As one of the three major malignant tumors in women, the morbidity of endometrial cancer is second only to that of cervical cancer and is increasing yearly. Its etiological mechanism is not clear, and the risk factors are numerous and common and are closely related to obesity, hypertension, diabetes, etc. The gut microbiota has many strains, which play a considerable part in normal digestion and absorption in the human body and the regulation of the immune response. In the last few years, research on the gut microbiota has been unprecedentedly popular, and it has been confirmed that the gut microbiota closely correlates with the occurrence and development of all kinds of benign and malignant diseases. In this article, the effects of the gut microbiota and its metabolites on the occurrence and development of endometrial cancer is reviewed, and its application in the prevention, diagnosis and treatment of endometrial cancer is explored.

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.

Substance use disorders (SUDs) involve a complex series of central and peripheral pathologies, leading to impairments in cognitive, behavioral, and physiological processes. Emerging evidence indicates a more significant role for the microbiome-gut-brain axis (MGBA) in SUDs than previously recognized. The MGBA is interconnected with various body systems by producing numerous metabolites, most importantly short-chain fatty acids (SCFAs), cytokines, and neurotransmitters. These mediators influence the human body's epigenome and transcriptome. While numerous epigenetic alterations in different brain regions have been reported in SUD models, the intricate relationship between SUDs and the MGBA suggests that the gut microbiome may partially contribute to the underlying mechanisms of SUDs. Promising results have been observed with gut microbiome-directed interventions in patients with SUDs, including prebiotics, probiotics, antibiotics, and fecal microbiota transplantation. Nonetheless, the long-term epigenetic effects of these interventions remain unexplored. Moreover, various confounding factors and study limitations have hindered the identification of molecular mechanisms and clinical applications of gut microbiome interventions in SUDs. In the present review, we will (i) provide a comprehensive discussion on how the gut microbiome influences SUDs, with an emphasis on epigenetic alterations; (ii) discuss the current evidence on the bidirectional relationship of gut microbiome and SUDs, highlighting potential targets for intervention; and (iii) review recent advances in gut microbiome-directed therapies, along with their limitations and future directions.

Fluoride exposure primarily occurs through contaminated water and leads to fluorosis, which is a global health concern. After ingestion, fluoride is absorbed via gastrointestinal tract, where it interacts with the gut microbiota. While animal studies have explored fluoride's effects on gut microbiota, no human studies have yet been conducted. Most research emphasizes metagenomic diversity, neglecting isolation and characterization of pure cultures for further applications. Additionally, the association between gut microbiota with fluorosis outcomes in fluoride-exposed populations is unexplored. This study characterizes and compares the cultivable gut microbiota in the fluoride-exposed population with (symptomatic, group II) or without (asymptomatic, group I) signs of skeletal fluorosis along with unexposed control (group III). Group I displayed higher abundance of Firmicutes (58.58 %), group II had predominance of Proteobacteria (61.25 %) while group III showed similar abundance of Proteobacteria (50.38 %) and Firmicutes (49.51 %). On analyzing short-chain fatty acid (SCFA) profiles, group I isolates produced higher isobutyric acid (1.31 ± 0.9 mM) than group II (0.71 ± 0.35 mM), while group II produced more isovaleric acid (0.8 ± 0.41 mM) than group I (0.61 ± 0.08 mM) (p < 0.05). These findings suggest that gut microbiota and SCFAs alteration may influence bone metabolism, affecting the fluorosis progression.

An ostomy, or stoma, is a surgically created percutaneous aperture from a hollow organ (e.g., small intestine) to the body's surface. Physicians may recommend an ostomy as a temporary or permanent solution to a range of disorders of the gastrointestinal tract, with up to 130 000 ostomies performed annually in the United States. An ostomy facilitates the expulsion of waste products, termed dejecta and circumvents the compromised organs. While an ostomy can be a lifesaving treatment, it is a disruption of regular digestive flow and has a number of associated complications including hernia, prolapse and necrosis. The most commonly observed complications are peristomal skin complications (PSCs), attributed to the leakage of dejecta onto the peristomal skin or the skin directly surrounding the stoma. Despite the prevalence of PSCs, little is known about the precise etiological factors that play a role in PSC formation. This review discusses the constituents of dejecta and their possible roles in PSC formation. Additionally, we identify a number of in vitro and in vivo skin models that could be used to study PSCs. Identification of the components of dejecta and understanding their interaction with skin models can facilitate the development of interventions to treat and prevent PSCs.

Obesity is a complex, chronic condition characterised by excess adiposity. Rates of obesity in childhood and adolescence are increasing worldwide, with a corresponding increase in adulthood. The aetiology of obesity is multifactorial and results from a combination of endocrine, genetic, environmental and societal factors. Population level approaches to reduce the prevalence of childhood obesity worldwide are urgently needed. There are wide-ranging complications from excess weight affecting every system in the body, which lead to significant morbidity and reduced life expectancy. Treatment of obesity and its complications requires a multi-faceted, biopsychosocial approach incorporating dietary, exercise and psychological treatments. Pharmacological treatments for treating childhood obesity have recently become available, and there is further development of new anti-obesity medications in the pipeline. In addition, bariatric surgery is being increasingly recognised as a treatment option for obesity in adolescence providing the potential to reverse complications related to excess weight. In this review, we present an update on the prevalence, aetiology, complications and treatment of childhood obesity.

The gut microbiota, a substantial group of microorganisms residing in the human body, profoundly impacts various physiological and pathological mechanisms. Recent studies have elucidated the association between gut dysbiosis and multiple organ diseases. Gut microbiota plays a crucial role in maintaining gastrointestinal stability, regulating the immune system and metabolic processes not only within the gastrointestinal tract but also in other organs such as the brain, lungs, and skin. Dysbiosis of the gut microbiota can disrupt biological functioning and contribute to the development of metabolic disorders. The Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) and CRISPR-associated proteins (Cas) modules are adaptive immune systems in numerous archaea and bacteria. CRISPR/Cas is a versatile gene-editing tool that enables modification of the genome in live cells, including those within the gut microbiota. This technique has revolutionized gene editing due to its simplicity and effectiveness. It finds extensive applications in diverse scientific arenas, facilitating the functional screening of genomes during various biological processes. Additionally, CRISPR has been instrumental in creating model organisms and cell lines for research purposes and holds great potential for developing personalized medical treatments through precise genetic alterations. This review aims to explore and discuss the possibilities of CRISPR/Cas and the current trends in using this technique for editing gut microbiota genes in various metabolic disorders. By uncovering the valuable potential of CRISPR/Cas in modifying metabolic disorders through the human gut microbiota, we shed light on its promising applications.

Convergent data across species paint a compelling picture of the critical role of the gut and its resident microbiota in several brain functions and disorders. The chemicals mediating communication along these sophisticated highways of the brain-gut-microbiome (BGM) axis include both microbiota metabolites and classical neurotransmitters. Amongst the latter, GABA is fundamental to brain function, mediating most neuronal inhibition. Until recently, GABA's role and specific molecular targets in the periphery within the BGM axis had received limited attention. Yet, GABA is produced by neuronal and non-neuronal elements of the BGM, and recently, GABA-modulating bacteria have been identified as key players in GABAergic gut systems, indicating that GABA-mediated signalling is likely to transcend physiological boundaries and species. We review the available evidence to better understand how GABA facilitates the integration of molecularly and functionally disparate systems to bring about overall homeostasis and how GABA perturbations within the BGM axis can give rise to multi-system medical disorders, thereby magnifying the disease burden and the challenges for patient care. Analysis of transcriptomic databases revealed significant overlaps between GABAAR subunits expressed in the human brain and gut. However, in the gut, there are notable expression profiles for a select number of subunits that have received limited attention to date but could be functionally relevant for BGM axis homeostasis. GABAergic signalling, via different receptor subtypes, directly regulates BGM homeostasis by modulating the excitability of neurons within brain centres responsible for gastrointestinal (GI) function in a sex-dependent manner, potentially revealing mechanisms underlying the greater prevalence of GI disturbances in females. Apart from such top-down regulation of the BGM axis, a diverse group of cell types, including enteric neurons, glia, enteroendocrine cells, immune cells and bacteria, integrate peripheral GABA signals to influence brain functions and potentially contribute to brain disorders. We propose several priorities for this field, including the exploitation of available technologies to functionally dissect components of these GABA pathways within the BGM, with a focus on GI and brain-behaviour-disease. Furthermore, in silico ligand-receptor docking analyses using relevant bacterial metabolomic datasets, coupled with advances in knowledge of GABAAR 3D structures, could uncover new ligands with novel therapeutic potential. Finally, targeted design of dietary interventions is imperative to advancing their therapeutic potential to support GABA homeostasis across the BGM axis.

Understanding when host-microbiome interactions are first established is crucial for comprehending normal development and identifying disease prevention strategies. Furthermore, bacterially derived metabolites play critical roles in shaping the intestinal immune system. Recent studies have demonstrated that memory T cells infiltrate human intestinal tissue early in the second trimester, suggesting that microbial components such as peptides that can prime adaptive immunity and metabolites that can influence the development and function of the immune system are also present in utero. Our previous study reported a unique fetal intestinal metabolomic profile with an abundance of several bacterially derived metabolites and aryl hydrocarbon receptor (AHR) ligands implicated in mucosal immune regulation.

In the current study, we demonstrate that a number of microbiome-associated metabolites present in the fetal intestines are also present in the placental tissue, and their abundance is different across the fetal intestine, fetal meconium, fetal placental villi, and the maternal decidua. The fetal gastrointestinal samples and maternal decidua samples show substantially higher positive correlation on the abundance of these microbial metabolites than the correlation between the fetal gastrointestinal samples and meconium samples. The expression of genes associated with the transport and signaling of some microbial metabolites is also detectable in utero.

We suggest that the microbiome-associated metabolites are maternally derived and vertically transmitted to the fetus. Notably, these bacterially derived metabolites, particularly short-chain fatty acids and secondary bile acids, are likely biologically active and functional in regulating the fetal immune system and preparing the gastrointestinal tract for postnatal microbial encounters, as the transcripts for their various receptors and carrier proteins are present in second trimester intestinal tissue through single-cell transcriptomic data. Video Abstract.

Enhancing the early embryo survival rate is important for increasing sow reproductive efficiency. Whether and how tryptophan influences early embryo survival and pregnancy outcomes in sows remains unknown.

The objective of this study was to investigate the effects of dietary tryptophan supplementation on the reproductive performance of sows.

A total of 128 multiparous Large White × Landrace sows were randomly assigned to 4 groups including the control group (dietary tryptophan concentration was 0.18% from weaning to estrus and 0.10% from day 1 to day 28 of pregnancy) or the low, medium, and high dose of tryptophan supplementation groups (dietary tryptophan levels were 0.27%, 0.36%, and 0.45% from weaning to estrus and 0.15%, 0.20%, and 0.25% from day 1 to day 28 of pregnancy). Primary porcine granulosa cells were isolated from porcine ovaries and treated with selected tryptophan metabolites to assess hormone levels in the cell supernatant.

Compared with the control group, the dietary high levels of tryptophan group increased the litter weight (P < 0.05) and showed an increasing trend in the born alive per litter (P = 0.06). Serum concentration of progesterone and estradiol and levels of tryptophan, kynurenine, xanthurenic acid, 2-aminobenzoic acid, and indoleamine 2,3-dioxygenase on day 28 of pregnancy were increased in the high concentration of tryptophan group (P < 0.05). In vitro experiments using primary porcine granulosa cell culture showed that tryptophan and 2-aminobenzoic acid increased progesterone and estradiol levels in the cell supernatant (P < 0.05). Dietary tryptophan supplementation increased the abundances of fecal beneficial bacteria such as Hydrogenoanaerobacterium and Lachnospiraceae in sows (P < 0.05).

Dietary tryptophan supplementation may enhance the pregnancy outcome of sows through the increase of tryptophan metabolites to strengthen steroid hormone secretion and the abundance of beneficial microbes.

Evidence suggests that the intestinal microbiome may play an important role in the pathogenesis and progression of acute critical illness in humans and other mammals, although evidence in small animal medicine is sparse. Moreover, the intestinal microbiota plays many important metabolic roles (production of short-chain fatty acids, trimethylamine-N-oxide, and normal bile acid metabolism) and is crucial for immunity as well as defense against enteropathogens. The use of probiotics and fecal microbiota transplantation as instruments to modulate the intestinal microbiota seems to be safe and effective in studies on critically ill dogs with acute gastrointestinal diseases.

Flaxseed (Linum usitatissimum L.) and chia seed (Salvia hispanica L.) have become increasingly popular in the design of various functional food products. However, information on their functional properties is scarce. The aim of this study is to comparatively evaluate the effects of the dietary fibers (DFs) of flaxseed and chia seed on colonic microbiota composition and metabolic outputs. The neutral and acidic monosaccharide compositions of DFs of flaxseed and chia seed were determined using gas chromatography/mass spectrometry (GC/MS) and spectrophotometer, respectively. Next, in vitro fecal fermentation assays were applied, and samples were collected at different time points for short-chain fatty acids (SCFA) measurements using GC, and fecal microbiota changes before and after fermentation were evaluated through 16S rRNA sequencing. The results revealed that DFs of flaxseed were dominated by xylose and uronic acid moieties, while that of chia seed was dominated by glucose units, indicating that their DFs are structurally different. Higher SCFA generations were observed in the case of flaxseed, suggesting that flaxseed DFs are more readily fermentable by gut microbiota. Flaxseed and chia seed DFs differentially impacted the microbiota compositions at the OTU level; for example, significant increases in the relative abundances of Acidaminococcaceae and Bacteroides stercoris related OTUs, which are known to be propionate producers, were observed in the case of flaxseed, but not chia seed. Interestingly, flaxseed, but not chia seed, DFs suppressed the growth of some pathogenic bacteria. Overall, this study suggests that the functionality of flaxseed and chia seed DFs in relation to colonic microbiota may differ, with flaxseed being more readily fermented and potentially promoting beneficial microbes to a greater extent. Thus, flaxseed could hold promise for developing functional food recipes aimed at supporting colonic health.

The organophosphorus pesticide chlorpyrifos (CPF) is widely utilized in agriculture to protect crops from pests and diseases. Concerns regarding its extensive use have emerged due to the substance's persistence, bioaccumulation, endocrine disruption, and associated toxicity, which may lead to various adverse reactions. In this study, 32 male C57BL/6 J mice were orally administered varying doses of CPF over a period of two weeks. Metabolic perturbations resulting from subacute exposure to CPF were assessed using LC-MS/MS-based untargeted metabolomics, alongside biochemical analysis and histopathological techniques. The 16S rRNA gene sequencing method was employed to evaluate changes in the gut microbial community within the cecal contents of mice exposed to CPF. In vivo studies have shown that CPF exposure induced dose-dependent damage and dysregulation of the intestinal microbiota in mouse colonic tissues. This was characterized by significant alterations in the gut microbiota, increased intestinal permeability and elevated levels of lipopolysaccharides. These changes may have compromised intestinal barrier function and facilitated the transfer of intestinal microbial metabolites and endotoxins to the liver, subsequently leading to liver injury. Collectively, this study elucidates a potential mechanism by which CPF triggers liver injury through alterations in the intestinal microbial community and increased intestinal permeability. These findings not only enhance our understanding of the toxicological effects of CPF but also contribute to the assessment of health risks associated with CPF exposure.

Inflammatory bowel disease (IBD) comprises chronic inflammatory conditions with complex mechanisms and diverse manifestations, posing significant clinical challenges. Traditional animal models and ethical concerns in human studies necessitate innovative approaches. This review provides an overview of human intestinal architecture in health and inflammation, emphasizing the role of microfluidics and on-chip technologies in IBD research. These technologies allow precise manipulation of cellular and microbial interactions in a physiologically relevant context, simulating the intestinal ecosystem microscopically. By integrating cellular components and replicating 3D tissue architecture, they offer promising models for studying host-microbe interactions, wound healing, and therapeutic approaches. Continuous refinement of these technologies promises to advance IBD understanding and therapy development, inspiring further innovation and cross-disciplinary collaboration.

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.

Increasing strain on feed resources has led to a gradual increase in feed input costs, making it necessary to improve feed efficiency in livestock and poultry. In this study, Hu sheep were divided into two groups (high and low feed conversion ratio [FCR]) according to the FCR. Based on 16S rDNA amplicon sequencing technology to compare rumen and small intestine microbial composition, the differences and similarities of production performance, expression level of intestinal nutrient-specific carrier, digestive enzyme activity, short-chain fatty acid (SCFA) content, muscle conventional nutrient content, and blood biochemical indexes of Hu sheep in high- and low-FCR groups were investigated, and correlation analysis was conducted. The results showed that Hu sheep in the low-FCR group had higher feed efficiency, average daily gain, and less fat deposition (P < 0.05). The difference in rumen microbial composition between the high- and low-FCR groups was significant (P < 0.05). Spearman's correlation analysis showed that FCR was significantly associated with production performance such as body weight, fat deposition, and dressing percentage (P < 0.05). The levels of digestive enzyme activity and nutrient transporter carrier expression in the small intestine were higher in the low-FCR group than in the high-FCR group. Therefore, FCR can be one of the important targets of concern in Hu sheep production. Combining FCR and regulating the gastrointestinal environment of Hu sheep by nutritional means can greatly improve the production performance and economic benefit of Hu sheep.

Feed costs account for a large portion of housed sheep. The purpose of comparing the performance and intestinal microbial composition of different FCR Hu sheep is to regulate the gastrointestinal microecology in production practice. This helps livestock producers choose low-FCR Hu sheep to maximize production costs, improve efficiency, and achieve the purpose of low-carbon production.

Background and Aim: The human gut microbiome plays a crucial role in maintaining health. Artificial sweeteners, also known as non-nutritive sweeteners (NNS), have garnered attention for their potential to disrupt the balance of the gut microbiome. This review explores the complex relationship between NNS and the gut microbiome, highlighting their potential benefits and risks. By synthesizing current evidence, we aim to provide a balanced perspective on the role of AS in dietary practices and health outcomes, emphasizing the need for targeted research to guide their safe and effective use. Methods: A comprehensive literature review was conducted through searches in PubMed and Google Scholar, focusing on the effects of artificial sweeteners on gut microbiota. The search utilized key terms including "Gut Microbiome", "gut microbiota", "Eubiosis", "Dysbiosis", "Artificial Sweeteners", and "Nonnutritive Sweeteners". Results: NNS may alter the gut microbiome, but findings remain inconsistent. Animal studies often report a decrease in beneficial bacteria like Bifidobacterium and Lactobacillus, and an increase in harmful strains such as Clostridium difficile and E. coli, potentially leading to inflammation and gut imbalance. Disruptions in short-chain fatty acid (SCFA) production and gut hormone signaling have also been observed. However, human studies generally show milder or no significant changes, highlighting the limitations in translating animal model findings directly to humans. Differences in study design, dosage, exposure time, and sweetener type likely contribute to these varied outcomes. Conclusions: While NNS offer certain benefits, including reduced caloric intake and improved blood sugar regulation, their impact on gut microbiome health raises important concerns. The observed reduction in beneficial bacteria and the rise in pathogenic strains underscore the need for caution in NNS consumption. Furthermore, the disruption of SCFA production and metabolic pathways illustrates the intricate relationship between diet and gut health.

Matrix metalloproteinases (MMPs) are key enzymes involved in extracellular matrix (ECM) remodeling, regulating a wide range of cellular and immune processes in both homeostatic and pathological conditions. Host-microbiota interactions play a critical role in maintaining ECM balance; however, during dysbiosis, this regulation is disrupted, leading to compromised barrier integrity, pathogen translocation into circulation, and the development of systemic diseases and cancer. This review highlights the bidirectional relationship between MMP expression/activity and microbiota dysbiosis, emphasizing tissue-specific alterations in MMP activity that contribute to disease progression. In addition, it integrates interdisciplinary evidence to illustrate the MMP-dependent mechanisms underlying various pathologies associated with oral and gut microbiome dysbiosis, including long-range effects through the gut-skin and gut-brain axes. Thus, this review introduces the emerging field of MatrixBiome, which explores the complex interactions between the ECM, microbiota, and host tissues. Finally, it also outlines therapeutic strategies to modulate MMP levels, either indirectly through microbiome-targeted approaches (e.g., prebiotics, probiotics, and postbiotics) or directly using MMP inhibitors, offering promising avenues for future clinical interventions.

Pathogenic infections can reshape the intestinal microbiota of aquatic animals, thereby impacting their health status. In this study, we aimed to investigate whether Vibrio parahaemolyticus infection induces dysbiosis in the intestinal bacterial community of Penaeus vannamei and to assess the associated ecological risks. Our findings revealed the deterministic processes in intestinal bacterial community assembly during bacterial infections, indicating that host selection, i.e., host immune response post-infection, has a significant influence on intestinal microbes. More importantly, we found that bacterial infection reshaped the intestinal community by reducing the relative abundance of probiotic Ruegeria species (e.g., R. atlantica, R. lacuscaerulensis, R. conchae, R. profundi, R. arenilitoris, R. pomeroyi) and increasing the relative abundance of Vibrio species (V. harveyi, V. sinaloensis, V. coralliilyticus, and V. brasiliensis). Significant negative correlations were observed between the relative abundance of these Ruegeria species and the relative abundance of Vibrio species. Moreover, the control P. vannamei contained a substantially higher number of keystone species belonging to Ruegeria in the bacterial community network, whereas bacterial infection individuals had few or no keystone species belonging to Ruegeria, with keystone species belonging to Vibrio becoming more prominent. Thus, the significant increase in Vibrio species abundance in the P. vannamei intestine following bacterial infection was associated with the marked reduction in Ruegeria species. Our findings will provide valuable insights into the complex interactions among bacterial infection, intestinal microbiota, and host health, and they provide guidance for the development of probiotics in promoting the healthy culture of P. vannamei.

The small intestine is an area of the digestive system difficult to access using current medical procedures, which prevents studies on the interactions between food, drugs, the small intestinal epithelium, and resident microbiota. Therefore, there is a need to develop novel microfluidic models that mimic the intestinal biological and mechanical environments. These models can be used for drug discovery and disease modeling and have the potential to reduce reliance on animal models. The goal of this study was to develop a small intestine on a chip with both enterocyte (Caco-2) and goblet (HT29-MTX) cells cocultured with Lacticaseibacillus rhamnosus biofilms, which is of one of several genera present in the small intestinal microbiota. L. rhamnosus was introduced following the establishment of the epithelial barrier. The shear stress within the device was kept in the lower physiological range (0.3 mPa) to enable biofilm development over the in vitro epithelium. The epithelial barrier differentiated after 5 days of dynamic culture with cell polarity and permeability similar to the human small intestine. The presence of biofilms did not alter the barrier's permeability in dynamic conditions. Under fluid flow, the complete model remained viable and functional for more than 5 days, while the static model remained functional for only 1 day. The presence of biofilm increased the secretion of acidic and neutral mucins by the epithelial barrier. Furthermore, the small intestine on a chip also showed increased MUC2 production, which is a dominant gel-forming mucin in the small intestine. This model builds on previous publications as it establishes a stable environment that closely mimics in vivo conditions and can be used to study intestinal physiology, food-intestinal interactions, and drug development.

In order to optimize diets for Bengal tiger cubs and improve their health condition and survival rates, we conducted microbiota and metabolomics analyses on fecal samples from Bengal tiger cubs fed goat and dog milk replacer formulae. The results showed that there were significant differences in fecal microorganisms and metabolites between the two groups. At the phylum level, the major components of the microbial composition in the feces of cubs were Firmicutes, Actinobacteriota, Proteobacteria, Bacteroidota and Fusobacteriota. In addition, the abundance of gut microbiota varied significantly between the two groups of tiger cubs. The fecal microbiota of the tiger cubs fed dog milk replacer powder exhibited an increase in probiotic bacteria (Anaerostipes and Clostridium_scindens) (p < 0.05), and the microbial community tended to be more balanced. Metabolomics data further elucidated that feeding different milk formulae significantly affected the fecal metabolites and metabolic pathways in the Bengal tiger cubs. In the dog milk replacer powder group, 76 metabolites were up-regulated (p < 0.05), and 278 metabolites were down-regulated (p < 0.05), particularly affecting the metabolism of vitamin D3, vitamin B5, isoleucine, valine, phenylalanine and oleic acid. At the same time, 19 metabolic pathways were affected (p < 0.05), including the amino acid metabolism, lipid metabolism and nucleotide metabolism pathways. In conclusion, this study confirms that milk formula composition affects the gut microbiota and metabolism of Bengal tiger cubs. These findings may provide new insights into how different milk powder formulae and dietary strategies influence the regulation of gut microbiota and overall health in Bengal tiger cubs.

The gut microbiome has emerged as a novel and intriguing focus in mood disorder research. Emerging evidence demonstrates the significant role of the gut microbiome in influencing mental health, suggesting a bidirectional communication between the gut and the brain. This review examines the latest findings on the gut-microbiota-brain axis and elucidates how alterations in gut microbiota composition can influence this axis, leading to changes in brain function and behavior. Although dietary interventions, prebiotics, probiotics, and fecal microbiota transplantation have yielded encouraging results, significant advances are needed to establish next-generation approaches that precisely target the neurobiological mechanisms of mood disorders. Future research must focus on developing personalized treatments, facilitated by innovative therapies and technological progress, which account for individual variables such as age, sex, drug history, and lifestyle. Highlighting the potential therapeutic implications of targeting the gut microbiota, this review emphasizes the importance of integrating microbiota research into psychiatric studies to develop more effective and personalized treatment strategies for mood disorders.

Modified Shi Hui San (MSHS) has shown excellent therapeutic effects on ulcerative colitis (UC) patients clinically in China. However, the exact mechanism underlying its effect remains unclear and needs to further investigation.

This study aimed to investigate the therapeutic effects of modified Shi Hui San decoction (MSHSD) in murine experimental colitis and explore its underlying mechanisms.

To examine the effects of MSHSD on UC, a murine model of colitis was induced using 2.5 % dextran sodium sulfate (DSS). The mice were then treated with MSHSD at the doses of 6.25 or 25 g/kg for 10 days. The progression of colitis was evaluated through clinical symptoms, histopathological analysis, evaluation of mucosal barrier integrity, biochemical assays, and analysis of the gut microbiota composition.

MSHSD administration markedly ameliorated experimental colitis in DSS-treated mice by suppressing inflammation, restoring the intestinal mucus barrier, alleviating oxidative stress, and reestablishing immunity. More importantly, it transformed the gut microbiota structure from an imbalanced state to a normal state.

These findings for the first time extend our understanding of the mechanisms, by which MSHSD ameliorates murine experimental colitis, and support the clinical use of MSHS for UC treatment.

Huntington's disease (HD) is a progressive neurodegenerative disorder characterized by motor dysfunction, cognitive decline, and emotional instability, primarily resulting from the abnormal accumulation of mutant huntingtin protein. Growing research highlights the role of intestinal microbiota and their metabolites, particularly short-chain fatty acids (SCFAs), in modulating HD progression. SCFAs, including acetate, propionate, and butyrate, are produced by gut bacteria through dietary fiber fermentation and are recognized for their neuroprotective properties. Evidence suggests that SCFAs regulate neuroinflammation, neuronal communication, and metabolic functions within the central nervous system (CNS). In HD, these compounds may support neuronal health, reduce oxidative stress, and enhance blood-brain barrier (BBB) integrity. Their mechanisms of action involve binding to G-protein-coupled receptors (GPCRs) and modulating gene expression through epigenetic pathways, underscoring their therapeutic potential. This analysis examines the significance of SCFAs in HD, emphasizing the gut-brain axis and the benefits of dietary interventions aimed at modifying gut microbiota composition and promoting SCFA production. Further research into these pathways may pave the way for novel HD management strategies and improved therapeutic outcomes.

Acute pancreatitis (AP) ranks among the most frequently encountered gastrointestinal diseases in the emergency department. Recent studies have increasingly emphasized the substantial connection among gut microbiota, inflammatory cytokines, and AP.

A two-sample Mendelian randomization (MR) study was conducted using summary statistics of gut microbiota (GM) from the largest available meta-analysis of genome-wide association studies conducted by the MiBioGen consortium (n=18,340). For cytokines, the data were obtained from a study that investigated genome variant associations with 41 inflammatory cytokines and growth factors (n=8293). The summary statistics of AP were obtained from the FinnGen consortium version R5 data (3022 cases and 195,144 controls). The inverse variance weighted (IVW) method was used as the main analysis, with MR-Egger and weighted median as complementary analytical methods. Sensitivity analyses were performed using Cochran's Q-test, MR-Egger intercept test, leave-one-out analyses, and MR-PRESSO. In addition, we employed the reverse MR analysis and MR Steiger method to estimate the orientations of exposure and outcome.

Among the 211 examined GM taxa, the IVW method revealed that Bacteroidales (odds ratio [OR]=1.412, 95% confidence interval [CI]:1.057 to 1.885, P=0.019), Eubacterium fissicatena group (OR=1.240, 95% CI:1.045 to 1.470, P=0.014), and Coprococcus3 (OR=1.481, 95 % CI:1.049 to 2.090, P=0.026) exhibited a positive association with AP. Conversely, Prevotella9 (OR=0.821, 95% CI:0.680 to 0.990, P=0.038), RuminococcaceaeUCG004 (OR=0.757, 95% CI:0.577 to 0.994, P=0.045), and Ruminiclostridium6 (OR=0.696, 95% CI:0.548 to 0.884, P=0.003) displayed a negative correlation with AP. Among the 41 inflammatory cytokines, only macrophage colony-stimulating factor (M_CSF, OR=0.894, 95% CI:0.847 to 0.943, P=0.037) exhibited a negative association with AP. Sensitivity analyses revealed no evidence of pleiotropy or heterogeneity. Nevertheless, the mediation analysis showed that M_CSF did not act as a mediating factor.

This two-sample MR study revealed causal associations between specific GM and inflammatory cytokines with AP, respectively. However, inflammatory cytokines did not appear to act as mediating factors in the pathway from GM to AP.

The human microbiome, a complex ecosystem of microorganisms inhabiting the body, plays a critical role in human health. Investigating its association with host traits is essential for understanding its impact on various diseases. Although shotgun metagenomic sequencing technologies have produced vast amounts of microbiome data, analyzing such data is highly challenging due to its sparsity, noisiness, and high feature dimensionality. Here, we develop MIOSTONE, an accurate and interpretable neural network model for microbiome-disease association that simulates a real taxonomy by encoding the relationships among microbial features. The taxonomy-encoding architecture provides a natural bridge from variations in microbial taxa abundance to variations in traits, encompassing increasingly coarse scales from species to domains. MIOSTONE has the ability to determine whether taxa within the corresponding taxonomic group provide a better explanation in a data-driven manner. MIOSTONE serves as an effective predictive model, as it not only accurately predicts microbiome-trait associations across extensive simulated and real datasets but also offers interpretability for scientific discovery. Both attributes are crucial for facilitating in silico investigations into the biological mechanisms underlying such associations among microbial taxa. Video Abstract.

Research on finding alternative protein sources to replace fishmeal (FM) has become a central issue in the nutrition field. Extensive research has been carried out on the replacement of FM with soybean meal (SBM); however, little is known about the replacement of FM with enzyme-treated SBM (ESBM). In this study, five isolipidic and isonitrogenous diets were formulated by substituting FM with ESBM at the levels of 0% (FM, control diet), 5% (ESBM25), 10% (ESBM50), and 15% (ESBM75) which were fed to juvenile shrimp for 8 weeks. And we found that replacing FM with ESBM at 5%-10% levels in shrimp diets had no impact on shrimp growth performance and feed utilization. However, substituting 10% ESBM for FM in the shrimp diets promoted the expression of growth-related genes and maintained consistent intestinal microbiota compared to the control group. Replacing FM with 15% ESBM in the shrimp diets inhibited shrimp growth, suppressed mTOR gene expression, and promoted the proliferation of harmful intestinal bacteria. Furthermore, replacing FM with different ESBM did not affect the intestinal health of shrimp. Taken together, our research provides that replacing FM with 10% ESBM is feasible. These findings not only enrich our knowledge of FM proteinogen replacement but also provide a reference for the use of ESBM as a substitute for FM in commercial feeds for shrimp Penaeus vannamei as well as other shrimp species.

Human health is greatly influenced by the gut microbiota and microbiota imbalance can lead to the development of diseases. It is widely acknowledged that the interaction of bacteria within competitive ecosystems is influenced by their specialized metabolites, which act, e.g., as antibacterials or siderophores. However, our understanding of the occurrence and impact of such natural products in the human gut microbiome remains very limited. As arylthiazole siderophores are an emerging family of growth-promoting molecules in pathogenic bacteria, we analyzed a metagenomic data set from the human microbiome and thereby identified the bil-BGC, which originates from an uncultured Bilophila strain. Through gene synthesis and BGC assembly, heterologous expression and mutasynthetic experiments, we discovered the arylthiazole natural products bilothiazoles A-F. While established activities of related molecules indicate their involvement in metal-binding and -uptake, which could promote the growth of pathogenic strains, we also found antibiotic activity for some bilothiazoles. This is supported by biosensor-experiments, where bilothiazoles C and E show PrecA-suppressing activity, while bilothiazole F induces PblaZ, a biosensor characteristic for β-lactam antibiotics. These findings serve as a starting point for investigating the role of bilothiazoles in the pathogenicity of Bilophila species in the gut.

Dietary protein level and amino acid (AA) balance are crucial determinants of animal health and productivity. Supplementing rumen-protected AAs in low-protein diets was considered as an efficient strategy to improve the growth performance of ruminants. The colon serves as a crucial conduit for nutrient metabolism during rumen-protected methionine (RPMet) and rumen-protected lysine (RPLys) supplementation, however, it has been challenging to clarify which specific microbiota and their metabolites play a pivotal role in this process. Here, we applied metagenomic and metabolomic approaches to compare the characteristic microbiome and metabolic strategies in the colon of lambs fed a control diet (CON), a low-protein diet (LP) or a LP diet supplemented with RPMet and RPLys (LR).

The LP treatment decreased the average daily weight gain (ADG) in lambs, while the LR treatment tended to elicit a remission in ADG. The butyrate molar concentration was greater (P < 0.05), while acetate molar concentration (P < 0.05) was lower for lambs fed the LP and LR diets compared to those fed the CON diet. Moreover, the LP treatment remarkably decreased total AA concentration (P < 0.05), while LR treatment showed an improvement in the concentrations of methionine, lysine, leucine, glutamate, and tryptophan. Metagenomic insights proved that the microbial metabolic potentials referring to biosynthesis of volatile fatty acids (VFAs) and AAs in the colon were remarkably altered by three dietary treatments. Metagenomic binning identified distinct microbial markers for the CON group (Alistipes spp., Phocaeicola spp., and Ruminococcus spp.), LP group (Fibrobacter spp., Prevotella spp., Ruminococcus spp., and Escherichia coli), and LR group (Akkermansia muciniphila and RUG099 spp.).

Our findings suggest that RPMet and RPLys supplementation to the low-protein diet could enhance the microbial biosynthesis of butyrate and amino acids, enriche the beneficial bacteria in the colon, and thereby improve the growth performance of lambs.

This review examines the current state of the supply chain management for Dicentrarchus labrax (sea bass) and Sparus aurata (sea bream), two key commercial fish species in the Mediterranean. It provides a comprehensive analysis of sustainable innovations in aquaculture, processing, and packaging, with particular attention to circular economy-based biopreservation techniques. A major focus is on the Integrated Multi-Trophic Aquaculture (IMTA) system, an advanced farming approach that enhances sustainability, promotes circular resource utilization, and improves fish welfare. By fostering ecological balance through the co-cultivation of multiple species, IMTA contributes to the overall quality of fish products for human consumption. Beyond aquaculture, the review addresses the critical challenge of food loss, which stems from the high perishability of fish during storage and processing. In this regard, it highlights recent advancements in biopreservation strategies, including the application of antagonistic microorganisms, their metabolites, and plant-derived extracts. Particular attention is given to the development of edible antimicrobial films, with a focus on the valorization of citrus processing by-products for their production. By centering on innovations specific to the Mediterranean context, this review underscores that a holistic, integrative approach to supply chain management is essential for transitioning the aquaculture sector toward greater efficiency and sustainability.

There is mounting evidence for the involvement of the immune system, neuroinflammation and disturbed gut microbiota, or dysbiosis, in attention-deficit/hyperactivity disorder (ADHD). Gut dysbiosis is strongly implicated in many physical, autoimmune, neurological, and neuropsychiatric conditions, however knowledge of its particular pathogenic role in ADHD is sparse. As such, this narrative review examines and synthesizes the available evidence related to inflammation, dysbiosis, and neural processes in ADHD. Minimal differences in microbiota diversity measures between cases and controls were found, however many relative abundance differences were observed at all classification levels (phylum to strain). Compositional differences of taxa important to key gut-brain axis pathways, in particular Bacteroides species and Faecalibacterium, may contribute to inflammation, brain functioning differences, and symptoms, in ADHD. We have identified one possible model of ADHD etiopathogenesis involving systemic inflammation, an impaired blood-brain barrier, and neural disturbances as downstream consequences of gut dysbiosis. Nevertheless, studies conducted to date have varied degrees of methodological rigour and involve diverse participant characteristics and analytical techniques, highlighting a need for additional research.

We explored the mechanisms underlying the improvement of postoperative ileus (POI) following probiotic pretreatment. We assessed intestinal permeability, inflammation, tight junction (TJ) protein expression in the gut epithelium, and plasma interleukin (IL)-17 levels in a guinea pig model of POI.

Guinea pigs were divided into control, POI, and probiotic groups. The POI and probiotic groups underwent surgery, but the probiotic group received probiotics before the procedure. The ileum and proximal colon were harvested. Intestinal permeability was measured via horseradish peroxidase permeability. Inflammation was evaluated via leukocyte count in the intestinal wall muscle layer, and calprotectin expression in each intestinal wall layer was analyzed immunohistochemically. TJ proteins were analyzed using immunohistochemical staining, and plasma IL-17 levels were measured using an enzyme-linked immunosorbent assay.

The POI group exhibited increased intestinal permeability and inflammation, whereas probiotic pretreatment reduced the extent of these POI-induced changes. Probiotics restored the expression of TJ proteins occludin and zonula occludens-1 in the proximal colon, which were increased in the POI group. Calprotectin expression significantly increased in the muscle layer of the POI group and was downregulated in the probiotic group; however, no distinct differences were observed between the mucosal and submucosal layers. Plasma IL-17 levels did not significantly differ among the groups.

Probiotic pretreatment may relieve POI by reducing intestinal permeability and inflammation and TJ protein expression in the gut epithelium. These findings suggest a potential therapeutic approach for POI management.

In the last decade, it has been discovered that intestinal flora can affect various organ-specific cancers by altering the body's energy balance, synthesizing genetic toxins and small signaling molecules, and initiating and modulating immune responses. In this review, we will focus on elucidating the role of intestinal flora based on its molecular mechanisms and its possible impact on head and neck cancers in the near future, and explore how it may be a novel approach to treating head and neck cancers in the future.

The intestinal microenvironment represents a complex and dynamic ecosystem, comprising a diverse range of epithelial and nonepithelial cells, a protective mucus layer, and a diverse community of gut microbiota. Understanding the intricate interplay between these components is essential for uncovering the mechanisms underlying intestinal health and disease. The development of intestinal organoids, three-dimensional (3-D) mini-intestines that closely mimic the architecture, cellular diversity, and functionality of the intestine, offers a powerful platform for investigating different aspects of intestinal physiology and pathology. However, current intestinal organoid models, mainly adult stem cell-derived organoids, lack the nonepithelial and microbial components of the intestinal microenvironment. As such, several coculture systems have been developed to coculture intestinal organoids with other intestinal elements including microbes (bacteria and viruses) and immune, stromal, and neural cells. These coculture models allow researchers to recreate the complex intestinal environment and study the intricate cross talk between different components of the intestinal ecosystem under healthy and pathological conditions. Currently, there are several approaches and methodologies to establish intestinal organoid cocultures, and each approach has its own strengths and limitations. This review discusses the existing methods for coculturing intestinal organoids with different intestinal elements, focusing on the methodological approaches, strengths and limitations, and future directions.

Non-communicable diseases (NCDs), such as type 2 diabetes (T2D) and metabolic dysfunction-associated fatty liver disease, have reached epidemic proportions worldwide. The global increase in dietary sugar consumption, which is largely attributed to the production and widespread use of cheap alternatives such as high-fructose corn syrup, is a major driving factor of NCDs. Therefore, a comprehensive understanding of sugar metabolism and its impact on host health is imperative to rise to the challenge of reducing NCDs. Notably, fructose appears to exert more pronounced deleterious effects than glucose, as hepatic fructose metabolism induces de novo lipogenesis and insulin resistance through distinct mechanisms. Furthermore, recent studies have demonstrated an intricate relationship between sugar metabolism and the small intestinal microbiota (SIM). In contrast to the beneficial role of colonic microbiota in complex carbohydrate metabolism, sugar metabolism by the SIM appears to be less beneficial to the host as it can generate toxic metabolites. These fermentation products can serve as a substrate for fatty acid synthesis, imposing negative health effects on the host. Nevertheless, due to the challenging accessibility of the small intestine, our knowledge of the SIM and its involvement in sugar metabolism remains limited. This review presents an overview of the current knowledge in this field along with implications for future research, ultimately offering potential therapeutic avenues for addressing NCDs.

Advances in minimally invasive surgeries and pre-operative treatments allow the preservation of anal function through lower anastomosis in patients with rectal cancer, often necessitating temporary diverting stomas owing to the risk of anastomotic leakage. Stoma closure is associated with a high rate of surgical site infections (SSIs). Various measures, including purse-string skin sutures and negative-pressure wound therapy, have been implemented, and some guidelines recommend purse-string skin sutures as the standard method of stoma closure. However, at our institution, we used linear skin closure with an SSI reduction bundle. This study describes our stoma closure method and retrospectively analyses surgical outcomes.

This retrospective study included patients aged ≥ 20 years who underwent loop stoma closure using linear skin sutures at our institution between January 2006 and March 2021. Our protocol emphasises the following: (1) pre-operative oral anti-microbials, (2) a surgical technique that distinctly separates clean and contaminated regions, and (3) wound closure to eliminate dead space. We evaluated the surgical outcomes, including the incidence of SSIs and other post-operative complications.

Ninety-two patients (53 men, 39 women; mean age, 59.4 years) underwent loop stoma closure. SSIs occurred in two patients (2.2%). No risk factors for SSIs were identified.

In our department, the incidence of SSIs after linear skin closure of stomas was low. Adherence to proper infection prevention practices can effectively mitigate SSIs, even with linear skin closure.

The gut microbiota emerged as a potential modulator of brain connectivity in health and disease. This systematic review details current evidence on the gut-brain axis and its influence on brain connectivity. The initial set of studies included 532 papers, updated to January 2024. Studies were selected based on employed techniques. We excluded reviews, studies without connectivity focus, studies on non-human subjects. Forty-nine papers were selected. Employed techniques in healthy subjects included 15 functional magnetic resonance imaging studies (fMRI), 5 diffusion tensor imaging, (DTI) 1 electroencephalography (EEG), 6 structural magnetic resonance imaging, 2 magnetoencephalography, 1 spectroscopy, 2 arterial spin labeling (ASL); in patients 17 fMRI, 6 DTI, 2 EEG, 9 structural MRI, 1 transcranial magnetic stimulation, 1 spectroscopy, 2 R2*MRI. In healthy subjects, the gut microbiota was associated with connectivity of areas implied in cognition, memory, attention and emotions. Among the tested areas, amygdala and temporal cortex showed functional and structural differences based on bacteria abundance, as well as frontal and somatosensory cortices, especially in patients with inflammatory bowel syndrome. Several studies confirmed the connection between microbiota and brain functions in healthy subjects and patients affected by gastrointestinal to renal and psychiatric diseases.

The human gut flora of trillions of bacteria is vital for general health and greatly influences digestion, immune system function, and brain development. Through neuronal, hormonal, and immunological channels, the gut-brain axis (GBA), a bidirectional communication network, links the gut microbiota to the central nervous system (CNS). This relationship has been linked to affective diseases, including depression and anxiety, as well as mental health issues. This review explores the intricate relationship between gut bacteria and mood disorders, focusing on how gut microbiota-host interactions, immune system modulation, and neurotransmitter control support mental health. The function of important microbial metabolites, including short-chain fatty acids (SCFAs), in preserving blood-brain barrier integrity and modulating neuroinflammation is covered in this review. It also examines the bidirectional impact between gut health and mental health, including how dysbiosis could aggravate mood disorders and how depressed states might change the composition of gut bacteria. Furthermore, we discuss how psychotropic drugs affect gut flora and consider other elements such as nutrition and lifestyle that affect gut microbiome composition. Potential paths for treating mood disorders through gut microbiota modification are presented as emerging treatment techniques, including probiotics, nutritional therapies, and precision medicine. The development of new therapeutic approaches for mood disorders depends on the awareness of the GBA. Gut bacteria significantly affect mental health through immune modulation, neurotransmitter generation, and other intricate processes. Future studies should concentrate on large, varied populations to better understand these interactions and to create customized treatments that combine gut microbiota modulation with conventional mental health therapies.

The combination of artificial intelligence (AI) with microbial technology marks the start of a major transformation, improving applications throughout biotechnology, especially in healthcare. With the capability of AI to process vast amounts of biological big data, advanced microbial technology allows for a comprehensive understanding of complex biological systems, advancing disease diagnosis, treatment and the development of microbial therapeutics. This mini review explores the impact of AI-integrated microbial technologies in healthcare, highlighting advancements in microbial biomarker-based diagnosis, the development of microbial therapeutics and the microbial production of therapeutic compounds. This exploration promises significant improvements in the design and implementation of health-related solutions, steering a new era in biotechnological applications.

Lipopolysaccharide (LPS) destroys intestinal mechanical barrier and causes apoptosis by triggering oxidative stress and inflammatory responses. Glutamine (Gln) can maintain normal intestinal function under various stressed or pathological conditions. Thereby, this study aims to evaluate the protection of glutamine on intestinal health of snakehead (Channa argus), specifically regarding the NF-κB/MLCK/MLC2 signaling pathway mediated by tight junction affecting oxidative stress, inflammation and apoptosis. In this work, a model of intestinal tight junction injury in intestine of snakehead was constructed by injecting 4 mg/mL LPS into anus for 96 h. Before constructing the model, fish were treated with different levels of alanyl-glutamine (Ala-Gln) (0 %, 0.3 %, 0.6 %, 0.9 %, 1.2 % and 1.5 %) for 56 days. Microstructure and ultra microstructure showed that LPS-induced obvious intestinal damage and tight connection destruction, while Gln effectively alleviated these phenomena. In addition, results also showed that Gln can effectively inhibit LPS-induced damage to intestinal tight junction (zo-1, occludin, claudin5, claudin1, nf-κb p65, mlck and mlc2), alleviate oxidative stress (nrf2, sod, gsh, gpx and cat), ameliorate intestinal inflammation (tnf-α, il-1β, il-8, tlr5 and tlr2), thereby reduce apoptosis (p38mapk, caspase9, caspase8, caspase3 and bax). Crucially, the above results were related to NF-κB/MLCK/MLC2 signaling pathway mediated by tight junction. In conclusion, Gln has a good protective effect on LPS-induced intestinal injury in northern snakehead, providing a new perspective for regulating fish intestinal health.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS), characterized by neurodegeneration, axonal damage, demyelination, and inflammation. Recently, gut dysbiosis has been linked to MS and other autoimmune conditions. Namely, gut microbiota has a vital role in regulating immune function by influencing immune cell development, cytokine production, and intestinal barrier integrity. While balanced microbiota fosters immune tolerance, dysbiosis disrupts immune regulation, damages intestinal permeability, and heightens the risk of autoimmune diseases. The critical factor in shaping the gut microbiota and modulating immune response is diet. Research shows that high-fat diets rich in saturated fats are associated with disease progression. Conversely, diets rich in fruits, yogurt, and legumes may lower the risk of MS onset and progression. Specific dietary interventions, such as the Mediterranean diet (MD) and ketogenic diet, have shown potential to reduce inflammation, support neuroprotection, and promote CNS repair. Probiotics, by restoring microbial balance, may also help mitigate immune dysfunction noted in MS. Personalized dietary strategies targeting the gut microbiota hold promise for managing MS by modulating immune responses and slowing disease progression. Optimizing nutrient intake and adopting anti-inflammatory diets could improve disease control and quality of life. Understanding gut-immune interactions is essential for developing tailored nutritional therapies for MS patients.