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Porcine epidemic diarrhea (PED), a highly contagious enteric disease caused by the porcine epidemic diarrhea virus (PEDV), is characterized by vomiting, diarrhea, and dehydration, leading to high mortality in newborn piglets and significant economic losses in the swine industry. The shortage of effective PED vaccines emphasizes the need to explore potent natural compounds for therapeutic intervention. It has been shown that glycerol monolaurate (GML) effectively inhibits PEDV replication in vivo and in vitro. Further investigation is needed to assess whether complex medium-chain triglycerides (CMCTs), composed of glyceryl tricaprylate/caprate (GTCC) and GML, offer an efficient anti-PEDV activity. In this study, piglets were orally infected with PEDV and exhibited typical clinical signs, including diarrhea and vomiting, accompanied by intestinal inflammation, oxidative stress, and tissue damage. CMCTs were administered orally twice daily for one week. In vivo findings indicate that CMCT treatment alleviated clinical signs and prevented weight loss. It significantly increased serum immunoglobulins (IgG, IgM, and IgA) and intestinal mucosal sIgA and MUC-2 levels, while reducing pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, and IL-17) and increasing antiviral interferons (IFN-α and IFN-γ), anti-inflammatory cytokines (IL-4 and IL-10), and IL-22. Antioxidant enzyme activities (T-AOC, SOD, GSH-Px, and CAT) were elevated, whereas oxidative stress markers (iNOS, NO, and MDA) were decreased. Expression of intestinal tight junction proteins claudin-1 and ZO-1 was restored. Moreover, CD4+ and CD8+ T cell populations increased, and the functions of regulatory T cells (Tregs) were restored. Gut microbiota analysis showed increased beneficial genera (Streptococcus and Ligilactobacillus) and decreased pathogenic Escherichia-Shigella. These results demonstrate that CMCTs mitigate PEDV infection by enhancing anti-inflammation, antioxidation, and intestinal barrier function, as well as modulating gut microbiota composition. This study improves the understanding of the pathogenesis of PEDV and highlights CMCTs as a promising therapeutic candidate for PED.

IBS often appears as bloating, altered bowel patterns, and abdominal pain (AP).Probiotics and SCFA may be useful in mucosal repair and symptom relief, according to earlier research, however there is currently a lack of systematic evidence supporting their therapeutic effectiveness across a variety of IBS subtypes. To investigate the impacts of probiotics on signs and intestinal barrier function (IBF) in individuals with multiple IBS subtypes, and evaluate the role of SCFA in this process. A double-blind randomized controlled trial (DBRCT) design was adopted. Using the Rome IV criteria, a total of 120 individuals with IBS were randomised to either the probiotic group (PG) or placebo group (PLG). The intervention lasted for 12 weeks with an additional 4-week follow-up. In addition to fecal SCFA (FSCFA) levels, intestinal permeability (L/M ratio), tight junction proteins (TJP), serum/fecal inflammatory markers, and adverse event occurrence, the primary endpoint (PEP) evaluated was IBS Symptom Severity Scale (IBS-SSS) scores. Subgroup analysis was performed in selected cases. In terms of symptom scores, there was a major correlation among group and time (F=9.314, P<0.001), and repeated-measures ANOVA showed that the PG's scores were considerably < than those of the control group (CG) beginning in week 8 (all P<0.01). Levels of acetate, propionate, and butyrate considerably increased after 12 weeks of intervention (all P<0.01). Intestinal permeability and Occludin significantly improved at weeks 8 and 12 (all P<0.0167), while important differences in Claudin-1 and Zonulin appeared only at week 12 (all P<0.0167). Inflammatory markers considerably decreased at week 12 (all P<0.0167). There were no statistically significant differences in adherence or adverse events (P>0.05). Reductions in symptom scores were positively connected with an increase in SCFAs (r=0.43, P=0.002). Subgroup analysis across multiple IBS subtypes indicated significant symptom relief at week 12 for all subtypes (all P<0.05). Probiotics significantly improved clinical symptoms in IBS patients of different subtypes by increasing short-chain fatty acid levels, repairing the intestinal barrier, and reducing inflammation.

Inflammatory bowel disease (IBD) is characterized by intestinal mucosal damage that exacerbates inflammation and promotes disease recurrence. Although hydrogel‐based therapies have shown potential for mucosal repair, challenges remain due to inadequate targeting and low hydrogel density, leading to ongoing infiltration of harmful substances and delayed mucosal healing. In this study, an inflammation‐targeting‐triggered healing hydrogel (ITTH hydrogel) is developed, composed of polyvinyl alcohol‐alginate microgels (PALMs) and a cyclodextrin polymer crosslinker (CPC). This hydrogel specifically targets inflamed colonic sites and crosslinks in situ to form a dense network. The results demonstrate that the ITTH hydrogel adheres effectively to inflamed colonic tissue in both IBD mouse models and human samples. The dense crosslinked network acts like the mucosal barrier, preventing the penetration of detrimental substances such as bacteria and small molecules, thereby protecting the underlying mucosal tissue. Furthermore, the ITTH hydrogel significantly improved therapeutic outcomes in mice with dextran sulfate sodium (DSS)‐induced colitis. These findings suggest that the ITTH hydrogel is a promising candidate for in situ reconstruction of colonic mucosa and the treatment of IBD. Inflammatory bowel disease (IBD) involves mucosal damage that exacerbates inflammation and recurrence. This study introduces an inflammation‐targeting‐triggered healing (ITTH) hydrogel, which specifically targets inflamed colonic tissue and undergoes in situ re‐crosslinking to form a dense barrier. This barrier prevents harmful substance infiltration, protects mucosal tissue, and significantly improves therapeutic outcomes.

To determine the mechanisms by which Weizmannia coagulans SANK70258 (WC) supplementation improved growth performance and coccidial symptoms, we assessed the gene expressions and the microbiota compositions in the small intestinal tissues and digestas of coccidium-infected broilers previously given WC or lasalocid-A sodium (AM). WC supplementation significantly upregulated the gene expressions related to intestinal immunity and barrier functions, such as IL17A, IL17F, IL10, cathelicidin-2 and pIgR. Body weights, and Claudin-1 and IL10 expressions were positively correlated (r = 0.41, p < 0.05 and r = 0.37, p = 0.06, respectively), whereas lesion scores of the small intestine and IL17A expression were negatively correlated (r = −0.33, p = 0.09). The microbiota analysis detected that genus Alistipes was more abundant in WC-supplemented broilers than in control, and positively correlated with body weights and Claudin-1 expression (r = 0.61, p < 0.05 and r = 0.51, p < 0.05, respectively). Intriguingly, genus Enterococcus was most abundant in WC-supplemented broilers and positively correlated with IL17A expression (r = 0.49, p < 0.05). Interestingly, Escherichia-Shigella was significantly more abundant in the small intestinal digestas of AM-administered broilers than in those of control. To summarize, WC supplementation modulated and immunostimulated the microbiotas of broilers, specifically genera Alistipes and Enterococcus, which led to the improvement of weight gain and coccidial symptoms, without disrupting the intestinal microbiota compositions, as AM did.

The intestine is the largest interface between the internal body and the external environment. The intestinal barrier is a dynamic system influenced by the composition of the intestinal microbiome and the activity of intercellular connections, regulated by hormones, dietary components, inflammatory mediators, and the enteric nervous system (ENS). Over the years, it has become increasingly evident that maintaining a stable intestinal barrier is crucial to prevent various potentially harmful substances and pathogens from entering the internal environment. Disruption of the barrier is referred to as 'leaky gut' or leaky gut wall syndrome and seems to be characterized by the release of bacterial metabolites and endotoxins, such as lipopolysaccharide (LPS), into the circulation. This condition, mainly caused by bacterial infections, oxidative stress, high-fat diet, exposure to alcohol or chronic allergens, and dysbiosis, appear to be highly connected with the development and/or progression of several metabolic and autoimmune systemic diseases, including obesity, non-alcoholic fatty liver disease (NAFLD), neurodegeneration, cardiovascular disease, inflammatory bowel disease, and type 1 diabetes mellitus (T1D). In this review, starting from a description of the mechanisms that enable barrier homeostasis and analyzing the relationship between this complex ecosystem and various pathological conditions, we explore the role of the gut barrier in driving systemic inflammation, also shedding light on current and future therapeutic interventions.

The gut microbiota is now considered as one of the key elements contributing to the regulation of host health. Virtually all our body sites are colonised by microbes suggesting different types of crosstalk with our organs. Because of the development of molecular tools and techniques (ie, metagenomic, metabolomic, lipidomic, metatranscriptomic), the complex interactions occurring between the host and the different microorganisms are progressively being deciphered. Nowadays, gut microbiota deviations are linked with many diseases including obesity, type 2 diabetes, hepatic steatosis, intestinal bowel diseases (IBDs) and several types of cancer. Thus, suggesting that various pathways involved in immunity, energy, lipid and glucose metabolism are affected.In this review, specific attention is given to provide a critical evaluation of the current understanding in this field. Numerous molecular mechanisms explaining how gut bacteria might be causally linked with the protection or the onset of diseases are discussed. We examine well-established metabolites (ie, short-chain fatty acids, bile acids, trimethylamine N-oxide) and extend this to more recently identified molecular actors (ie, endocannabinoids, bioactive lipids, phenolic-derived compounds, advanced glycation end products and enterosynes) and their specific receptors such as peroxisome proliferator-activated receptor alpha (PPARα) and gamma (PPARγ), aryl hydrocarbon receptor (AhR), and G protein-coupled receptors (ie, GPR41, GPR43, GPR119, Takeda G protein-coupled receptor 5).Altogether, understanding the complexity and the molecular aspects linking gut microbes to health will help to set the basis for novel therapies that are already being developed.

Disruptions in the intestinal epithelial barrier can result in devastating consequences and a multitude of disease syndromes, particularly among preterm neonates. The association between barrier dysfunction and intestinal dysbiosis suggests that the intestinal barrier function is interactive with specific gut commensals and pathogenic microbes. In vitro and in vivo studies demonstrate that probiotic supplementation promotes significant upregulation and relocalization of interepithelial tight junction proteins, which form the microscopic scaffolds of the intestinal barrier. Probiotics facilitate some of these effects through the ligand-mediated stimulation of several toll-like receptors that are expressed by the intestinal epithelium. In particular, bacterial-mediated stimulation of toll-like receptor-2 modulates the expression and localization of specific protein constituents of intestinal tight junctions. Given that ingested prebiotics are robust modulators of the intestinal microbiota, prebiotic supplementation has been similarly investigated as a potential, indirect mechanism of barrier preservation. Emerging evidence suggests that prebiotics may additionally exert a direct effect on intestinal barrier function through mechanisms independent of the gut microbiota. In this review, we summarize current views on the effects of pro- and prebiotics on the intestinal epithelial barrier as well as on non-epithelial cell barrier constituents, such as the enteric glial cell network. Through continued investigation of these bioactive compounds, we can maximize their therapeutic potential for preventing and treating gastrointestinal diseases associated with impaired intestinal barrier function and dysbiosis.

Weaning is considered to be one of the most critical periods in pig production, which is related to the economic benefits of pig farms. However, in actual production, many piglets are often subjected to weaning stress due to the sudden separation from the sow, the changes in diet and living environment, and other social challenges. Weaning stress often causes changes in the morphology and function of the small intestine of piglets, disrupts digestion and absorption capacity, destroys intestinal barrier function, and ultimately leads to reduced feed intake, increased diarrhea rate, and growth retardation. Therefore, correctly understanding the effects of weaning stress on intestinal health have important guiding significance for nutritional regulation of intestinal injury caused by weaning stress. In this review, we mainly reviewed the effects of weaning stress on the intestinal health of piglets, from the aspects of intestinal development, and intestinal barrier function, thereby providing a theoretical basis for nutritional strategies to alleviate weaning stress in mammals in future studies.

Zonulin is the master regulator of endothelial and epithelium tight junctions, modulating both gut and blood-brain barriers. 3 We analysed stool faecal microbiota and plasma in 50 subjects who self-reported to be asymptomatic for gastrointestinal physical disorders; 22 volunteers met Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition criteria for a depressive disorder or an anxiety disorder (DEP/ANX), and 28 more were control reference subjects (NODEPANX). Figure 2; Plasma LPS endotoxin, zonulin and fatty acid-binding protein-2 (FABP2) blood markers of gut dysbiosis and gut permeability pathophysiological epithelium integrity. 3 4 Analysis of variance yielded significant mean differences (p<0.05) (see online supplementary material ). Funding: University of Florida Clinical and Translational Science Institute grant (BRS, CJP) from the National Center For Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR001427; National Institute of Health (NIH) grants HL33610, HL56921 (MKR, CJP); UM1 HL087366 (CJP); Gatorade Trust through funds distributed by the University of Florida, Department of Medicine (CJP); PCORI-OneFlorida Clinical Research Consortium CDRN-1501-26692 (CJP); and internal funds from the University of Florida Department of Physiology and Functional Genomics (BRS, MKR).

Correspondence to Prof An Hendrix, Laboratory of Experimental Cancer Research, Department of Radiation Oncology and Experimental Cancer Research, Ghent University, Ghent 9000, Belgium; an.hendrix@ugent.be We read with interest recent papers reporting on the impact of gut microbiota on several aspects of health and disease due to altered intestinal permeability resulting in systemic immune activation by pathogen-associated molecular patterns (PAMP), a process termed microbial translocation.1–4 Common to these studies is the analysis of systemic lipopolysaccharide (LPS), the major outer membrane PAMP of Gram-negative bacteria, to quantitatively assess microbial translocation. Online supplementary table 1 summarises individual patient characteristics; 25 donors asymptomatic of intestinal barrier dysfunction (12 healthy volunteers and 13 patients with cancer during chemotherapy without GI side effects suggestive for intestinal mucositis) and 24 patients with clinically well-defined intestinal barrier dysfunction (13 patients with IBD, 5 patients with cancer with radiation or chemotherapy-induced intestinal mucositis and 6 treatment-naive patients with HIV). [...]LPS-positive bacterial EV are present in plasma, are able to induce immune activation and correlate with impaired barrier integrity in patients diagnosed with IBD, HIV and cancer therapy-induced intestinal mucositis (figure 2).