Search Results (184)

Emerging evidence implicates the gut–brain axis in the pathophysiology of schizophrenia, yet literature regarding specific microbiome alterations remains inconsistent. This study aims to synthesize evidence on gut microbiota diversity and taxonomic composition in individuals with schizophrenia compared to healthy controls. Unlike prior meta-analyses, this study integrates quantitative alpha diversity synthesis with cross-taxonomic qualitative analysis and contextualizes findings within functional frameworks of the gut–brain axis, highlighting the methodological heterogeneity that limits biological interpretation. A systematic review and meta-analysis were conducted following PRISMA 2020 guidelines. Electronic databases (Web of Science, PubMed, MDPI) were searched for observational studies published between 2017 and 2025. Forty-eight studies met inclusion criteria for qualitative synthesis, with 14 providing sufficient data for random-effects meta-analyses of alpha diversity. Meta-analyses revealed no statistically significant differences in alpha diversity indices (Shannon, Simpson, Chao1, ACE, Observed) between patients and controls, despite high heterogeneity. Conversely, beta diversity analyses generally demonstrated significant differences in microbial community composition. Taxonomic synthesis identified recurrent but heterogeneous dysbiotic patterns characterized by the depletion of short-chain fatty acid-producing taxa (e.g., Faecalibacterium, Roseburia, Lachnospiraceae) and enrichment of pro-inflammatory taxa (e.g., Proteobacteria, Fusobacterium). Schizophrenia is associated with evidence of compositional alterations and functional shifts rather than a global loss of microbial richness. These findings highlight candidate taxa that may warrant further investigation in biomarker-focused studies and microbiome-based therapeutics. However, these findings should be interpreted cautiously due to substantial heterogeneity and limited control for key confounders such as antipsychotic medication, diet, and life-style factors. Full article

Recent studies have reported skin microbiome dysbiosis in patients with photodermatoses, featuring enriched Staphylococcus aureus colonization and decreased microbiome diversity. We propose that ultraviolet radiation (UVR), along with atypical antimicrobial peptides, may exert selective pressure on the skin microbiome, while cytokine dysregulation and a reduction in commensal bacteria amplify microbial dysbiosis. Dysbiotic microorganisms further release pathogen-associated patterns and virulence factors, and activate tissue-resident memory T cells, which collectively contribute to local inflammation. These mechanisms establish the skin microbiome as a potential target for early intervention. Potential therapeutic strategies may include antibiotics, phototherapy, bleach baths, phage therapy, and microbiota-based therapies. This review integrates current findings from microbial ecology, molecular biology, and host immunology to outline a conceptual framework linking UVR exposure, microbiome alterations, and cutaneous immune responses, while emphasizing the current limitations and evidence gaps in this field. Full article

Background: Obesity and its related metabolic complications, including non-alcoholic fatty liver disease (NAFLD) and insulin resistance, constitute an escalating global public health challenge, with high-fat diet (HFD) exposure recognized as a primary etiological driver. This study aimed to systematically evaluate the therapeutic effects of pepper leaf extracts (PLE), spinach extracts (SE), and obeticholic acid (OCA) on HFD-induced metabolic dysfunction in mice. Methods: Integrated phenotypic, histopathological, gut microbial, bile acid, and metabolomic analyses were applied to evaluate the intervention effects. Results: Our results demonstrated that 16-week dietary intervention with PLE, SE, or OCA all effectively mitigated HFD-induced obesity, pathological adipose remodeling, hepatic steatosis, systemic insulin resistance, and intestinal barrier dysfunction. Mechanistically, PLE effectively restored intestinal barrier integrity and reshaped the dysbiotic gut microbiota, with a marked enrichment of beneficial bacterial taxa closely linked to intestinal barrier maintenance, and normalized the disrupted cecal bile acid profile in HFD-fed mice. Furthermore, untargeted metabolomic analysis revealed that PLE reprogrammed disordered systemic metabolism, with significant modulation of key pathways involved in bile acid homeostasis, amino acid metabolism, and energy metabolism. Conclusions: In summary, this study provides evidence that PLE effectively attenuates HFD-induced metabolic disorders through modulation of the gut microbiota–bile acid–metabolome axis and restoration of intestinal barrier integrity. The superior therapeutic efficacy of PLE compared with SE and OCA, coupled with its favorable safety profile, positions PLE as a promising novel natural candidate for the prevention and treatment of obesity and its associated metabolic complications. Full article

Limosilactobacillus fermentum MC1 is an exopolysaccharide (EPS)-producing strain with previously determined probiotic potential in vitro. This study aimed to investigate the in vivo capacity of the MC1 strain or its EPSs to modulate intestinal microbiota and assess its anti-inflammatory effects in both healthy and dysbiotic conditions. Therefore, Lb. fermentum MC1 and its EPSs were administered to a mouse model of dextran sulfate sodium (DSS)-induced colitis (DIC) and to a healthy group, and the effects were observed. Microbiome analysis was used to detect taxonomic differences between treatments. According to the results, administration of the MC1 strain and MC1-EPSs significantly altered gut microbiome composition at different taxonomic levels. The most notable effect was an increased relative abundance of Firmicutes and decreased levels of Candidatus saccharibacteria. Llb. fermentum MC1, and its EPS administration positively affected several disease parameters: reduced disease activity index (DAI), reduced mouse colitis histology index (MCHI), reduced expression of inflammation-related genes and levels of bleeding, and induced polarization of M1 macrophages to the M2-like macrophage phenotype in the DIC mice. These results, along with those related to the induction of antioxidant enzymes and changes in NF-κB-related gene expression, suggest that strain MC1 and MC1-EPSs could be further investigated for their capacity to alleviate DSS-induced histopathological changes and modulate pro-inflammatory cytokine gene expression in colon tissue, which positively correlates with the secretion of inflammatory cytokines, the delay of intestinal inflammation and the maintenance of intestinal barrier function. The obtained data provide a basis for further research into the potential application of intact or microencapsulated Llb. fermentum MC1 cells and its EPSs in colitis therapy. Full article

Background: Gut microbiota alterations are increasingly recognized as key contributors to the development and clinical course of inflammatory bowel disease (IBD), particularly in pediatric patients, in whom microbial maturation and immune regulation are still evolving. Objective: This study aimed to assess intestinal microbiota composition and dysbiosis severity in pediatric IBD, with comparative analyses according to disease phenotype (Crohn’s disease versus ulcerative colitis) and therapeutic strategy (biologic versus non-biologic treatment). Methods: A prospective cohort of 60 pediatric patients diagnosed with IBD based on Porto criteria was evaluated. Fecal samples were obtained at baseline and after three months of combined standard IBD treatment and adjunct microbiota-targeted therapy, and were analyzed using an AI-assisted microbiota profiling platform. A semi-quantitative dysbiosis score was calculated based on the relative abundance of proinflammatory taxa and depletion of short-chain fatty acid (SCFA)-producing bacteria. Microbial parameters were correlated with clinical and therapeutic variables, including the Organism of Interest metric and the Gut Microbiota Index (GMI). Results: Dysbiosis severity was significantly higher in patients with Crohn’s disease compared with ulcerative colitis (9.65 ± 1.44 vs. 8.42 ± 1.88, p = 0.037). Patients receiving biologic therapy showed a trend toward lower dysbiosis scores and improved microbial indices, although statistical significance was not reached. Severe dysbiosis was identified in 46.7% of the cohort. Strong positive correlations were observed between the dysbiosis score, Organism of Interest metric and GMI (r = 0.68–0.72, p < 0.01). Conclusions: Pediatric IBD is associated with a reproducible dysbiotic profile, more pronounced in Crohn’s disease and partially modulated by biologic therapy. The observed correlations between microbiota-derived indices support their potential utility as complementary markers of intestinal microbial imbalance and disease activity. Full article

The escalating consumption of red meat is a potent environmental risk factor for inflammatory bowel disease (IBD), which is characterized by compromised expression of the xenobiotic transporter P-glycoprotein (MDR1/ABCB1). While gut microbiota metabolize dietary tryptophan into diverse indole derivatives that function as aryl hydrocarbon receptor (AhR) ligands, their differential regulation of MDR1 remains an unresolved AhR paradox. Here, we investigated the mechanisms by which two distinct metabolites, indole-3-acetic acid (IAA) and skatole, regulate MDR1 expression in human colonic epithelial Caco-2 cells. We observed that IAA selectively enhances MDR1 protein stability via an AhR-dependent pathway without inducing de novo transcription, suggesting a mechanism we term enhanced proteostasis mediated by the AhR-Hsp90 complex. Conversely, skatole, a toxic dysbiotic metabolite linked to red meat intake, triggered a time-dependent depletion of MDR1 and potently abrogated the protective efficacy of IAA. Our findings are consistent with a model in which skatole acts as a putative structural disruptor, potentially destabilizing the chaperone complex essential for MDR1 integrity. This destruction is facilitated by a key bacterial enzyme, indoleacetate decarboxylase (IAD), which is a pH-dependent metabolic switch in the gut. The modern Western diet, characterized by high protein and low fiber content, elevates colonic pH, thereby activating IAD to convert protective IAA into toxic skatole. These findings provide a molecular framework for the red meat–microbiome–barrier failure axis and highlight the restoration of the IAA/skatole balance through dietary intervention as a promising therapeutic strategy. Full article

Social wasps, including hornets, are increasingly recognized not only as invasive pests but also as farmed insects; however, their gut microbiota and associated diseases remain poorly characterized. In indoor rearing facilities for the hornet Vespa analis in Dehong, Yunnan, China, we observed recurrent larval disease with weakness, larvae falling from the nests, and high mortality. To identify the causative agent and its effects on the gut community, we isolated bacteria from diseased larvae, characterized them by morphology, biochemical tests, and 16S rRNA gene sequencing, and then established an oral infection model. A red-pigmented isolate, designated YR2, was identified as Serratia marcescens. Oral inoculation with YR2 reproduced disease signs and significantly increased larval mortality, and a phenotypically consistent S. marcescens isolate was reisolated from infected larval guts. Amplicon sequencing showed that healthy larvae harbored gut communities dominated by Proteobacteria, whereas infection was associated with reduced diversity and a dysbiotic shift with enrichment of Enterobacterales. Our results support S. marcescens as a strong candidate pathogen associated with larval disease and mortality in Vespa analis under indoor-rearing conditions. Our findings provide a basis for pathogen surveillance and microbiota management in indoor hornet husbandry, and support improved biosecurity and health monitoring practices. Full article

Background: The human gut microbiome is highly complex, and its composition is strongly influenced by dietary patterns. Alterations in microbiome structure have been associated with a range of diseases, including type 2 diabetes mellitus. However, the underlying mechanisms for this remain poorly understood. In this study, a novel in vitro approach was utilized to investigate the interplay between gut bacteria, dietary metabolites, and metabolic dysfunction. Methods: Two representative gut bacterial species—Bacteroides thetaiotaomicron and Lactobacillus fermentum—were isolated from human faecal samples and subjected to controlled dietary manipulation to mimic eubiotic and dysbiotic conditions. Metabolites produced under these conditions were extracted, characterized, and quantified. To assess the functional impact of these metabolites, we utilized the INS-1 832/3 insulinoma cell line, evaluating insulin sensitivity through glucose-stimulated insulin secretion and ERK1/2 activation. Results: Our findings demonstrate that metabolites derived from high-carbohydrate/high-fat diets exacerbate metabolic dysfunction, whereas those generated under high-fibre conditions significantly enhance insulin secretion and glucose-dependent ERK1/2 activation in co-culture compared to monocultures. Conclusions: This work systematically disentangles the complex interactions between gut microbiota, diet, and disease, providing mechanistic insights into how microbial metabolites contribute to the onset of metabolic disorders. Full article

Rectifying the microbiome perturbed by Eimeria invasion might alleviate the adverse effects of coccidia on broiler growth. This study employed an in vitro fermentation model to investigate the direct, host-independent effects of two probiotics—Lactobacillus rhamnosus (LR) and Bacillus subtilis (BS)—on the cecal microbiome and metabolome perturbed by Eimeria tenella. Four in vitro fermentation treatments consisted of a healthy control (cecal slurry samples from health broilers), an Eimeria-disturbed control (slurry samples from infected broilers), an LR treatment (Eimeria-infected slurry + 3 × 10⁵ of LR cfu/mL), and a BS treatment (Eimeria-disturbed group + 3 × 10⁵ of BS cfu/mL). 16S rRNA sequencing and metabolomic analysis revealed that Eimeria infection resulted in an increase in microbial alpha diversity, promoted opportunistic pathogens, including Helicobacter and Bacteroides, and suppressed commensals like Lactobacillus, concurrently altering 530 intracellular metabolites. Probiotic supplementation partially restored microbial composition. Notably, LR inoculation rectified 107 metabolites across pathways including galactose metabolism and phosphotransferase systems, primarily affecting membrane phospholipid balance. In contrast, BS addition restored only 64 metabolites, largely related to secondary metabolism. The current in vitro study indicates that LR can directly modulate key metabolic disturbances in a dysbiotic microbiota, while the BS may be more dependent on host-mediated interactions. Full article

Background. The establishment and diversity of the gut microbiota during early childhood are fundamental for immune regulation and metabolic processes, with factors such as prematurity, delivery method, antibiotic treatment, and breastfeeding significantly impacting microbiome development and potential health outcomes. Objectives/Methods. This comparative study examined the gut microbiota composition in children aged 6–8 and 9–12 months, born via spontaneous labor at ≥38 weeks’ gestation, who either did not receive antibacterial therapy or required beta-lactam antibiotics. The composition of the colonic microbiota was analyzed in these fecal samples using a quantitative real-time PCR (qRT-PCR). Results. Significant differences in microbiota composition were observed between groups. Children treated with antibiotics exhibited a statistically significant reduction in alpha diversity indices (Shannon and Simpson), along with decreased colonization of key functionally important microorganisms, including obligate anaerobic bacteria such as Faecalibacterium prausnitzii, Clostridium leptum, Bacteroides spp., and metabolically active Bifidobacteria (B. bifidum, B. breve, B. longum). Conclusions. These microbiota alterations may adversely affect child health by diminishing microbial balance and functional potential, especially during this critical period of immune and metabolic development. The decline in anti-inflammatory, short-chain fatty acid-producing bacteria elevates the risk for allergic, atopic, dysbiotic, and metabolic conditions. Recognizing these impacts underscores the importance of strategies to supports microbiota restoration after antibiotic use, such as probiotics, prebiotics, and dietary interventions. Further research should focus on microbiota recovery dynamics to facilitate early intervention and optimize pediatric health outcomes. Overall, understanding antibiotic effects on gut microbiota can guide more judicious treatment approaches, reducing long-term health risks. Full article

For decades, cancer risk has been explained mainly by local factors. However, emerging evidence shows that the oral microbiome acts as a systemic modifier of oncogenesis well beyond the head and neck. This review synthesizes clinical and mechanistic data linking dysbiotic oral communities, especially Porphyromonas gingivalis, Fusobacterium nucleatum, and Treponema denticola, to malignancies across gastrointestinal, respiratory, hepatobiliary, pancreatic, breast, and urogenital systems. We summarize organ-specific associations from saliva, tissue, and stool studies, noting the recurrent enrichment of oral taxa in tumor and peri-tumoral niches of oral, esophageal, gastric, colorectal, lung, pancreatic, liver, bladder, cervical, and breast cancers. Convergent mechanisms include the following: (i) persistent inflammation (lypopolysacharide, gingipains, cytolysins, and collagenases); (ii) direct genotoxicity (acetaldehyde, nitrosation, and CDT); (iii) immune evasion/suppression (TLR/NLR signaling, MDSC recruitment, TAN/TAM polarization, and TIGIT/CEACAM1 checkpoints); and (iv) epigenetic/signaling rewiring (NF-κB, MAPK/ERK, PI3K/AKT, JAK/STAT, WNT/β-catenin, Notch, COX-2, and CpG hypermethylation). Plausible dissemination along an oral–gut–systemic axis, hematogenous, lymphatic, microaspiration, and direct mucosal transfer enables distal effects. While causality is not yet definitive, cumulative data support oral dysbiosis as a clinically relevant cofactor, motivating biomarker-based risk stratification, saliva/stool assays for early detection, and microbiome-targeted interventions (periodontal care, antimicrobials, probiotics, and microbiota modulation) alongside conventional cancer control. Full article

Intestinal health is essential for maintaining systemic physiological balance through nutrient absorption, immune regulation, and host–microbiota interactions. Atractylodes macrocephala (Baizhu), a traditional medicinal plant long used for gastrointestinal dysfunction, has attracted growing interest because its polysaccharides (AMPs) show promises in intestinal disorders. In this review, we summarize preclinical studies on AMPs identified through searches of PubMed, Web of Science, ScienceDirect, Google Scholar and the China National Knowledge Infrastructure (CNKI), focusing on their extraction, purification, structural features and gut-related activities. Experimental evidence suggests that AMPs are metabolized by gut microbiota into short-chain fatty acids and other bioactive metabolites that regulate mucosal immunity, enhance epithelial barrier function and modulate host metabolic pathways. AMPs have been shown to promote the growth of beneficial taxa, restore dysbiotic communities, up-regulate tight junction proteins, suppress intestinal inflammation and modulate gut–brain axis signaling involved in intestinal motility and visceral sensitivity. These actions underlie their protective effects reported in models of irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), colorectal cancer, chemotherapy-induced mucosal injury, and metabolic-associated systemic inflammation. Overall, current data support AMPs as microbiota-modulating, immunomodulatory, epithelial-protective and neuro-regulatory agents with potential as functional food-derived interventions for intestinal health. In this review, we also highlight key limitations and priorities for future research on structure–function relationships and clinical translation. Full article

Background: Rotavirus gastroenteritis (RVGE) remains a leading cause of severe infant diarrhea worldwide, with growing evidence supporting the role of the gut microbiome in modulating the disease. However, the interplay between early-life demographic factors, the gut microbiome, and their combined impact on RVGE clinical severity remains inadequately characterized, particularly in specific geographic populations. Aim: We aimed to investigate how demographic determinants shape gut microbiome composition and function in RVGE and how these features relate to clinical severity. Methods: In our comprehensive case–control study of 165 infants (120 RVGE cases and 45 healthy controls, aged 0–12 months), we utilized 16S rRNA sequencing combined with advanced statistical modeling and machine learning to investigate how demographic factors influence microbiome composition and clinical outcomes. Results: RVGE cases exhibited significantly reduced bacterial diversity (Kruskal–Wallis, Static = 14.85, p < 0.001) and distinct patterns, with community structure most strongly associated with dehydration severity (PERMANOVA; R² = 0.15, p < 0.001). Substantial taxonomic alterations were identified characterized by depletion of beneficial commensals including Akkermansia (LDA score = 3.8, p < 0.001), Faecalibacterium (Random Forest AUC = 0.82, p < 0.001), and Bifidobacterium (r = −0.42 with breastfeeding, p < 0.001), alongside enrichment of inflammation-associated taxa such as Escherichia-Shigella (WBC; r = 0.49, p < 0.001, and CRP; r = 0.56, p < 0.001), Streptococcus (LDA score = 4.2, p < 0.001), and Staphylococcus. Proteobacteria was the top potential biomarker of severe outcomes (Random Forest AUC = 0.85), with abundance positively correlated with systemic inflammation (CRP: r = 0.51, p = 0.003). Functional predictions revealed increased lipopolysaccharide biosynthesis (ko00540) and reduced butanoate metabolism (ko00650, p < 0.001) in severe disease. Importantly, demographic factors significantly modulated clinical outcomes: cesarean-delivered, formula-fed infants presented the most dysbiotic profiles and experienced 3.2-fold longer hospitalization (95% CI: 1.8–5.6, p < 0.001) than vaginally delivered, breastfed infants did. Conclusions: Collectively, these findings demonstrate that early-life demographic factors potentially shape the gut microbiome composition and function, may influence RVGE severity and recovery trajectories, thus providing candidate biomarkers for risk stratification and identifying targets for microbiota-based interventions. Full article

Persistent diarrhea remains a significant cause of morbidity in young children, yet the role of gut microbiota has not been fully clarified. This prospective study evaluated the diversity and predicted functions of the gut microbiota in 30 children aged 6–24 months with persistent diarrhea of unknown etiology (patient group, PG) and 30 healthy controls (healthy group, HG). Nearly full-length 16S rRNA genes from fecal bacterial metagenomic DNA were sequenced and taxonomically annotated. Subsequently, all downstream analyses, including diversity assessment, differential abundance and functional prediction analyses, and data visualization, were performed using R software (version 4.5.0, 2025). The PG showed lower Shannon and higher Simpson indices than the HG (p < 0.05), reflecting reduced microbial diversity. At the phylum level, Firmicutes predominated in the PG, whereas Actinobacteriota, Bacteroidota, and Verrucomicrobiota were more abundant in the HG (|log₂FC| > 1 and FDR < 0.05). At the genus and species levels, the PG exhibited a marked depletion of essential commensals such as Bifidobacterium longum, Faecalibacterium, Lactobacillus, and Eubacterium, alongside an enrichment of opportunistic taxa including Klebsiella, Enterococcus lactis, and Streptococcus spp. (FDR < 0.05). Functional predictions using PICRUSt2 indicated an enrichment of carbohydrate metabolism and reductions in amino acid metabolism, B-vitamin pathways, and the biosynthesis of endogenous antibiotics (FDR < 0.05). These findings suggest that the PG harbors a dysbiotic gut microbiota characterized by reduced diversity, depletion of key commensal taxa, expansion of opportunistic bacteria, and potentially adverse shifts in metabolic functions. Full article

Xanthohumol (XN), a polyphenol from hops (Humulus lupulus), exhibits antioxidant, anti-inflammatory, antihyperlipidemic, and chemo-preventive activity. Preclinical evidence suggests gut microbiota are critical to mediating some of these bioactivities. Nevertheless, its precise impact on human gut microbiota, particularly at supplemental doses, remains poorly characterized. We evaluated 200 mg/day XN for 3 weeks on human gut microbiota in a eubiotic and dysbiotic model using the Simulator of the Human Intestinal Microbial Ecosystem (SHIME^®). Functional assessments of microbiota included quantification of XN metabolites, short-chain fatty acids (SCFAs), and untargeted metabolomics of the digestive metabolome. Bacterial composition was assessed by 16S rRNA gene sequencing. XN reduced alpha-diversity and short-chain fatty acid production in both models, as well as altered taxa abundance variably between models. XN disrupted bile acid metabolism through inhibition of microbial bile salt hydrolase (BSH). The modulation of bile acid metabolism has important implications for host-level bioactivity of XN. Full article