Search Results (455)

Autism Spectrum Disorder (ASD) is frequently accompanied by gastrointestinal disturbances, dietary selectivity, and altered stress responses, with growing evidence pointing to gut–brain axis involvement. While intestinal microbiota has been extensively studied, the role of the oral microbiota remains underexplored. This study investigates the associations between oral microbiota composition and behavioral, gastrointestinal, dietary, and neuroendocrine parameters in children with ASD. A total of 45 children aged 2–18 years comprised the study group. Data collection included oral swabs for 16S rRNA gene sequencing, salivary cortisol sampling, dietary records, and standardized behavioral assessments using the Vineland Adaptive Behavior Scale. A total of 363 microbial species across 11 phyla were identified. Significant correlations were observed between specific bacterial taxa and functional gastrointestinal disorders (FGIDs), dietary patterns, salivary cortisol rhythms, and functioning. Children with FGIDs, food selectivity, or macronutrient imbalances exhibited enriched pro-inflammatory taxa (e.g., Selenomonas, Megasphaera), whereas those with typical cortisol secretion or higher adaptive functioning showed greater microbial diversity and abundance of health-associated genera (e.g., Bifidobacterium dentium). These findings suggest that oral microbiota profiles may reflect systemic physiological and neurobehavioral traits in children with ASD. Further longitudinal studies are needed to clarify causal relationships and support the development of microbiota-targeted interventions. Full article

Background: Ulcerative colitis (UC), characterized by chronic intestinal inflammation, epithelial barrier dysfunction, and immune imbalance demands novel ameliorative strategies beyond conventional approaches. Methods: In this study, the probiotic properties of Lactobacillus paracaseiL21 (L. paracaseiL21) and its ability to ameliorate colitis were evaluated using an in vitro lipopolysaccharide (LPS)-induced intestinal crypt epithelial cell (IEC-6) model and an in vivo dextran sulfate sodium (DSS)-induced UC mouse model. Results: In vitro, L. paracaseiL21 decreased levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-8) while increasing anti-inflammatory IL-10 levels (p < 0.05) in LPS-induced IEC-6 cells, significantly enhancing the expression of tight junction proteins (ZO-1, occludin, claudin-1), thereby restoring the intestinal barrier. In vivo, both viable L. paracaseiL21 and its heat-inactivated postbiotic (H-L21) mitigated weight loss, colon shortening, and disease activity indices, concurrently reducing serum LPS and proinflammatory mediators. Interventions inhibited NF-κB signaling while activating HIF1α/AhR pathways, increasing IL-22 and mucin MUC2 to restore goblet cell populations. Gut microbiota analysis showed that both interventions increased the abundance of beneficial gut bacteria (Lactobacillus, Dubococcus, and Akkermansia) and improved faecal propanoic acid and butyric acid levels. H-L21 uniquely exerted an anti-inflammatory effect, marked by the regulation of Dubosiella, while L. paracaseiL21 marked by the Akkermansia. Conclusions: These results highlight the potential of L. paracaseiL21 as a candidate for the development of both probiotic and postbiotic formulations. It is expected to provide a theoretical basis for the management of UC and to drive the development of the next generation of UC therapies. Full article

This study elucidates how the quorum-sensing (QS) signal 3OC12-HSL exacerbates enterotoxigenic E. coli (ETEC) pathogenicity and intestinal barrier dysfunction. In vitro, 3OC12-HSL enhanced ETEC C83902 growth (66.7% CFU increase at 8 h) and dysregulated stress/growth genes (e.g., eight-fold rmf upregulation under static conditions). In synthetic gut microbiota, 3OC12-HSL selectively augmented E. coli colonization (37.6% 16S rDNA increase at 12 h). Murine studies revealed 3OC12-HSL reduced jejunal villus height (381.5 μm vs. 543.2 μm in controls), elevated serum LPS, D-lactate, and DAO, and altered microbial composition (Firmicutes/Bacteroidetes imbalance). The lactonase AiiA reversed these effects by degrading 3OC12-HSL. It abrogated bacterial growth stimulation (in vitro CFU restored to baseline), normalized microbiota diversity (Shannon index recovered to control levels), suppressed pro-inflammatory cytokines (IL-6/TNF-α reduction), and restored intestinal integrity (villus length: 472.5 μm, 20.5% increase vs. ETEC-infected mice). Our findings establish AiiA as a potent quorum-quenching agent that counteracts ETEC virulence via targeted signal inactivation, highlighting its translational value. Full article

Mycotoxins represent a group of highly toxic secondary metabolites produced by diverse fungal pathogens. Mycotoxin contaminations frequently occur in foods and feed and pose significant risks to human and animal health due to their carcinogenic, mutagenic, and immunosuppressive properties. Notably, deoxynivalenol, zearalenone, fumonisins (mainly including fumonisins B1, B2, and FB3), aflatoxin B1 (AFB1), and T-2/HT-2 toxins are the major mycotoxin contaminants in foods and feed. Undoubtedly, exposure to these mycotoxins can disrupt gut health, particularly damaging the intestinal epithelium in humans and animals. In this review, we summarized the detrimental effects caused by these mycotoxins on the intestinal health of humans and animals. The fundamental molecular mechanisms, which cover the induction of inflammatory reaction and immune dysfunction, the breakdown of the intestinal barrier, the triggering of oxidative stress, and the intestinal microbiota imbalance, were explored. These signaling pathways, such as MAPK, Akt/mTOR, TNF, TGF-β, Wnt/β-catenin, PKA, NF-kB, NLRP3, AHR, TLR2, TLR4, IRE1/XBP1, Nrf2, and MLCK pathways, are implicated. The abnormal expression of micro-RNA also plays a critical role. Finally, we anticipate that this review can offer new perspectives and theoretical foundations for controlling intestinal health issues caused by mycotoxin contamination and promote the development of prevention and control products. Full article

Background/Objectives: Inflammatory bowel disease (IBD) is characterized by chronic relapsing and remitting inflammation of the gastrointestinal tract. Fecal microbiota transplantation (FMT) has emerged as an FDA-approved treatment for recurrent Clostridioides difficile infections (CDIs), with promising potential in patients with IBD. This manuscript aimed to provide a comprehensive and updated review of the available literature on fecal microbiota transplantation, its clinical use in IBD in general, as well as in patients with IBD and CDI. Methods: An extensive literature search was performed from October 2024 to March 2025. All publications available within PubMed, Medline, Embase, Google Scholar, and Cochrane databases were reviewed. All original articles, case reports, review articles, systematic reviews, and meta-analyses were included. Qualitative and quantitative data were both extracted. Discussion: Intestinal microbiota is an integral part of the human body, and dysbiosis (an imbalance in the gut’s microbial community) has been linked with several pathologies. Dysbiosis in IBD is marked by reduced beneficial bacteria and increased pro-inflammatory pathogens, contributing to mucosal damage and immune dysregulation. FMT has emerged as a solution to dysbiosis, with the first case recorded in 1917. FMT has been successful in treating patients with CDI. The diagnostic value of the gut microbiome is currently being explored as a possible therapeutic approach to IBD. Several studies have assessed FMT in patients with IBD and CDI with promising results in both ulcerative colitis (UC) and Crohn’s disease (CD) but varying efficacy based on administration routes, donor selection, and processing methods. In the context of recurrent CDI in patients with IBD, FMT demonstrates a high cure rate and potential benefit in concurrently improving IBD activity. However, risks such as IBD flare-ups post-FMT remain a concern. Conclusions: FMT holds promising potential in the management of CDI in patients with IBD. By restoring microbial diversity and correcting dysbiosis, FMT offers a novel, microbiota-targeted alternative to conventional therapies. While data support its efficacy in improving disease remission, variability in outcomes underscores the need for standardized protocols and additional large-scale, controlled studies. Continued research efforts into donor selection, treatment regimens, and long-term safety will be critical to optimizing FMT’s role in IBD and CDI care as well as improving patient outcomes. Full article

Oxidative stress directly or indirectly contributes to the development and progression of various diseases; therefore, regulating oxidative stress is a promising strategy for preventing or treating these conditions. The unique substances in soybeans, soy isoflavones, notably genistein, which have a strong antioxidant capacity, are considered to regulate various signaling pathways, alleviate oxidative stress, and improve gut microbiota imbalance as well as mitochondrial dysfunction. In this literature review, we summarize the latest research on genistein, providing evidence of its development and application as a potential drug for preventing and treating five selected diseases (Parkinson’s disease, Alzheimer’s disease, diabetes mellitus, cardiovascular disease, and cancers). The literature was searched using keywords that include tripartite combinations of genistein and oxidative stress, along with each of the five selected diseases, from PubMed, Science Direct, and Google Scholar between 2014 and 2024. According to current in vitro, in vivo, and clinical trials, we comprehensively discuss the therapeutic dose used to target various disease entities to achieve optimal efficacy and meet safety requirements. Moreover, considering the poor water solubility and limited bioavailability of genistein, strategies for improving its therapeutic efficacy, such as combining it with exercise, existing medications, and advanced technologies, as well as applying nanotechnology, were assessed. Therefore, this review aims to provide robust evidence for the development and application of genistein as a potential therapeutic agent or functional food for preventing and treating these diseases. Full article

Inflammatory Bowel Disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), results from dysregulated immune responses that drive chronic intestinal inflammation. Neutrophils, as key effectors of the innate immune system, contribute to IBD through multiple mechanisms, including the release of reactive oxygen species (ROS), pro-inflammatory cytokines, and neutrophil extracellular traps (NETs). NETs are web-like structures composed of DNA, histones, and associated proteins including proteolytic enzymes and antimicrobial peptides. NET formation is increased in IBD and has a context-dependent role; under controlled conditions, NETs support antimicrobial defense and tissue repair, whereas excessive or dysregulated NETosis contributes to epithelial injury, barrier disruption, microbial imbalance, and thrombotic risk. This review examines the roles of neutrophils and NETs in IBD. We summarize recent single-cell and spatial-omics studies that reveal extensive neutrophil heterogeneity in the inflamed gut. We then address the dual role of neutrophils in promoting tissue damage—through cytokine release, immune cell recruitment, ROS production, and NET formation—and in supporting microbial clearance and mucosal healing. We also analyze the molecular mechanisms regulating NETosis, as well as the pathways involved in NET degradation and clearance. Focus is given to the ways in which NETs disrupt the epithelial barrier, remodel the extracellular matrix, contribute to thrombosis, and influence the gut microbiota. Finally, we discuss emerging therapeutic strategies aimed at restoring NET homeostasis—such as PAD4 inhibitors, NADPH oxidase and ROS pathway modulators, and DNase I—while emphasizing the need to preserve antimicrobial host defenses. Understanding neutrophil heterogeneity and NET-related functions may facilitate the development of new therapies and biomarkers for IBD, requiring improved detection tools and integrated multi-omics and clinical data. Full article

Intestinal inflammation involves barrier impairment, immune hyperactivation, and oxidative stress imbalance. Bioactive polysaccharides universally alleviate inflammation via anti-inflammatory, antioxidant, and microbiota-modulating effects, yet exhibit distinct core mechanisms. Elucidating these differences is vital for targeted polysaccharide applications. This research examines distinct regulatory pathways through which diverse bioactive polysaccharides mitigate lipopolysaccharide-triggered intestinal inflammation in male Kunming (KM) mice. This experiment employed Lentinula edodes polysaccharide (LNT), Auricularia auricula polysaccharide (AAP), Cordyceps militaris polysaccharide (CMP), Lycium barbarum polysaccharide (LBP), and Brassica rapa polysaccharide (BRP). The expression levels of biomarkers associated with the TLR4 signaling pathway, oxidative stress, and intestinal barrier function were quantified, along with comprehensive gut microbiota profiling. The results showed that all five polysaccharides alleviated inflammatory responses in mice by inhibiting inflammatory cytokine release, reducing oxidative damage, and modulating gut microbiota, but their modes of action differed: LBP significantly suppressed the TLR-4/MyD88 signaling pathway and its downstream pro-inflammatory cytokine expression, thereby blocking inflammatory signal transduction and reducing oxidative damage; LNT and CMP enhanced the body’s antioxidant capacity by increasing antioxidant enzyme activities and decreasing malondialdehyde (MDA) levels; AAP and BRP enriched Akkermansia (Akk.) within the Verrucomicrobia (Ver.) phylum, upregulating tight junction protein expression to strengthen the intestinal mucosal barrier and indirectly reduce oxidative damage. This research demonstrates that different polysaccharides alleviate inflammation through multi-target synergistic mechanisms: LBP primarily inhibits inflammatory pathways; AAP and BRP focus on intestinal barrier protection and microbiota modulation; and LNT and CMP exert effects via antioxidant enzyme activation. These data support designing polysaccharide blends that leverage complementary inflammatory modulation mechanisms. Full article

Schizophrenia is a complex psychiatric disorder traditionally linked to neurotransmitter dysregulation, particularly within dopamine and glutamate pathways. However, recent evidence implicates the gut–brain axis as a potential contributor to its pathophysiology. This perspective article proposes a systems-level understanding of schizophrenia that incorporates the role of gut microbial dysbiosis specifically, reductions in short-chain fatty acid (SCFA)-producing taxa, and elevations in pro-inflammatory microbes. These imbalances may compromise gut barrier integrity, stimulate systemic inflammation, and disrupt neurochemical signaling in the brain. We synthesize findings from animal models, clinical cohorts, and microbial intervention trials, highlighting mechanisms such as SCFA regulation, altered tryptophan–kynurenine metabolism, and microbial impacts on neurotransmitters. We also explore microbiome-targeted interventions like probiotics, prebiotics, dietary strategies, and fecal microbiota transplantation (FMT) and their potential as adjunctive therapies. While challenges remain in causality and translation, integrating gut–brain axis insights may support more personalized and biologically informed models of schizophrenia care. Full article

Ulcerative colitis (UC) is a chronic inflammatory bowel disease driven by immune dysregulation, microbiota imbalance, and intestinal barrier dysfunction. Despite its global burden, effective therapies remain limited. This study explores the therapeutic potential of Agrocybe cylindracea polysaccharides (ACP) in a dextran sulfate sodium (DSS)-induced murine colitis model. High-performance liquid chromatography (HPLC)-characterized ACP was administered orally to BALB/c mice following colitis induction. ACP treatment significantly reduced Disease Activity Index (DAI) scores, preserved colon length, and restored intestinal barrier integrity by upregulating tight junction proteins. Mechanistically, ACP modulated immune homeostasis, suppressing pro-inflammatory cytokines (IL-17, IL-23, CRP) while enhancing anti-inflammatory mediators (IL-4, TGF-β). Furthermore, ACP inhibited hepatic TLR4/MyD88/NF-κB signaling, attenuated systemic inflammation, and reshaped gut microbiota composition by enriching beneficial taxa and reducing pathogenic Bacteroides. These findings demonstrate ACP multi-target efficacy in colitis, positioning it as a promising natural therapeutic for UC. Full article

Emerging evidence highlights the critical role of the gut microbiota in the development and progression of eating disorders (EDs), particularly in women, who are more frequently affected by these conditions. Women with anorexia nervosa, bulimia nervosa, and binge eating disorder exhibit distinct alterations in gut microbiota composition compared to healthy controls. These alterations, collectively termed dysbiosis, involve reduced microbial diversity and shifts in key bacterial populations responsible for regulating metabolism, inflammation, and gut–brain signaling. The gut microbiota is known to influence appetite regulation, mood, and stress responses—factors closely implicated in the pathogenesis of EDs. In women, hormonal fluctuations related to menstruation, pregnancy, and menopause may further modulate gut microbial profiles, potentially compounding vulnerabilities to disordered eating. Moreover, the restrictive eating patterns, purging behaviors, and altered dietary intake often observed in women with EDs exacerbate microbial imbalances, contributing to intestinal permeability, low-grade inflammation, and disturbances in neurotransmitter production. This evolving understanding suggests that microbiota-targeted therapies, such as probiotics, prebiotics, dietary modulation, and fecal microbiota transplantation (FMT), could complement conventional psychological and pharmacological treatments in women with EDs. Furthermore, precision nutrition and personalized microbiome-based interventions tailored to an individual’s microbial and metabolic profile offer promising avenues for improving treatment efficacy, even though these approaches remain exploratory and their clinical applicability has yet to be fully validated. Future research should focus on sex-specific microbial signatures, causal mechanisms, and microbiota-based interventions to enhance personalized treatment for women struggling with eating disorders. Full article

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver condition. Its prevalence is estimated to further increase. The gut–liver axis, which represents both anatomical and functional connections, contributes significantly to the development of MASLD. Dysbiosis, characterized by an imbalance in gut microbiota, can exacerbate the disease by increasing intestinal permeability, which permits harmful bacteria and their components to enter the bloodstream. This review sought to explore the impact of probiotics, prebiotics, and synbiotics on the treatment of MASLD. Method: The methodology for scoping reviews in accordance with Prisma-ScR guidelines was followed. A comprehensive search was conducted in databases such as PubMed, Scopus, and Medline. Out of 1390 studies screened, 25 were selected for the final analysis. Results: The findings of this scoping review highlight the therapeutic potential of probiotics, prebiotics, and synbiotics in the management and treatment of MASLD, as showcased by the existing literature. Conclusions: This scoping review offers important insights into the advantages of probiotics, prebiotics, and synbiotics in the treatment of MASLD. The limitations identified in this study emphasize the necessity for larger, long-term, and geographically diverse studies in order to obtain more solid scientific results. Full article

Background/Objectives: The gut microbiota (GM) is pivotal for immune regulation, metabolism, and neurodevelopment. Infants undergoing surgery for congenital gastrointestinal anomalies are especially prone to microbial imbalances, with a paucity of beneficial bacteria (e.g., Bifidobacteria and Bacteroides) and diminished short-chain fatty acid production. Dysbiosis has been associated with severe complications, including necrotizing enterocolitis, sepsis, and feeding intolerance. This narrative review aims to critically examine strategies for microbiota modulation in this high-risk cohort. Methods: An extensive literature analysis was performed to compare the evolution of GM in healthy neonates versus those requiring gastrointestinal surgery, synthetizing strategies to maintain eubiosis, such as early nutritional interventions—particularly the use of human milk—along with antibiotic management and supplementary treatments including probiotics, prebiotics, postbiotics, and lactoferrin. Emerging techniques in metagenomic and metabolomic analysis were also evaluated for their potential to elucidate microbial dynamics in these patients. Results: Neonates undergoing gastrointestinal surgery exhibit significant alterations in microbial communities, characterized by reduced levels of eubiotic bacteria and an overrepresentation of opportunistic pathogens. Early initiation of enteral feeding with human milk and careful antibiotic stewardship are linked to improved microbial balance. Adjunctive therapies, such as the administration of probiotics and lactoferrin, show potential in enhancing gut barrier function and immune modulation, although confirmation through larger-scale studies remains necessary. Conclusions: Modulating the GM emerges as a promising strategy to ameliorate outcome in neonates with congenital gastrointestinal surgical conditions. Future research should focus on the development of standardized therapeutic protocols and the execution of rigorous multicenter trials to validate the efficacy and safety of these interventions. Full article

Rheumatoid arthritis (RA) is a chronic autoimmune disease that has a serious impact on both human health and animal production. The gut microbiota is a large and complex symbiotic ecosystem in animals, and the imbalance of gut microbiota is closely related to the pathogenesis of numerous diseases, including RA. The interactions among the gut microbiota, intestinal barrier, and immune system play key roles in maintaining intestinal homeostasis and affecting the development of RA. Regulating intestinal flora and metabolites provides new ideas for the prevention and treatment of RA. Probiotics can regulate the balance of intestinal flora and metabolites, improve the immune environment, and provide novel therapeutic strategies against RA. In order to summarize the role of gut microbiota and metabolite remodeling in the development and management of RA, this review will elaborate on the role of intestinal flora imbalance in the pathogenesis of RA and assess prospective therapeutic approaches that target the gut flora. Understanding the interaction among intestinal flora, metabolites, and RA will help to clarify the pathogenesis of RA and develop innovative and personalized therapeutic interventions against chronic autoimmune diseases. Full article

Plateau environments present unique mental health challenges owing to stressors including hypoxia, low temperatures, and intense ultraviolet (UV) radiation. These factors induce structural and functional alterations in the gut microbiota, disrupting gut-brain axis homeostasis and contributing to the higher prevalence of depression in plateau regions relative to flatland areas. For example, studies report that 28.6% of Tibetan adults and 29.2% of children/adolescents on the Qinghai-Tibet Plateau experience depression, with increasing evidence linking this trend to alterations in the gut microbiota. Dysbiosis contributes to depression through three interconnected mechanisms: (1) Neurotransmitter imbalance: Reduced bacterial diversity impairs serotonin synthesis, disrupting emotional regulation. (2) Immune dysregulation: Compromised gut barrier function allows bacterial metabolites to trigger systemic inflammation via toll-like receptor signaling pathways. (3) Metabolic dysfunction: Decreased short-chain fatty acid levels weaken neuroprotection and exacerbate hypothalamic-pituitary-adrenal axis stress responses. Current interventions—including dietary fiber, probiotics, and fecal microbiota transplantation—aim to restore microbiota balance and increase short-chain fatty acids, alleviating depressive symptoms. However, key knowledge gaps remain in understanding the underlying mechanisms and generating population-specific data. In conclusion, existing evidence indicates an association between plateau environments, the gut microbiota, and depression, but causal relationships and underlying mechanisms require further empirical investigation. Integrating multiomics technologies to systematically explore interactions among high-altitude environments, the microbiota and the brain will facilitate the development of precision therapies such as personalized nutrition and tailored probiotics to protect mental health in high-altitude populations. Full article