?

The study analyzed 70 oral (salivary) samples collected from three groups: 32 patients with throat cancer, nine patients with a vocal cord polyp, and 29 healthy individuals serving as normal controls. All participants were drawn from a clinical setting where throat cancer and vocal cord polyp diagnoses had been made, alongside disease-free comparison subjects.

What were the most important findings?

The salivary microbiota of throat cancer patients was significantly different from that of polyp patients and healthy individuals, with beta diversity clearly divergent in the cancer group. Alpha diversity was significantly reduced in cancer patients, as shown by the Chao1 estimator (P = 8.1e-05), Simpson index (P = 0.0045), and Shannon index (P = 0.0071). The genera Aggregatibacter, Pseudomonas, Bacteroides, and Ruminiclostridium were significantly enriched in throat cancer patients compared with the other two groups, a result confirmed by qPCR. A diagnostic model built from these bacterial constituents achieved 87.5% accuracy in distinguishing cancer patients from the other groups.

What are the greatest implications of this study?

These findings suggest that reduced salivary microbial diversity and enrichment of specific bacterial genera may serve as biological indicators associated with throat cancer. The strong diagnostic accuracy of the bacteria-based model points to the potential for salivary microbiota profiling as a non-invasive tool to help distinguish throat cancer from benign vocal cord polyps and healthy states. Because this is an association-based study, further research is needed to determine whether these microbial shifts are causal, secondary to tumor presence, or influenced by other factors before clinical application.

What was studied?

Condyloma acuminatum (CA) is a benign epithelium hyperplasia mainly caused by human papillomavirus (HPV), which is now the second most common viral sexually transmitted infection (STI) in China. In total, 90% of CA patients are caused by the low-risk HPV 6 and 11. Aside from low-risk HPV infection there are likely other factors within the local microenvironment that contribute to CA and there has been related research before. In this study, 62 vaginal specimens were analyzed using 16S rRNA gene sequencing. The diversity of the vaginal microbiota was higher and the composition was different with LR-HPV infection. While the relative abundance of dominant Firmicutes was lower, Actinobacteria, Proteobacteria, and Fusobacteria phyla were significantly higher; at the genus level Gardnerella, Bifidobacterium, Sneathia, Hydrogenophilus, Burkholderia, and Atopobium were higher. This study firstly confirmed a more accurate and comprehensive understanding of the relationship between low-risk HPV infection and vaginal microbiota, in order to provide a theoretical basis for further research on the occurrence and development of CA.

What was studied?

The mucosa-associated gut microbiota directly modulates epithelial and mucosal function. In this study, we investigated the mucosa-associated microbial community in patients with inflammatory bowel disease (IBD), using endoscopic brush samples.

Who was studied?

A total of 174 mucus samples from 43 patients with ulcerative colitis (UC), 26 with Crohn's disease (CD) and 14 non-IBD controls were obtained by gentle brushing of mucosal surfaces using endoscopic cytology brushes. The gut microbiome was analyzed using 16S rRNA gene sequencing.

What were the most important findings?

There were no significant differences in microbial structure among different anatomical sites (the ileum, cecum and sigmoid colon) within individuals. There was, however, a significant difference in microbial structure between CD, UC and non-IBD controls. The difference between CD and non-IBD controls was more marked than that between UC patients and non-IBD controls. α-Diversity was significantly lower in UC and CD patients than non-IBD controls. When comparing CD patients with non-IBD controls, the phylum Proteobacteria was significantly increased and the phyla Firmicutes and Bacteroidetes were significantly reduced. These included a significant increase in the genera Escherichia, Ruminococcus (R. gnavus), Cetobacterium, Actinobacillus and Enterococcus, and a significant decrease in the genera Faecalibacterium, Coprococcus, Prevotella and Roseburia. Comparisons between CD and UC patients revealed a greater abundance of the genera Escherichia, Ruminococcus (R. gnavus), Clostridium, Cetobacterium, Peptostreptococcus in CD patients, and the genera Faecalibacterium, Blautia, Bifidobacterium, Roseburia and Citrobacter in UC patients.

What are the greatest implications of this study?

Mucosa-associated dysbiosis was identified in IBD patients. CD and UC may be distinguishable from the mucosa-associated microbial community structure.

What was studied?

Exposure to ambient fine particulate matter (PM2.5) correlates with abnormal glucose homeostasis, but the underlying biological mechanism has not been fully understood. The gut microbiota is an emerging crucial player in the homeostatic regulation of glucose metabolism. Few studies have investigated its role in the PM2.5 exposure-induced abnormalities in glucose homeostasis.

Who was studied?

C57Bl/6J mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CAP) for 12 months using a versatile aerosol concentration enrichment system (VACES) that was modified for long-term whole-body exposures. Their glucose homeostasis and gut microbiota were examined and analysed by correlation and mediation analysis.

What were the most important findings?

Intraperitoneal glucose tolerance test (IPGTT) and insulin tolerance test (ITT) showed that CAP exposure markedly impaired their glucose and insulin tolerance. Faecal microbiota analysis demonstrated that the impairment in glucose homeostasis was coincided with decreased faecal bacterial ACE and Chao-1 estimators (the indexes of community richness), while there was no significant change in all faecal fungal alpha diversity estimators. The Pearson's correlation analyses showed that the bacterial richness estimators were correlated with glucose and insulin tolerance, and the mediation analyses displayed a significant mediation of CAP exposure-induced glucose intolerance by the alteration in the bacterial Chao-1 estimator. LEfSe analyses revealed 24 bacterial and 21 fungal taxa differential between CAP- and FA-exposed animals. Of these, 14 and 20 bacterial taxa were correlated with IPGTT AUC and ITT AUC, respectively, and 5 fungal taxa were correlated with abnormalities in glucose metabolism.

What are the greatest implications of this study?

Chronic exposure to PM2.5 causes gut dysbiosis and may subsequently contribute to the development of abnormalities in glucose metabolism.

What was studied?

The study examined how the fatty acid profile of the maternal diet during gestation and lactation shapes the development of the offspring gut microbiota. It also tested whether these maternal fatty acid effects translate into later metabolic health outcomes in offspring fed a high-fat diet. The researchers used a transgenic mouse model capable of endogenously producing n-3 polyunsaturated fatty acids (PUFA), allowing them to compare offspring exposed to higher versus lower maternal n-3 PUFA levels.

Who was studied?

The subjects were murine (mouse) offspring from dams with differing endogenous n-3 PUFA production during gestation or lactation. Both male and female offspring were assessed, and offspring were subsequently fed a high-fat diet to evaluate metabolic outcomes into adulthood. The abstract does not give specific animal numbers, so no precise cohort size can be stated.

What were the most important findings?

Higher maternal n-3 PUFA production during gestation or lactation significantly reduced weight gain and markers of metabolic disruption in male offspring on a high-fat diet, but had no significant effect on weight gain in female offspring. Reduced maternal n-3 PUFA exposure was linked to significantly depleted Epsilonproteobacteria, Bacteroides, and Akkermansia, along with a higher relative abundance of Clostridia. The maternal fatty acid profile during lactation had a more profound influence on offspring microbiota and metabolism than exposure in utero, and this effect on microbiota composition and function persisted into adulthood after lifelong high-fat diet feeding.

What are the greatest implications of this study?

The findings suggest that maternal n-3 PUFA status during lactation can durably reprogram the offspring gut microbiota in a sex-specific way, with lasting consequences for metabolic health. This points to the early postnatal period, particularly lactation, as a key window in which maternal diet could be targeted to influence lifelong obesity risk. The results also highlight a potential mechanistic link between modern Western dietary patterns low in n-3 PUFA, the intestinal microbiome, and metabolic disease susceptibility.

What was studied?

The aim of this study was to investigate the characteristics and composition of intestinal microbiota in children with refractory epilepsy after ketogenic diet (KD) therapy and to explore the bacterial biomarkers related to clinical efficacy.

Who was studied?

We prospectively analyzed 20 patients (14 males, 6 females) treated with KD. Clinical efficacy, electroencephalogram (EEG) changes, and laboratory tests were evaluated, and fecal specimens were obtained prior to and 6 months after therapy. The composition of gut microbiota was analyzed by 16S rDNA sequencing, and we screened the possible flora associated with efficacy of the KD.

What were the most important findings?

After 6 months of treatment, 2 patients were seizure free, 3 had ≥ 90% seizure reduction, 5 had a reduction of 50-89%, and 10 had < 50% reduction. All 10 responders showed an improvement in EEG. Compared with baseline, fecal microbial profiles showed lower alpha diversity after KD therapy and revealed significantly decreased abundance of Firmicutes and increased levels of Bacteroidetes. We also observed that Clostridiales, Ruminococcaceae, Rikenellaceae, Lachnospiraceae, and Alistipes were enriched in the non-responsive group.

What are the greatest implications of this study?

The results show that the KD can reduce the species richness and diversity of intestinal microbiota. The changes of gut microbiota may be associated with different efficacy after KD, and specific gut microbiota may serve as an efficacy biomarker and a potential therapeutic target in patients with refractory epilepsy.

What was studied?

The esophageal microbiome has been proposed to be involved in a range of diseases including the esophageal adenocarcinoma cascade; however, little is currently known about its function and relationship to the host. Here, the esophageal microbiomes of 106 prospectively recruited patients were assessed using 16S rRNA and 18S rRNA amplicon sequencing as well as shotgun sequencing, and associations with age, gender, proton pump inhibitor use, host genetics, and disease were tested.

What were the most important findings?

The esophageal microbiome was found to cluster into functionally distinct community types (esotypes) defined by the relative abundances of Streptococcus and Prevotella. While age was found to be a significant factor driving microbiome composition, bacterial signatures and functions such as enrichment with Gram-negative oral-associated bacteria and microbial lactic acid production were associated with the early stages of the esophageal adenocarcinoma cascade. Non-bacterial microbes such as archaea, Candida spp., and bacteriophages were also identified in low abundance in the esophageal microbiome. Specific host SNPs in NOTCH2, STEAP2-AS1, and NREP were associated with the composition of the esophageal microbiome in our cohort.

What are the greatest implications of this study?

This study provides the most comprehensive assessment of the esophageal microbiome to date and identifies novel signatures and host markers that can be investigated further in the context of esophageal adenocarcinoma development.

What was studied?

This study examined the bacterial community composition of the bronchial airway, sampled by protected bronchial brushing, in relation to atopic asthma. The researchers used 16S rRNA gene sequencing to characterize the bronchial bacterial microbiome and inferred community-level functional profiles from the sequencing data. They compared microbiome composition across groups and examined associations with clinical and inflammatory features, including type 2-related inflammation markers and the change in airway hyperresponsiveness following six weeks of inhaled fluticasone treatment.

Who was studied?

The study included 42 adults with steroid-naive atopic asthma, 21 adults with atopy but no asthma, and 21 nonatopic healthy control subjects. All participants underwent bronchial brushing to obtain airway samples for bacterial profiling. The asthmatic group had not yet received corticosteroid treatment at the time of initial sampling, allowing comparison before and after six weeks of fluticasone.

What were the most important findings?

The bronchial microbiome differed significantly among the three groups. Asthmatic subjects were uniquely enriched in members of the Haemophilus, Neisseria, Fusobacterium, and Porphyromonas genera compared with the atopy-only and healthy control groups. These compositional differences suggest that microbiome features are more closely tied to the asthma phenotype itself than to atopy or aeroallergen sensitization alone.

What are the greatest implications of this study?

By comparing steroid-naive asthmatics, atopic non-asthmatics, and healthy controls, the study helps disentangle whether bronchial microbiome changes reflect asthma, atopy, or corticosteroid treatment. Enrichment of specific bacterial genera in asthmatic airways points to potential microbial targets or biomarkers relevant to asthma pathophysiology. The examination of microbiome relationships to corticosteroid responsiveness also raises the possibility that airway bacterial composition could inform understanding of treatment response in asthma.

What was studied?

This study examined whether melatonin's known ability to reduce body weight and improve energy balance is linked to changes in the gut microbiota. Mice were fed a high fat diet (HFD) to induce obesity, and melatonin was administered to test its effects on body weight, liver steatosis, low-grade inflammation, and insulin resistance. High-throughput pyrosequencing of the 16S rRNA gene was used to characterize shifts in gut microbiota composition following melatonin treatment. The study compared microbiota profiles across HFD, melatonin-treated HFD, and normal chow diet (NCD) groups.

Who was studied?

The subjects were mice fed either a high fat diet or a normal chow diet, with a subset of high fat diet mice receiving melatonin supplementation. The abstract does not specify the number of animals, their strain, sex, or age. This was an animal model study rather than a human cohort, designed to isolate diet and melatonin effects on the gut microbiota.

What were the most important findings?

Melatonin reduced body weight, liver steatosis, and low-grade inflammation, and improved insulin resistance in HFD-fed mice. High fat diet feeding altered 69 operational taxonomic units (OTUs) compared to the normal chow diet group, and melatonin supplementation reversed 14 of these OTUs back toward the NCD configuration. Melatonin decreased overall richness and diversity of the gut microbiota, lowered the Firmicutes-to-Bacteroidetes ratio, and increased the abundance of the mucin-degrading bacterium Akkermansia, which is associated with healthy mucosa. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, hydrogen sulfide, or sulfur metabolism.

What are the greatest implications of this study?

The findings suggest that melatonin's protective effects against diet-induced obesity and metabolic dysfunction may be mediated in part through remodeling of the gut microbiota. The partial reversal of HFD-induced OTU changes and the boost in Akkermansia point to a plausible microbiota-mediated pathway supporting mucosal health and metabolic improvement. This positions melatonin as a candidate modulator of gut microbiota composition in the context of obesity, warranting further mechanistic and translational research.

What was studied?

This study examined the gut microbiota composition and metabolic functionality associated with functional constipation (FC), a common gastrointestinal disorder whose precise causes remain unclear. The researchers used 16S rRNA-based microbial profiling to characterize bacterial community composition, then applied shotgun metagenomics to assess the functional, metabolic capabilities of the gut microbiome. The goal was to clarify inconsistent prior findings and identify a clearer link between microbiota composition and constipation symptoms.

Who was studied?

The 16S rRNA analysis included 147 stool samples collected from 68 individuals with functional constipation, compared against samples from 79 healthy subjects. A smaller subset, five FC individuals and five healthy subjects, underwent deeper shotgun metagenomic sequencing on a MiSeq platform to evaluate microbial metabolic pathways. No further demographic details are given in the abstract.

What were the most important findings?

Individuals with functional constipation showed depletion of gut bacteria belonging to Bacteroides, Roseburia, and Coprococcus 3 compared to healthy subjects. Functionally, healthy subjects' microbiomes were enriched in pathways for carbohydrate, fatty acid, and lipid metabolism relative to those with constipation. In contrast, the microbiomes of constipated individuals showed high abundance of genes involved in hydrogen production, methanogenesis, and glycerol degradation. The abstract does not report findings related to Desulfovibrio, sulfate-reducing bacteria, or hydrogen sulfide.

What are the greatest implications of this study?

The findings suggest that functional constipation is associated with both compositional and functional shifts in the gut microbiome, not just changes in which taxa are present. The elevated hydrogen production and methanogenesis capacity in FC microbiomes point to altered gas metabolism as a potentially important factor in constipation. These composition and metabolic differences could offer candidate microbial targets or biomarkers for future research into functional constipation.

What was studied?

Cesarean (C-section) delivery, recently shown to cause excess weight gain in mice, perturbs human neonatal gut microbiota development due to the lack of natural mother-to-newborn transfer of microbes. Neonates excrete first the in-utero intestinal content (referred to as meconium) hours after birth, followed by intestinal contents reflective of extra-uterine exposure (referred to as transition stool) 2 to 3 days after birth. It is not clear when the effect of C-section on the neonatal gut microbiota emerges. We examined bacterial DNA in carefully-collected meconium, and the subsequent transitional stool, from 59 neonates [13 born by scheduled C-section and 46 born by vaginal delivery] in a private hospital in Brazil. Bacterial DNA was extracted, and the V4 region of the 16S rRNA gene was sequenced using the Illumina MiSeq (San Diego, CA, USA) platform. We found evidence of bacterial DNA in the majority of meconium samples in our study. The bacterial DNA structure (i.e., beta diversity) of meconium differed significantly from that of the transitional stool microbiota. There was a significant reduction in bacterial alpha diversity (e.g., number of observed bacterial species) and change in bacterial composition (e.g., reduced Proteobacteria) in the transition from meconium to stool. However, changes in predicted microbiota metabolic function from meconium to transitional stool were only observed in vaginally-delivered neonates. Within sample comparisons showed that delivery mode was significantly associated with bacterial structure, composition and predicted microbiota metabolic function in transitional-stool samples, but not in meconium samples. Specifically, compared to vaginally delivered neonates, the transitional stool of C-section delivered neonates had lower proportions of the genera Bacteroides, Parabacteroides and Clostridium. These differences led to C-section neonates having lower predicted abundance of microbial genes related to metabolism of amino and nucleotide sugars, and higher abundance of genes related to fatty-acid metabolism, amino-acid degradation and xenobiotics biodegradation. In summary, microbiota diversity was reduced in the transition from meconium to stool, and the association of delivery mode with microbiota structure, composition and predicted metabolic function was not observed until the passing of the transitional stool after meconium.

What was studied?

Differences in the composition of the gut microbial community have been associated with diseases such as obesity, Crohn's disease, ulcerative colitis and colorectal cancer (CRC). We used 454 titanium pyrosequencing of the V1-V2 region of the 16S rRNA gene to characterize adherent bacterial communities in mucosal biopsy samples from 33 subjects with adenomas and 38 subjects without adenomas (controls). Biopsy samples from subjects with adenomas had greater numbers of bacteria from 87 taxa than controls; only 5 taxa were more abundant in control samples. The magnitude of the differences in the distal gut microbiota between patients with adenomas and controls was more pronounced than that of any other clinical parameters including obesity, diet or family history of CRC. This suggests that sequence analysis of the microbiota could be used to identify patients at risk for developing adenomas.