Inflammatory bowel diseases (IBD), including ulcerative colitis and Crohn's disease, arise from various factors such as dietary, genetic, immunological, and microbiological influences. The gut microbiota plays a crucial role in the development and treatment of IBD, though the exact mechanisms remain uncertain. Current research has yet to definitively establish the beneficial effects of the microbiome on IBD. Bacteria and viruses (both prokaryotic and eukaryotic) are key components of the microbiome uniquely related to IBD. Numerous studies suggest that dysbiosis of the microbiota, including bacteria, viruses, and bacteriophages, contributes to IBD pathogenesis. Conversely, some research indicates that bacteria and bacteriophages may positively impact IBD outcomes. Additionally, plant metabolites play a crucial role in alleviating IBD due to their anti-inflammatory and microbiome-modulating properties. This systematic review discusses the role of the microbiome in IBD pathogenesis and evaluates the potential connection between plant metabolites and the microbiome in the context of IBD pathophysiology.

Chronic infection with Toxoplasma gondii (T. gondii) results in severe damages to the integrity of intestinal barrier, however, both the underlying mechanism and feasible intervention strategies are still little known. Here, we found that both the chronic infection of T. gondii and transplanting gut microbiota from T. gondii-infected mice severely impaired the mice intestinal integrity, which was characterized by significantly decreased thickness of inner mucus layer and down-regulated expression of three tight junction proteins Occludin, ZO-1, and Claudin (p < 0.05). Moreover, T. gondii infection also led to mice intestinal microbiota dysbiosis, especially butyrate-producing bacteria, and significantly changed the expression of several senescence-associated markers, including 6- and 7- fold upregulation for P16, P21, and 6-fold downregulation for Lamin B1 at mRNA levels, and 2-fold downregulation for β-galactosidase at protein levels (p < 0.05). Interestingly, subsequent administration with dietary butyrate could alleviate T. gondii-induced intestinal integrity impairment and cell senescence, revealing a significant increase of the inner mucus layer thickness (p < 0.001), and a remarkable decrease in P16, P21, β-galactosidase expression levels while an upregulation of Lamin B1 expression (p < 0.05). Taken together, our study revealed that T. gondii-induced dysbiosis of gut microbiota, especially butyrate-producing bacteria, contributes to the intestinal impairment, potentially via promoting cell senescence. In addition, administration with the metabolite, butyrate, could be a promising therapeutic measure against T. gondii infection.

The gut microbiota plays a crucial role in human health, but its impact on lipid metabolism remains unclear. Understanding the causal relationship between gut bacteria and lipid profiles is essential for developing strategies to prevent and treat dyslipidemia and cardiovascular diseases. This study aimed to assess this relationship using two-sample Mendelian randomization (MR). Data for both exposure and outcomes were obtained from the IEU-GWAS database, with lipid profile data sourced from a publication. Genome-wide significant single nucleotide polymorphisms (SNPs), which were independent of outcome factors but correlated with exposure variables, were identified as instrumental variables. Several MR methods, including weighted analysis, maximum likelihood, inverse variance weighting (IVW), MR-Egger, and weighted median, were applied. Colocalization analysis further validated the findings. The analysis revealed microbial groups with causal relationships to ApoA1, ApoB, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol, and triglycerides. Reverse MR and colocalization analysis provided additional confirmation of these results. This study offers new evidence of the causal link between gut microbiota and lipid profiles, providing insights for improving lipid profiles and reducing cardiovascular disease risk.

Epigallocatechin-3-gallate (EGCG), a major catechin in green tea, exhibits potent antioxidant and disease-preventive properties, but its application is limited by poor stability and bioavailability. This study aimed to address these challenges by preparing and characterizing three EGCG-loaded nanoparticles: chitosan-EGCG-tripolyphosphate nanoparticles (CE-NPs), β-cyclodextrin-EGCG (BE-NPs), and EGCG-nanostructured lipid carriers (NE-NPs). BE-NPs exhibited the highest loading performance and retention rate under thermal environment (89.78 % after 10 h at 80 °C). NE-NPs had the highest EGCG stability in alkaline condition (45 % after 4 h at pH 7.4). Compared to free EGCG, all NPs significantly improved in vitro bioaccessibility following incubation in simulated gastrointestinal digestion for 4 h; BE-NPs enhanced oral bioavailability by 1.71 times in vivo. Additionally, CE-NPs and NE-NPs increased the relative abundance of Faecalibaculum, Erysipelotrichaceae, and Bifidobacterium in the colons of Sprague-Dawley rats. These findings suggest that BE-NPs are a promising nano-delivery system for enhancing EGCG stability and bioavailability in healthy organisms.

Sleep-disordered breathing (SDB) is characterized by recurrent reductions or interruptions in airflow during sleep, termed hypopneas and apneas, respectively. SDB impairs sleep quality and is linked to substantive health issues including cardiovascular and metabolic disorders, as well as cognitive decline. Recent evidence suggests a link between gut microbiota (GM) composition and sleep apnea. Indeed, GM, a community of microorganisms residing in the gut, has emerged as a potential player in various diseases, and several studies have identified associations between sleep apnea and GM diversity along with shifts in bacterial populations. Additionally, the concept of "leaky gut," a compromised intestinal barrier with potentially increased inflammation, has emerged as another key player in the potential bidirectional relationship between GM and sleep apnea. One of the potential effectors could be extracellular vesicles (EVs) underlying gut-brain communication pathways that are relevant to sleep regulation and function. Thus, therapeutic implications afforded by targeting the GM or exosomes for sleep apnea management have surfaced as promising areas of research. This review explores current understanding of the relationship between GM, exosomes and sleep apnea, highlighting key research dynamics and potential mechanisms. A comprehensive review of the literature was conducted, focusing on studies investigating GM composition, intestinal barrier function and gut-brain communication in relation to sleep apnea.

Gut microbiota dysbiosis induced by antibiotic use weakens its colonization resistance against opportunistic pathogens, increasing the risk of invasion and infection. While probiotics have the potential to restore the impaired gut microbial structure and prevent respiratory tract infections, the effectiveness of specific strains and the underlying mechanisms remain largely unexplored. In this study, the preventive effects of a novel butyrate-producing bacterium, Clostridium cellabutyricum YQ-FP-027T against Pseudomonas aeruginosa infection after antibiotic exposure were investigated in antibiotic-pretreated mice model.

Phenotypic characterizations including the bacterial load in the lung, the assessment of gene expression of immune factors in lung tissue using qPCR, and detection of gut microbial composition using 16S rRNA sequencing were conducted. Pulmonary bacterial load and expression levels of immune factors of lung tissue, and gut microbial composition were evaluated.

Our results demonstrated that YQ-FP-027T ameliorated lung tissue integrity, significantly reduced pulmonary bacterial burden, and decreased the expression of interleukin-1β and TNF-α, while enhancing the expression of interleukin-10 and cathelicidin-related antimicrobial peptide. Furthermore, YQ-FP-027T increased the abundance of Lachnospiraceae in the gut and reduced the abundance of opportunistic pathogens such as Enterococcaceae and Helicobacteraceae.

These results suggest YQ-FP-027T exerts probiotic effects by restoring gut microbiota balance, enhancing intestinal barrier function, and positively influencing pulmonary immune responses through the gut-lung axis. This study reveals the preventive potential of YQ-FP-027T against P. aeruginosa infection in the context of gut microbiota dysbiosis, offering a novel preventive strategy.

Micro- and nanoplastics (MNPLs) are emerging environmental pollutants that have garnered significant attention over the past few decades due to their detrimental effects on human health through various exposure pathways. This study investigates the impact of MNPLs on gut microbiota, utilizing Drosophila melanogaster as a model organism. Drosophila was selected for its microbiota's similarities to humans and its established role as an accessible and well-characterized model system. To analyze microbiota, full-length 16S rRNA gene sequencing was performed using the Nanopore sequencing platform, enabling comprehensive profiling of the microbial populations present in the samples. As models of MNPLs, two commercial polystyrene nanoplastics (PS-NPLs, 61.20 and 415.22 nm) and one lab-made polylactic acid nanoplastic (PLA-NPLs, 463.90 nm) were selected. As a positive control, zinc oxide nanoparticles (ZnO-NPs) were used. The observed findings revealed that exposure to MNPLs induced notable alterations in gut microbiota, including a reduction in bacterial abundance and shifts in species composition. These results suggest that MNPLs exposure can lead to microbial dysbiosis and potential gut health disruptions through its interaction, either with the gut epithelial barrier or directly with the resident microorganisms.

Previous studies have revealed the association between gut microbiota (GM) and temporomandibular joint inflammation, which leads to temporomandibular joint disorders (TMD). However, the causality of the associations remains unknown. This Mendelian randomization (MR) study aims to clarify the causal relationships between GM and TMD. We employed a two-sample MR approach to analyze GM data from the MiBioGen consortium, including 18,340 participants and 211 taxa, and TMD data from the FinnGen consortium R10 release, including 6314 cases and 222,498 controls. Various MR methods, including inverse-variance weighted (IVW), MR-Egger, and weighted median analyses, alongside comprehensive sensitivity analyses, were used to assess causality. After comprehensive sensitivity analyses, the study found causal links between 6 certain GM at the genus level and TMD, including Eubacterium fissicatena group (IVW's odds ratio [OR] = 1.18; 95% confidence interval [CI]: 1.02-1.37; P = .027), Catenibacterium (IVW's OR = 1.33; 95% CI: 1.11-1.59; P = .002), Oxalobacter (IVW's OR = 0.85; 95% CI: 0.75-0.97; P = .013), Ruminococcaceae NK4A214 (IVW's OR = 0.80; 95% CI: 0.66-0.99; P = .036), and Senegalimassilia (IVW's OR = 0.75; 95% CI: 0.59-0.96; P = .024). Following replication verification analysis, Catenibacterium (FDR = .04) at the genus level were positively correlated to the risk of TMD. The reverse MR analysis revealed that TMD had no significant effect on the 6 GMs. The findings of this MR study support a strong and negative causal association between genus Catenibacterium and TMD, highlighting potential targets for the prevention and treatment of TMD.

The use of antibiotics unbalances the intestinal microbiota. Probiotics, prebiotics, and synbiotics are alternatives for these unbalances. The effects of a new synbiotic composed of probiotic Saccharomyces boulardii CNCM I-745 and fructans from Agave salmiana (fAs) as prebiotics were assessed to modulate the intestinal microbiota. Two probiotic presentations, the commercial probiotic (CP) and the microencapsulated probiotic (MP) to improve those effects, were used to prepare the synbiotics and feed Wistar rats subjected to antibiotics (AB). Eight groups were studied, including five controls and three groups to modulate the microbiota after the use of antibiotics: G5: AB + MP-synbiotic, G6: AB + CP-synbiotic, and G8: AB + fAs. All treatments were administered daily for 7 days. On days 7 and 21, euthanasia was performed, cecum tissue was recovered and used to evaluate histological analysis and to study microphotograph by TEM, and finally, bacterial DNA was extracted and 16S rRNA gene metabarcode sequencing was performed. Histological analysis showed less epithelial damage and more abundance of the intestinal microbiota in the groups G5, G6, and G8 in comparison with the AB control group after 7 days. Microphotograph of the cecum at 2 weeks post treatment showed that G5 and G6 presented beneficial effects in epithelial reconstruction. Interestingly, in the groups that used the synbiotic without AB (G3 and G4) in addition to contributing to the recovery of the autochthonous microbiota, it promotes the development of beneficial microorganisms; those results were also achieved in the groups that used the synbiotic with AB enhancing the bacterial diversity and regulating the impact of AB.

Microplastics are recognised as ubiquitous pollutants as they are now found in all terrestrial and marine ecosystems. The interactions between microbiota and microplastics are an issue of fundamental importance in studying and maintaining global health. Microplastics alter the structures and functions of microbial communities, resulting in adverse health effects. A comprehensive understanding of these effects through interdisciplinary research is essential to mitigate pollution and protect the health of ecosystems. The review aims to explore these interactions within a One Health framework. Indeed, a deeper understanding of the processes involved in the interaction between microbiota and microplastics could pave the way for new and promising strategies to mitigate the harmful effects of microplastics on ecosystems and human health.

Selenium-enriched tea represents an ideal source of selenium supplements, yet its effects on mice with intestinal disorders remain under-documented. Therefore, we have carried out relevant research.

We determined the main chemical components of selenium-enriched green tea and evaluated the antioxidant and anti-inflammatory effects of selenium-enriched green tea extract and changes in intestinal flora of antibiotic-induced intestinal disease mice through BALB/c mouse experiments.

The main chemical components of selenium-enriched green tea and green tea are significantly different. Selenium-enriched green tea is characterized by a high selenium content, with tea polyphenols, flavonoids, tea polysaccharides and catechins being the primary constituents. The results of animal experiments indicate that the extract of green tea rich in selenium increased the content of antioxidant factors in the intestines of mice and reduced the levels of intestinal inflammatory factors. This was also confirmed by mRNA gene expression determination. In addition, selenium-enriched green tea extracts can reduce the weight loss and intestinal pathological damage induced by antibiotics, promote the colonization of Bifidobacterium and Lactobacillus in the intestinal tract of mice and inhibit the growth of Escherichia coli and Enterococcus in the intestinal tract.

Selenium-enriched green tea has high nutritional content. It demonstrates superior potential in alleviating oxidative stress and inflammatory responses caused by intestinal diseases, and plays a role in regulating the intestinal flora. © 2025 Society of Chemical Industry.

Diabetic kidney disease (DKD) is a persistent disorder that occurs as a result of long-term diabetes mellitus with genetic and environmental risk factors. The identification of DKD associated single-nucleotide polymorphisms (SNPs) is pivotal for patient screening. This manuscript briefly outlines the pathophysiology and the role of genetic factors in DKD expansion. It further discusses the utility of bioinformatic tools and laboratory techniques requried for the identification of DKD-specific SNPs along with integrated data analysis pipelines valuable to enhance the accuracy of genetic interpretation. A comparative analysis of various SNPs has also been made across diverse Asian populations in conjunction with environmental and lifestyle factors. The clinical relevance of SNPs in predicting DKD progression and stratifying patient risk is highlighted, with focus on gene-specific pathways and associated functional outcomes. The advances in genetic screening, gene-specific therapies, and microbiome-based therapy should help expand the utility of SNPs-based identification of DKD under diverse clinical settings. A structured clinical decision-making framework is proposed to support customized treatment based on SNP profiles. However, this domain has yet to gain widespread recognition with regard to variability in the effects of SNPs across diverse demographies, challenges in clinical translation, and ethical considerations in genetic testing.

Obesity has become a global health crisis driven by genetic, environmental, and lifestyle factors, often linked to gut microbiome imbalances. Probiotics, particularly Lactobacillus and Bifidobacterium strains, have shown promise in clinical trials by promoting weight loss, improving lipid profiles, and addressing gut dysbiosis associated with obesity. This review surveys the literature on the microbiome and obesity, emphasizing the clinical relevance of probiotics in treatment strategies. Our comprehensive PubMed search highlights the mechanisms through which probiotics influence metabolic health, including their effects on inflammation and appetite regulation. We also explore promising future research directions and the potential for integrating probiotics into clinical practice. While results are encouraging, the evidence is limited by strain variability, small sample sizes, short trial durations, and individual differences in microbiota composition. More extensive, long-term studies with standardized methods are crucial to confirm the effectiveness of probiotics as viable anti-obesity treatments.

The gut microbiome refers to the collective genomes of the approximately 1,000-1,150 microbial species found in the human gut, called the gut microbiota. Changing the gut microbiota composition has been shown to affect cardiovascular health significantly. Numerous studies have demonstrated the part that gut microbiota and its metabolites play in the development and course of several illnesses, including colon cancer, heart failure, stroke, hypertension, and inflammatory bowel disease. With cardiovascular diseases responsible for more than 31% of all fatalities globally, conditions like hypertension, atherosclerosis, and heart failure are serious global health issues. Developing preventive measures to fight cardiovascular diseases requires understanding how the gut microbiota interacts with the cardiovascular system. Understanding the distinctive gut microbiota linked to cardiovascular diseases has been made possible by microbial sequencing analysis. The gut microbiota and cardiovascular diseases are closely related, and more profound knowledge of this association may result in treatment strategies and broad guidelines for enhancing cardiovascular health through gut microbiome modification. This review summarizes the role of gut microbiota in cardiovascular diseases, highlighting their influence on disease progression and potential therapeutic implications.

The urobiome, or urinary tract microbiome, has emerged as a crucial component in maintaining urinary health and defending against infections. Recent advances in next-generation sequencing (NGS) have debunked the long-held belief that the urinary tract is sterile, revealing a unique ecosystem of microorganisms. The urobiome interacts with the urothelium and mucosa-associated lymphoid tissue (MALT) to support local immunity, playing an integral role in defending the urinary tract against pathogens. Through complex communication processes like quorum sensing, the urobiome regulates microbial behavior and controls interactions with host tissues, helping to prevent pathogen colonization and infection. However, dysbiosis in the urobiome can disrupt this balance, making the urinary tract more susceptible to infections, including urinary tract infections (UTIs). Studies have highlighted specific microbial compositions associated with both healthy and disease states, suggesting that shifts in the urobiome may correlate with various urological diseases. Furthermore, microbial diversity within the urinary tract differs by factors such as age and gender, reflecting the dynamic nature of the urobiome. Future research focusing on the interplay between the urobiome, host immune defenses, and pathogenic mechanisms may lead to innovative diagnostic and therapeutic approaches. Understanding how microbial composition changes during disease states could enable targeted treatments, potentially reducing reliance on antibiotics and minimizing resistance issues. The urobiome thus represents a promising frontier in urology, with implications for enhancing urinary health and treating infections more effectively.

Gut microbiome has a considerable impact on the central nervous system via the "gut-brain axis". Neuroepigenome emerges as the interface between environment and genes, potentially help conveying the signals derived from the microbiome to the brain tissue. While only a limited number of studies have implicated epigenetic roles in the gut-brain axis, this review explores how gut microbiome might impact various brain-based epigenetic mechanisms, including DNA methylation, histone modification, ncRNA and RNA methylation, notably in the context of the specific neural complications. Among the epigenetic mechanisms, histone acetylation was most well-studied with respect to its relationships with gut microbiome, exerting a dynamic influence on gene expression in the brain. Furthermore, the pathways connecting gut bacteria to neuroepigenome were summarized, highlighting the roles of metabolites such as butyrate, propionate, acetate, lactate, and folate. Of particular interest, the roles of butyrate are emphasized due to their outstanding inhibitory activity towards histone deacetylases (HDACs), among other mechanisms. It is worth noting that some indirect gut-brain pathways may also be associated with the interplay between microbiome and neuroepigenome, while IL-6 has been found to effectively transmit microbe-derived signals to histone methylation in brains. Finally, we recapitulate the future perspectives critical to understanding this gut-brain crosstalk, such as clarifying the cause-and-effect relationship, bacterial cross-feeding within the gut, and the mechanisms underlying the site-specific histone modification in the brain. Together, this review attempts to consolidate our current knowledge about the "microbiome-neuroepigenome interplay" and propose a conceptual pathway to decipher the gut-brain axis in various neurological conditions.

Endometriosis (EM) and adenomyosis (AM) are interrelated gynecological disorders characterized by the aberrant presence of endometrial tissue and are frequently linked with chronic pelvic pain and infertility, yet their pathogenetic mechanisms remain largely unclear. In this cross-sectional study, we analyzed endometrial samples from 244 participants, split into 91 EM patients, 56 AM patients, and 97 healthy controls (HC). We conducted untargeted liquid chromatography-mass spectrometry (LC-MS) and 5R 16S rRNA sequencing to examine endometrial metabolome and microbiome profiles. Additionally, we integrated transcriptomic analysis using nine transcriptomic data sets to investigate the biological basis of these conditions. Metabolomic profiling and 16S rRNA sequencing revealed distinct metabolic and microbial signatures. Specific pathways, including linoleic acid and glycerophospholipid metabolism, show significant alterations in both conditions. Notably, four metabolites, including phosphatidylcholine 40:8 [PC(40:8)], exhibited marked changes in both EM and AM, suggesting shared pathological features. Furthermore, taxonomic analysis identified unique bacterial species associated with each condition, particularly those belonging to the phylum Proteobacteria, which correlated with altered metabolic signatures. Machine learning models demonstrated high predictive accuracy for differentiating between AM, EM, and HC based on metabolic and microbial signatures. Integrative analysis with transcriptomic data highlighted distinct pathways related to immune response and signaling transduction for each condition. Our study provides fresh insights into the pathogenesis of AM and EM through a multi-omic approach, suggesting potential inconsistencies in the underlying pathogenetic mechanisms.

Existing research highlighted a connection between endometriosis (EM) and adenomyosis (AM), underscoring their overlapping symptoms and potential shared pathophysiological mechanisms. Although the role of microbiota in inflammatory conditions has been acknowledged, comprehensive investigations into the endometrial microbiota in cases of EM and AM have been limited. Previous studies identified distinct microbial communities associated with these conditions; however, they were constrained by small sample sizes and a lack of integrated analyses of microbiota and metabolomics. Furthermore, the ongoing debate over whether EM and AM should be classified as separate diseases or related phenotypes emphasizes the necessity for further exploration of their molecular interactions. Our study uncovers distinct microbial and metabolic signatures associated with each condition, revealing both shared and unique pathways that may contribute to their pathogenesis. Furthermore, the integration of transcriptomic data offers valuable insights into the complex interactions underlying these disorders.

Age, metabolic inflammation, sleep patterns, lifestyle choices, and gut microbiome composition were investigated as factors influencing functional strength. The Northern German FoCus cohort subgroup (394 women, 233 men) was categorized into six groups based on weekly sports activity and handgrip strength (HGS) measurements. The analyses included anthropometric data, clinical biochemistry, medication, sleep duration, healthy lifestyle score (HLS), 16 S rRNA gut microbiota, serum and urine metabolomics, bile acids, and an adapted dietary inflammatory index (ADII) score. Associations were found between age, inflammation, and low functional strength, with sleep duration increasing the odds and a healthy lifestyle decreasing the risk. Urine metabolomics revealed differences in enrichment analyses. No significant differences were observed in the Chao1 and InVSimpson indices between the groups. At the genus level, some species were associated with daily sports activity, whereas others were associated with HGS measurements. Clostridium XIVa was found only in high- and medium-HGS groups, while Alistipes, Odoribacter, and Streptococcus decreased with activity. Thus, tailored lifestyle interventions may reduce the risk of poor functional strength.

This study aimed to investigate whether enema is associated with nervous system injury caused by diquat poisoning using a population-based case-control analysis. Medical records of patients with acute diquat poisoning admitted to the hospital from January 2018 to January 2024 were retrospectively collected. Central nervous system injury symptoms following diquat poisoning defined the case group, while the control group were matched 1:2 on population-based without nervous system injury in diquat poisoning patients. Conditional logistic regression models were used for analysis. We identified 101 diquat poisoning patients with nervous system injury and selected 202 diquat poisoning patients without nervous system injury. Diquat poisoning patients performed 2 and ≧ 3 enemas had ORs of nervous system injury of 3.084 (95% CI 1.230, 7.734) and 4.693 (95% CI 1.408, 15.645) compared with diquat poisoning patients with no enema, respectively. Further analyses were performed in various age subgroups. The ORs of conducting 2 and ≧ 3 enemas were dramatically higher among case group than control group in subgroup aged ≧ 60 years old (OR  10.184, 14.982 respectively). We concluded that enema may be associated with an increased risk of nervous system injury caused by DQ poisoning, particularly among the elderly.

The existing body of evidence has highlighted gut microbiota as a versatile regulator of body wellness affecting not only multiple physiological metabolisms but also the function of remote organs. Emerging studies revealed a reciprocal relationship between physical exercise and intestinal microbiota, suggesting that physical exercise could enhance gut health, including regulating intestinal barrier integrity, increasing microbial diversity, and promoting beneficial microbial metabolism. Furthermore, the beneficial outcomes of exercise on the intestine may also promote brain health through the gut-brain axis. Diet is an important factor in boosting exercise performance and also greatly impacts the structure of gut microbiota. Abundant research has reported that diet alongside exercise could exert beneficial effects on metabolism, immune regulation, and the neuropsychiatric system. In this paper, we used a narrative review, primarily searching PubMed, Web of Science, and Elsevier, to review the existing research on how moderate-intensity exercise promotes gut health, and we introduced the effects of exercise on the nervous system through the gut-brain axis. We also proposed dietary strategies targeting the regulation of gut microbiota to provide guidelines for boosting brain health. This review highlights that moderate exercise and a healthy diet promote gut and brain health.

Malignant ascites is a common complication of advanced ovarian cancer (OC) and gastrointestinal cancer (GI), significantly impacting metastasis, quality of life, and survival. Increased intestinal permeability can lead to blood or lymphatic infiltration and microbial translocation from the gastrointestinal or uterine tract. This study aimed to identify microbiota-derived metabolites in ascites from OC (stages II-III and IV) and GI patients, assessing their roles in tumor progression.

Malignant ascites samples from 18 OC and GI patients were analyzed using a four-dimensional (4D) untargeted metabolomics approach combining reversed-phase (RP) and hydrophilic interaction liquid chromatography (HILIC) with trapped ion mobility spectrometry time-of-flight mass spectrometry (timsTOF-MS). Additonally, a targeted flow cytometry-based cytokine panel was used to screen for inflammatory markers. Non-endogenous, microbiota-derived metabolites were identified through the Human Microbial Metabolome Database (MiMeDB).

OC stage IV exhibited metabolic profiles similar to GI cancers, while OC stage II-III differed significantly. Stage IV OC patients exhibited higher levels of 11 typically microbiome-derived metabolites, including 1-methylhistidine, 3-hydroxyanthranilic acid, 4-pyridoxic acid, biliverdin, butyryl-L-carnitine, hydroxypropionic acid, indole, lysophosphatidylinositol 18:1 (LPI 18:1), mevalonic acid, N-acetyl-L-phenylalanine, and nudifloramide, and lower levels of 5 metabolites, including benzyl alcohol, naringenin, o-cresol, octadecanedioic acid, and phenol, compared to stage II-III. Correlation analysis revealed positive associations between IL-10 and metabolites such as glucosamine and LPCs, while MCP-1 positively correlated with benzyl alcohol and phenol.

4D metabolomics revealed distinct metabolic signatures in OC and GI ascites, highlighting microbiota-derived metabolites involved in lipid metabolism and inflammation. Metabolites like 3-hydroxyanthranilic acid, indole, and naringenin may serve as markers of disease progression and underscore the microbiota's role in shaping malignant ascites and tumor biology.

The gut microbiota represents a rich and adaptive microbial network inhabiting the gastrointestinal tract, performing key functions in nutrient processing, immune response modulation, intestinal wall protection, and microbial defense. Its composition remains highly personalized and responsive to external influences, including lifestyle patterns, physical activity, body composition, and nutritional intake. The interactions of the gut microbiota with bodily systems are conventionally interpreted as broad systemic impacts on organ balance. Yet, emerging research-exemplified by the gut microbiota-brain axis-suggests the potential existence of more targeted and direct communication mechanisms. Dysbiosis, characterized by microbial ecosystem disturbance, generates multiple metabolic compounds capable of entering systemic circulation and reaching distant tissues, notably including ocular structures. This microbial imbalance has been associated with both systemic and localized conditions linked to eye disorders. Accumulating scientific evidence now supports the concept of a gut-retina axis, underscoring the significant role of microbiota disruption in generating various retinal pathologies. This review comprehensively investigates gut microbiota composition, functional dynamics, and dysbiosis-induced alterations, with specific focus on retinal interactions in age-related macular degeneration, diabetic retinopathy, glaucoma, and retinal artery occlusion. Moreover, the review explores microbiota-targeted therapeutic strategies, including precision nutritional interventions and microbial transplantation, as potential modulators of retinal disease progression.

Ulcerative colitis (UC) is an idiopathic inflammatory bowel disease. Glycyrrhiza pallidiflora polysaccharide (GPP) is an important constituent of a species of Glycyrrhiza pallidiflora, but its therapeutic mechanism in UC mice is not clear. A dextran sulphate sodium salt (DSS)-induced mouse model of UC was established, and GPP was extracted by ultrasound-assisted extraction, optimised to a GPP content of 25.66% by one-factor optimisation. The effects of different doses (100, 200, 300 mg/kg) of GPP on UC were investigated. The results showed that GPP could delay the trend of weight loss, reduce the DAI score and decrease colon damage in mice, and GPP had a better ameliorative effect on enteritis, which provided a theoretical basis for studying the effect of natural products on UC.

A burgeoning corpus of evidence indicates that S24-7 is integral to human health, with links to obesity, inflammation, metabolism, and dietary interactions. In the present study, we conducted a comprehensive review of the S24-7 literature from the past 10 years, augmented by an evaluation of research trends using both quantitative and qualitative approaches. From the Web of Science (WoS) database, we retrieved 903 research articles and four review articles pertaining to S24-7, also known as Muribaculaceae, that were published between January 1, 2014, and January 1, 2024. Employing software tools such as R, Biblioshiny, VOSviewer, the Bibliometric Analysis Platform, and Pajek, we performed visual mapping and correlation analyses on the collected documents. Our analysis revealed China and the United States as the leading publishers in the field of S24-7 research. The top three academic journals for S24-7 family research are Food and Function, Frontiers in Microbiology, and Nutrition. Among individual contributors, Zhang Y stands out with 31 publications and an h-index of 13, representing 3.42% of the 907 articles analyzed. Jiangnan University leads in institutional output with 46 publications. Keyword analysis underscores that S24-7 research is concentrated on examining the family's associations with obesity, inflammation, metabolism, and diet. This study highlights notable contributions from various countries, institutions, journals, and researchers, shedding light on the influence of the S24-7 family on human health. It serves to inform future research directions and clinical applications concerning the S24-7 flora.

Frailty is an ageing-associated geriatric syndrome that severely affects the functional status, quality of life and life expectancy of older adults. Immune dysfunction and chronic inflammation play crucial roles in frailty, and this study aimed to explore the correlation between the intestinal microbiota and frailty.

A cross-sectional survey was conducted using a comprehensive geriatric assessment of older individuals who underwent medical checkups at the Health Management Center from April 2023 to May 2024. A total of 672 older individuals who met the inclusion criteria were included and divided into a healthy control group and a frail case group. Clinical data, as well as blood and stool samples, were collected. The data from the two groups were analysed with 16S rRNA sequencing in 20 and 30 cases, respectively. SPSS 25.0 was used for statistical analysis.

There were significant differences in income, smoking, and globulin levels between the two groups, while there were no differences in age or sex. There was no significant difference in the abundance or species evenness of intestinal bacteria between the two groups. However, the abundance of accessory bacteria, bifidobacteria, and Escherichia coli in the frail group was greater than that in the control group. Specifically, Escherichia-Shigella was significantly upregulated and fit well into the prediction model of frailty.

The gut microbiota of frail older individuals underwent significant changes in structural composition, and the presence of Escherichia-Shigella may be a diagnostic marker for debilitating diseases. These findings provide an essential clinical reference value for developing methods for preventing or alleviating frailty based on specific microbial communities.

Animal models are an essential part of translational research for the purpose of improving human health. The pig is a potential human research model that can be used to assess the effects of dietary interventions, pathologies, and drugs on gut health and the microbiome, due to its anatomical and physiological similarity to humans. It is recognised that a healthy gut is closely linked to the prevention of several chronic diseases, including obesity, diabetes, gastrointestinal inflammation, as well as neurological and cardiovascular diseases. The use of prebiotics and probiotics plays an important role in maintaining a healthy digestive system, which is responsible for modulating all other body functions. The present review focuses on the applications of prebiotics and probiotics in the pig as an animal model in healthy and diseased conditions, in order to highlight the efficacy of these molecules in the perspective of human health outcomes. The data support the use of prebiotics to improve intestinal health in both healthy and diseased states. In addition, the use of human microbiota-associated (HMA) gnotobiotic pigs provided a good model to study the intestinal and systemic immune response and microbiota composition following probiotic supplementation after a vaccine or virus challenge.

Pu-erh tea, a dark tea from China, is classified into raw and ripened types. Both have significant anti-obesity effects. Polyphenols are among their major bioactive components. This study aimed to explore the anti-obesity properties and mechanisms of raw (R-TP) and ripened (F-TP) Pu-erh tea polyphenols.

The results showed that R-TP and F-TP significantly reduced body weight, improved insulin resistance, and enhanced glucose and lipid metabolism in high-fat-diet (HFD)-induced obese mice. Mild differences were observed in their impact on fat metabolism, carbohydrate metabolism, and inflammation levels. Both R-TP and F-TP were able to restore the disrupted intestinal flora caused by HFD treatment, returning them to a composition and levels similar to those of normal mice. Interestingly, the gut microbiota of all the mice could be reclassified into three enterotypes (enterotype Type-1, Type-2, and Type-HFD). Lactobacillaceae predominated in Type-1. Lactobacillaceae, Muribaculaceae, and Lachnospiraceae were the most common in Type-2. Type-HFD was primarily composed of Atopobiaceae, Lachnospiraceae, Lactobacillaceae, Ruminococcaceae, and Erysipelotrichaceae. The small differences in the effects of R-TP and F-TP may be due to variations in enterotypes.

These findings indicate that R-TP and F-TP can alleviate obesity by regulating the enterotype of gut microbiota, suggesting that they possess the potential for application in the treatment of obesity and the development of anti-obesity agents. © 2025 Society of Chemical Industry.

Given the complex relationship between the gut microbiome and chronic kidney disease (CKD), exploring the potential role and scope of microbiota-targeted therapies in pediatric CKD is highly relevant. We aim to provide an overview of gut-targeted therapeutic strategies, including nutritional interventions (fiber, phytochemicals, fermented foods, and traditional Chinese medicines), probiotics, synbiotics, oral absorbents, and fecal microbial transplantation. Enhancing physical activity and preventing constipation are additional strategies that may promote gut microbiome health. In a uremic environment, gut microbiota-targeted therapies could potentially rebalance the gut microbiota, improve gut barrier function, decrease uremic toxin concentrations, enhance the production of short-chain fatty acids (SCFA), and reduce inflammation. While research in adult CKD patients has provided insights into these approaches, there are limited data in children with CKD. This review aims to summarize potential targeted therapies for restoring a balanced gut microbiota, emphasizing the need for studies that evaluate their effects on clinical outcomes in pediatric CKD.

Decades of research have made clear that host-associated microbiomes touch all facets of health. However, effective therapies that target the microbiome have been elusive given its inherent complexity. Here, we experimentally examined diet-microbe-host interactions through a complex systems framework, centered on dietary oxalate. Using multiple, independent molecular, rodent, and in vitro experimental models, we found that microbiome composition influenced multiple oxalate-microbe-host interfaces. Importantly, the administration of the oxalate-degrading specialist, Oxalobacter formigenes, was only effective against a poor oxalate-degrading microbiota background and gives critical new insights into why clinical intervention trials with this species exhibit variable outcomes. Data suggest that, while heterogeneity in the microbiome impacts multiple diet-host-microbe interfaces, metabolic redundancy among diverse microorganisms in specific diet-microbe axes is a critical variable that may impact the efficacy of bacteriotherapies, which can help guide patient and probiotic selection criteria in probiotic clinical trials.

Obesity is recognized as a global epidemic that can result in changes in the human body and metabolism. Accumulating evidence indicates that gut microbiota (GM) can affect the development of obesity. The GM not only plays a crucial role in digesting and absorbing nutrients, but also in maintaining the overall health of the host. Dietary supplements such as non-starch polysaccharides are mainly fermented by the GM in the colon. Recent findings suggest that shaping the GM through the prebiotic function of non-starch polysaccharides may be a viable strategy against obesity. In this paper, the effects of non-starch polysaccharides on host health, together with their prebiotic function influencing the GM to control obesity via the gut-target organ axis, are reviewed. Potential perspectives of non-starch polysaccharides exhibiting anti-obesity effects via the gut-target organ axis are proposed for future research.

Schistosomiasis japonica is a parasitic disease that seriously endangers human health. Patients with advanced Schistosoma japonicum infection often suffer from cirrhosis and portal hypertension. Splenectomy has been widely used in the treatment of these patients. Previous studies have confirmed that S. japonicum infection is closely related to the gut microbiota, but the impact of splenectomy on the gut microbiota of patients with advanced S. japonicum infection remains unclear. This study used 16sRNA sequencing technology to compare the differences in intestinal flora between patients with advanced S. japonicum infection who underwent splenectomy and non-surgical patients. We focused on the changes in the species composition, diversity and functions of the intestinal flora. Our study shows that dysbiosis of the gut microbiome occurred in patients with advanced S. japonicum infection, including changes in abundance and diversity and the disorder of biological function. The intestinal flora structure, diversity and function of patients who underwent splenectomy were significantly changed compared with those who did not undergo surgery.

Diet modulates gut microbiome composition and function. However, determining causal links between diet-gut microbiome interactions and human health is complicated by inconsistencies in the evidence, arising partially from variability in research methods and reporting. Widespread adoption of standardized best practices would advance the field but require those practices to be identified, consolidated, and discussed. This umbrella review aimed to identify recommended best practices, define existing gaps, and collate considerations for conducting research on diet-gut microbiome interactions and their impact on human health outcomes. Reviews meeting inclusion criteria and published after 2013 were identified using a systematic search. Recommendations, considerations, and gaps relating to the best practices associated with study design, participant selection, dietary intervention/assessment, biological sample collection, and data analysis and reporting were extracted and consolidated. Eight narrative reviews were included. Several general points of agreement were identified, and a recurring theme was that best practices are dependent upon the research aims, outcomes, and feasibility. Multiple gaps were also identified. Some, such as suboptimal diet assessment methods and lack of validated dietary intake biomarkers, are particularly relevant to nutrition science. Others, including defining a "healthy" gut microbiome and the absence of standardized sample and data collection/analysis protocols, were relevant specifically to gut microbiome research. Gaps specific to diet-gut microbiome research include the underrepresentation of microbiome-modulating dietary components in food databases, lack of knowledge regarding interventions eliciting changes in the gut microbiome to confer health benefits, lack of in situ measurement methods, and the need to further develop and refine statistical approaches for integrating diet and gut microbiome data. Future research and cross-disciplinary exchange will address these gaps and evolve the best practices. In the interim, the best practices and considerations discussed herein, and the publications from which that information was extracted provide a roadmap for conducting diet-gut microbiome research. This trial was registered at PROSPERO as CRD42023437645.

Rheumatoid arthritis is a chronic autoimmune disorder characterized by destructive, symmetric joint inflammation and synovitis, resulting in substantial disability that profoundly compromises patients' quality of life. Its pathogenesis encompasses complex interactions between genetic and environmental factors. Recent advances in bacterial DNA sequencing technologies have uncovered a significant correlation between the human gut microbiota composition and rheumatoid arthritis progression. Growing clinical and experimental evidence establishes the gut-joint axis as a crucial mediator in rheumatoid arthritis pathogenesis. Comprehensive investigation of gut microbial communities and their metabolites' influence on rheumatoid arthritis mechanisms, coupled with the elucidation of microbiome's bidirectional regulatory effects in disease development, not only deepens our understanding of pathological processes but also establishes a theoretical framework for developing novel diagnostic biomarkers and personalized therapeutic interventions to enhance patient outcomes.

Cardiovascular diseases (CVDs), including heart failure (HF), hypertension, myocardial infarction (MI), and atherosclerosis, are increasingly linked to gut microbiota dysbiosis and its metabolic byproducts. HF, affecting over 64 million individuals globally, is associated with systemic inflammation and gut barrier dysfunction, exacerbating disease progression. Similarly, hypertension and MI correlate with reduced microbial diversity and an abundance of pro-inflammatory bacteria, contributing to vascular inflammation and increased cardiovascular risk. Atherosclerosis is also influenced by gut dysbiosis, with key microbial metabolites such as trimethylamine-N-oxide (TMAO) and short-chain fatty acids (SCFAs) playing crucial roles in disease pathogenesis. Emerging evidence highlights the therapeutic potential of natural compounds, including flavonoids, omega-3 fatty acids, resveratrol, curcumin, and marine-derived bioactives, which modulate the gut microbiota and confer cardioprotective effects. These insights underscore the gut microbiota as a critical regulator of cardiovascular health, suggesting that targeting dysbiosis may offer novel preventive and therapeutic strategies. Further research is needed to elucidate underlying mechanisms and optimize microbiome-based interventions for improved cardiovascular outcomes.

From a biological point of view, Diversity, Equity, and Inclusion (DEI) are important at multiple levels, which include our genetics, microbiomes, diets, and all organ system interactions. Considering only DEI's sociological aspects is equivalent to the error of "throwing out the baby with the bath water." Variances in microbial diversity within our microbiomes might affect our health through systemic interactions affecting metabolites, maintaining immune homeostasis, and wound healing of cellular damage from an infection, physical stress, or psychological trauma. An imbalance of our immune cell subsets, both innate and adaptive, and the microbes in any of our microbiomes might lead to more cellular damage from excessive inflammation and oxidative stress and less immune regulation. The immune dysregulation may occur due to the loss of endometrial barriers enabling the spread of microbes, environmental pollutants, and allergens. Heat waves, sleep deprivation, and increased prevalence of pollutants such as polychlorinated biphenyls, which weaken endothelial barriers, may be responsible for the enhanced prevalence of physical and psychological stresses. Leakage of our useful gut microbiota into the periphery might initiate inflammatory responses, and an altered gut microbiome might affect the gut-brain axis that influences physical and mental health.

Eurotium cristatum (EC), the dominant fungus in Fuzhuan brick tea, has significant applications in food fermentation and pharmaceutical industries, exhibiting probiotic properties, but further investigation of its intestinal benefits is required. This study characterized the EC-520 strain through whole genome sequencing and evaluated its effects on rat colons using histomorphology, 16S rRNA sequencing, and untargeted metabolomics. The genomic analysis revealed that EC-520 possessed a 28.37 Mb genome distantly related to Aspergillus flavus. The 16S results demonstrated that EC-520 significantly increased the abundance of Bacteroidota (p < 0.05) while decreasing the Proteobacteria and Firmicutes/Bacteroidota ratio (the F/B ratio); at the genus level, it elevated Muribaculaceae and Clostridia_UCG-014 while reducing harmful bacteria. The metabolomic results showed that EC-520 also significantly altered tryptamine, caproic acid, isocaproic acid, and erucic acid (p < 0.05). Additionally, the Spearman's correlation analysis revealed that Muribaculaceae_unclassified and Clostridia_UCG-014_unclassified were significantly positively correlated with tryptamine, caproic acid, isocaproic acid, and erucic acid. Therefore, this study suggested that EC-520 enhanced the colon barrier and increased the abundance of Muribaculaceae_unclassified and Clostridia_UCG-014_unclassified, thus promoting the secretion of tryptamine and affecting the release of 5-hydroxytryptamine (5-HT). It also promoted the secretion of certain fatty acids, enhancing the balance of the colonic microbiota. This study provides a new view for a comprehensive understanding of EC's regulatory role in the colon.

Stress in dog breeding leads to significant physiological and psychological burdens, including anxiety, reduced appetite, weakened immune function, gut microbiota imbalance, and even death. Currently, there are various pharmacological interventions for stress management, but few focus on gut health. This study evaluates the potential of a novel strain, Enterococcus faecium Kimate-X, in alleviating transport stress and improving gut health in dogs, providing an alternative to traditional pharmacological treatments. In vitro experiments showed that Kimate-X significantly enhanced the activities of superoxide dismutase (SOD) and catalase (CAT) while reducing the levels of malondialdehyde (MDA) and tumor necrosis factor-α (TNF-α) in RAW 264.7 macrophage cells. In vivo, dogs supplemented with Kimate-X exhibited significantly lower cortisol levels after transport, indicating reduced stress. Metagenomic analysis revealed increased gut microbiota diversity and higher concentrations of short-chain fatty acids (acetate, propionate, and butyrate) in fecal samples. This study systematically uncovers the mechanism by which Enterococcus faecium Kimate-X alleviates transport stress through modulation of the gut microbiota. These findings provide new scientific evidence supporting the use of probiotics as a novel approach to stress management in animals.

Alzheimer's disease (AD) has emerged as a global public health priority characterized by escalating prevalence and the limited efficacy of current therapeutic approaches. Although the pathological complexity of AD is well-recognized, its underlying etiology remains incompletely elucidated. Current research highlights a bidirectional gut-brain axis (GBA) interaction, wherein gut microbiome perturbations may impair intestinal barrier stability, influence immune responses, and blood-brain barrier permeability through microbial metabolite-mediated pathways, thereby contributing to AD pathophysiology. Notably, probiotics demonstrate therapeutic potential by restoring gut microbiome homeostasis, reinforcing intestinal barrier integrity, and mitigating neuroinflammatory responses via GBA. This review focuses on investigating the gut microbiome alterations in AD pathogenesis, the interaction of probiotics with GBA, and its significance in AD pathogenesis. By synthesizing current clinical evidence, this review aims to establish a scientific foundation for probiotic-based interventions as a novel therapeutic strategy in AD management.

While growing evidence highlights the role of gut microbiota and inflammatory proteins in cancer, with cancer-related inflammation now considered the seventh hallmark of cancer, the direct causal relationships between specific microbiota, cancer, and the potential mediating effects of inflammatory proteins have not been fully established.

We employed Mendelian randomization (MR) to assess the causal relationships between gut microbiota, inflammatory proteins, and eighteen distinct cancers using data from extensive genome-wide association studies (GWAS). The primary statistical method utilized was inverse variance weighting (IVW). We also investigated whether inflammatory proteins could mediate the effects of gut microbiota on cancer development.

Our findings revealed 42 positive and 49 inverse causal impacts of gut microbiota on cancer risk (P < 0.05). Additionally, we identified 32 positive and 28 inverse causal relationships between inflammatory proteins and cancer risk. Moreover, genus Collinsella decreased the risk of lung cancer by decreasing levels of T-cell surface glycoprotein CD5 (mediating effect = 16.667%), while genus Ruminococcaceae UCG005 increased the risk of mesothelioma by increasing levels of CCL4 (mediating effect = 5.134%).

Our study provides evidence for a causal association between gut microbiota, inflammatory proteins, and eighteen different cancer types. Notably, the T-cell surface glycoprotein CD5 and CCL4 were identified as mediators linking the genus Collinsella with lung cancer and the genus Ruminococcaceae UCG005 with mesothelioma, respectively.