Intestinal Mucosal Barrier Research Articles

Effects of ethanol extract from senna leaf (EESL) on inflammation and oxidative stress in mice: A non-targeted metabolomic study.

Senna leaf is a commonly used medication for treating constipation, and long-term use can cause damage to the intestinal mucosa and lead to drug dependence. But the exact mechanism remains unclear. Using non-targeted metabolomics technology to study the mechanism of senna leaf ethanol extract (EESL) inducing inflammation and oxidative stress in mice and causing side effects. EESL was administered to mice by gavage to detect inflammation and oxidative stressrelated factors in mice, and the EESL components and differential metabolites in mouse plasma were analyzed using non-targeted metabolome techniques. 23 anthraquinone compounds were identified in the EESL, including sennoside and their derivatives. Administration of EESL to mice resulted in a significant increase in pro-inflammatory factors, IL-1β, and IL-6 in the plasma, while the levels of IgA significantly decreased. The levels of oxidative stress significantly increased, and the intestinal mucosal integrity was impaired. 21 endogenous in plasma metabolites were identified as differential metabolites related with taurine and taurine metabolism, glycerophospholipid metabolism, arachidonic acid metabolism, tryptophan metabolism, and sphingolipid metabolism. These metabolic pathways are related to oxidative stress and inflammation. Senna leaf can inhibit the expression of tight junction proteins in the intestinal mucosa and disrupt intestinal mucosal barrier integrity, exacerbating oxidative stress and inflammation induced by bacterial LPS entering the bloodstream. In addition, the impact of Senna leaf on tryptophan metabolism may be linked to the occurrence of drug dependence.

Tryptophan Metabolites Improve Intestinal Mucosal Barrier via the Aryl Hydrocarbon Receptor-Interleukin-22 Pathway in Murine Dextran Sulfate Sodium-Induced Pouchitis.

Pouchitis is the commonest complication after ileal pouch-anal anastomosis for ulcerative colitis. The protective effect of tryptophan metabolites on the mucosal barrier may be an effective method for treating pouchitis. The role of tryptophan metabolites on pouchitis remained unclear. We aimed to establish a murine model of dextran sulfate sodium-induced pouchitis to examine the roles of tryptophan metabolites in its pathogenesis. This is a study combined clinical patient data and animal research. A total of 22 patients were enrolled: 5 with familial adenomatous polyposis after ileal pouch-anal anastomosis, eight ulcerative colitis patients after ileal pouch-anal anastomosis patients with pouchitis, and 9 ulcerative colitis patients after ileal pouch-anal anastomosis with normal pouch. The demographic data and fecal samples of patients were collected. Male C57BL/6 mice were purchased from a licensed breeder and underwent ileal pouch-anal anastomosis to establish murine model of pouch. The bloods, feces, tissues of mice were collected. This study was performed in an academic medical center in China. The demographic data of patients were observational collected. The mice underwent ileal pouch-anal anastomosis were divided into six groups: control group with chow diet, dextran sulfate sodium, 6-formylindolo[3,2-b] carbazole + dextran sulfate sodium, high tryptophan diet + dextran sulfate sodium, CH-223191 + dextran sulfate sodium, indole-3-carboxaldehyde + dextran sulfate sodium. Animals were sacrificed after dextran sulfate sodium for 7 days. Fecal tryptophan metabolite level and microbiome composition, the severity of pouchitis, intestinal mucosal barrier function, and activation of the aryl hydrocarbon receptor-interleukin 22 pathway were assessed. Patients with pouchitis had lower fecal microbial diversity and indole-3-acetic acid levels. In murine pouchitis model, high-tryptophan diet increased fecal levels of 3-indoleglyoxylic acid, indole-3-aldehyde, and indole. A high-tryptophan diet and intraperitoneal aryl hydrocarbon receptor ligand 6-formylindolo[3,2-b] carbazole injection alleviated pouchitis. Tryptophan metabolites improved pouch mucosal barriers. aryl hydrocarbon receptor inhibitors exacerbated experimental pouchitis and disrupted the mucosal barrier; however, the aryl hydrocarbon receptor ligand indole-3-carboxaldehyde reversed this effect. This study was limited by small human sample size and lacking an Aryl hydrocarbon receptor knockout mouse model. A high-tryptophan diet and aryl hydrocarbon receptor ligand alleviated dextran sulfate sodium-induced pouchitis in murine ileal pouch-anal anastomosis model, which might be through regulating epithelial tight junctions and promoting goblet-cell differentiation, as well as maintaining the integrity and function of the mucosal barrier. This study provides a rationale for the clinical application of Aryl hydrocarbon receptor ligands in the treatment of pouchitis. See Video Abstract.

GYY4137, as a slow-releasing H2S donor, ameliorates sodium deoxycholate–induced chronic intestinal barrier injury and gut microbiota dysbiosis

IntroductionNumerous studies have revealed that a long-term high-fat diet can raise intestinal deoxycholate acid concentration, which can harm intestinal mucosal barrier function in several ways. This study aims to verify the protective effect of GYY4137, as a slow-releasing H2S donor, on microbiome disturbance and the chronic injury of the intestinal mucosal barrier function caused by sodium deoxycholate.MethodsCaco-2 monolayer and mouse models were treated with a relatively high concentration of sodium deoxycholate (1.0 mM and 0.2%, respectively) for longer periods (32 h and 12 weeks, respectively) to understand the effects of GYY4137 on sodium deoxycholate–induced chronic intestinal barrier dysfunction and its fundamental mechanisms.ResultsA relatively long period of sodium deoxycholate treatment can remarkably increase the intestinal barrier permeability, alter the distribution and expression of tight junction proteins and generate the production of pro-inflammatory cytokines (TNF-α and IL-1β) in the Caco-2 monolayers and mouse models. Moreover, it can activate the MLCK-P-MLC2 pathway in the Caco-2 monolayers, which was further confirmed using RNA sequencing. The body weight, intestinal barrier histological score, and TUNEL index of sodium deoxycholate-treated mice worsened. In addition, an induced microbiome imbalance was observed in these mice. The above variations can be reversed with the administration of GYY4137.ConclusionThis study demonstrates that GYY4137 ameliorates sodium deoxycholate–induced chronic intestinal barrier injury by restricting the MLCK-P-MLC2 pathway while elevating the expression level of tight junction proteins, anti-apoptosis and maintaining the microbiome’s homeostasis.

Chicoric acid exerts therapeutic effects in DSS-induced ulcerative colitis by targeting the USP9X/IGF2BP2 axis.

Chicoric acid, a hydroxycinnamic acid, exhibits anti-inflammation activities. However, the specific mechanisms underlying the effects of chicoric acid on dextran sulfate sodium (DSS)-induced colitis remain unclear. Here, we aimed to elucidate the molecular mechanisms underlying the protective effects of chicoric acid in DSS-induced colitis. Mice with DSS-induced colitis (UC mice) were treated for a week with chicoric acid. Symptoms of colitis, colonic pathology, inflammation-related indicators, and intestinal mucosal barrier function were evaluated. RNA sequencing was performed on colon tissues to obtain differentially expressed genes. The deubiquitinating enzyme USP9X was selected, and the inhibitory and targeting effects of chicoric acid on USP9X were subsequently determined. In vivo and in vitro, DSS-induced colitis was treated with USP9X inhibitors WP1130 and EOAI3402143. Ubiquitination label-free quantitative proteomic analysis was performed to identify protein peptides that may undergo de-ubiquitination by USP9X. Co-immunoprecipitation (Co-IP), immunohistochemistry and western blotting were used to validate in vivo and in vitro results. Chicoric acid significantly alleviated clinical activity and histological changes, inhibited pro-inflammatory cytokine production and improved integrity of the intestinal barrier in UC mice. Moreover, chicoric acid suppressed USP9X expression in colonic tissues from UC mice. Furthermore, USP9X contributed to promoting the onset of UC and that insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) was deubiquitinated by USP9X. Chicoric acid ameliorated DSS-induced colitis by targeting the USP9X/IGF2BP2 axis, indicating that targeting the USP9X/IGF2BP2 axis presents a promising and innovative therapeutic approach for the treatment of UC.

Toxicological Characteristics of Bacterial Nanocellulose in an In Vivo Experiment-Part 2: Immunological Endpoints, Influence on the Intestinal Barrier and Microbiome.

Bacterial nanocellulose (BNC) is considered a promising alternative to microcrystalline cellulose, as well as an ingredient in low-calorie dietary products. However, the risks of BNC when consumed with food are not well characterized. The aim of this study is to investigate the impact of BNC on immune function, the intestinal microbiome, intestinal barrier integrity, and allergic sensitization in subacute experiments on rats. Male Wistar rats received BNC with a diet for eight weeks in a dose range of 1-100 mg/kg of body weight. The measurements of serum levels of cytokines, adipokines, iFABP2, indicators of cellular immunity, composition of the intestinal microbiome, and a histological study of the ileal mucosa were performed. In a separate four-week experiment on a model of systemic anaphylaxis to food antigen, BNC at a dose of 100 mg/kg of body weight did not increase the severity of the reaction or change the response of IgG antibodies. Based on dose-response effects on immune function, the non-observed adverse effect level for BNC was less than 100 mg/kg of body weight per day. The effects of BNC on the gut microbiome and the intestinal mucosal barrier were not dose-dependent. Data on the possible presence of prebiotic effects in BNC have been obtained.

Enteromorpha prolifera Polysaccharide Alleviates Acute Alcoholic Liver Injury in C57 BL/6 Mice through the Gut-Liver Axis and NF-κB Pathway.

Enteromorpha prolifera polysaccharide (EP2) protection against acute alcoholic liver injury (AALI) in mice was investigated. By integration of physiological indicators, gut microbiota, and short-chain fatty acids (SCFAs), the mechanism of EP2 in alleviating AALI was disclosed. The results showed that EP2 significantly ameliorated alcohol-induced abnormal transaminase activities, liver and intestinal systemic inflammation, and intestinal environmental disorders. EP2 significantly reduces liver and serum LPS contents by 1.69-fold and 1.54-fold. Furthermore, inhibition of the NF-κB signaling pathway by EP2 reduced the production of proinflammatory cytokines such as TNF-α (1.83-fold), IL-6 (11.09-fold), and IL-1β (1.99-fold). EP2 restored SCFAs to normal levels by upregulating the abundance of beneficial bacteria (Colidextribacter, Ruminococcus, unclassified_Lachnospiraceae, and Akkermansia). The alleviation of AALI by EP2 occurs through protection of the intestinal mucosal barrier and reduction of LPS permeating in serum. The decrease in LPS inactivates the NF-κB signaling pathway and prevents inflammation. In short, EP2 regulates the gut-liver axis and inflammation, alleviating effects in AALI mice.

Fecal Microbiota Transplantation Induced by Wumei Pills Improves Chemotherapy-Induced Intestinal Mucositis in BALB/c Mice by Modulating the TLR4/MyD88/NF-κB Signaling Pathway.

Our previous studies have found that Wumei Pills can regulate the intestinal flora to inhibit chemotherapy-induced intestinal mucositis (CIM). However, there is still insufficient evidence to confirm that intestinal flora is the main link in the regulation of CIM by Wumei Pills, and its downstream mechanism is still unclear. We first obtained the signal pathway of the intervention of Wumei Pill on CIM through network pharmacological analysis and then transplanted the bacterial solution into CIM mice, combined with Western Blot, HE, ELISA and other biological technology-related proteins and inflammatory factors. It showed that 97 kinds of effective ingredients and 205 kinds of targets of Wumei pills were screened out and the potential mechanism of Wumei Pills on CIM may be the NF-κB signaling pathway. In contrast with the control group, the results displayed that the weight, food intake, and mice's colon length were apparently decreased in the 5-Fu group, while the diarrhea score was increased. However, FMT reversed this change, and the difference was statistically significant. Additionally, FMT could improve the pathological state of inflammatory cell infiltration in mice, reduce histopathological scores of colon and jejunum, decrease the expression levels of IL-1β, MPO, TNF-α, and IL-6, reverse the activation of signaling pathway named TLR4/Myd88/ NF-κB and down-regulate protein expression, thereby exerting its anti-inflammatory activities. Further experiments have found that FMT could reverse the decreasing of tight junction proteins and mucins caused by 5-Fu, thereby repairing the intestinal mucosal barrier, and FMT could also increase the content of acetic acid, propanoic acid, and butanoic acid in the feces of 5-Fu group. FMT can defend the intestinal mucosal barrier integrality by increasing the content of exercise fatty acids, and its mechanism may be in connection with its inhibition of TLR4/My- D88/NF-κB signal pathway to relieve inflammation.

Therapeutic effects of fecal microbial transplantation on alcoholic liver injury in rat models

ObjectiveDisruption of gut microbiota is closely related to the progression of alcoholic liver disease (ALD). This study aimed to explore the therapeutic effect of fecal microbiota transplantation (FMT) in ALD rats using a combination of microbiological and metabolomic techniques. MethodsThree liver injury rat models were constructed using alcohol, CCL4, and alcohol combined with CCL4, and administered an FMT treatment comprising the fecal microbiota of healthy rats via the gastric route for 12 consecutive weeks. We measured the therapeutic effect of FMT treatment on liver inflammation, intestinal mucosal barrier, and bacterial translocation in ALD rats using 16S rRNA and UPLC-Q/TOF-MS technology to detect the effects of FMT on the intestinal microbiota and metabolic patterns of ALD rats. ResultsFMT treatment effectively improved liver function, prolonged survival time, improved the intestinal mucosal barrier, reduced bacterial translocation, alleviated liver inflammation, and delayed the progression of liver fibrosis in three types of liver injury models. The microbiome and metabolomic results showed that FMT can effectively improve gut microbiota disorder in ALD rats and improve metabolic patterns by regulating metabolic pathways such as the arachidonic acid and retinol pathways. ConclusionFMT treatment could reverse alcohol induced liver injury by improving gut microbiota and metabolic patterns in ALD rats, and oral FMT could be an effective therapeutic approach for ALD.

Cimicifuga heracleifolia kom. Attenuates ulcerative colitis through the PI3K/AKT/NF-κB signaling pathway

Ethnopharmacological relevanceCimicifuga heracleifolia Kom. (C. heracleifolia) has demonstrated efficacy in treating gastrointestinal disorders, including splenasthenic diarrhea. Ulcerative colitis (UC), a chronic inflammatory bowel disease, shares similarities with splenasthenic diarrhea. However, the pharmacological effects of C. heracleifolia on UC and the underlying mechanisms remain unexplored. Aim of the studyThe present study investigates the therapeutic potential and mechanisms of C. heracleifolia in UC. MethodsInitially, network pharmacology analysis, encompassing ingredient screening, target prediction, protein-protein interaction (PPI) network analysis, and enrichment analysis, was employed to predict the mechanisms of C. heracleifolia. The findings were further validated using transcriptomics and functional assays in a dextran sulfate sodium (DSS)-induced UC model. Additionally, bioactive compounds were identified through surface plasmon resonance (SPR) analysis, molecular docking, and cell-based assays. ResultsA total of 52 ingredients of C. heracleifolia were screened, and 32 key targets were identified within a PPI network comprising 285 potential therapeutic targets. Enrichment analysis indicated that the anti-UC effects of C. heracleifolia are mediated through immune response modulation and the inhibition of inflammatory signaling pathways. In vivo experiments showed that C. heracleifolia mitigated histological damage in the colon, reduced the expression of phosphorylated Akt1, nuclear factor-kappa B (NF-κB) p65, and inhibitor of Kappa B kinase α/β (IKKα/β), suppressed the content of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and enhanced the expression of tight junction proteins. Moreover, cimigenoside, caffeic acid, and methyl caffeate were identified as the bioactive constituents responsible for the UC treatment effects of C. heracleifolia. ConclusionsIn summary, this study is the first to demonstrate that C. heracleifolia exerts therapeutic effects on UC by enhancing the intestinal mucosal barrier and inhibiting the phosphatidylinositol 3-kinase (PI3K)/AKT/NF-κB signaling pathway. These findings offer valuable insights into the clinical application of C. heracleifolia for UC management.

Microbiota activation and regulation of adaptive immunity.

In the mucosa, T cells and B cells of the immune system are essential for maintaining immune homeostasis by suppressing reactions to harmless antigens and upholding the integrity of intestinal mucosal barrier functions. Host immunity and homeostasis are regulated by metabolites produced by the gut microbiota, which has developed through the long-term coevolution of the host and the gut biome. This is achieved by the immunological system's tolerance for symbiote microbiota, and its ability to generate a proinflammatory response against invasive organisms. The imbalance of the intestinal immune system with commensal organisms is causing a disturbance in the homeostasis of the gut microbiome. The lack of balance results in microbiota dysbiosis, the weakened integrity of the gut barrier, and the development of inflammatory immune reactions toward symbiotic organisms. Researchers may uncover potential therapeutic targets for preventing or regulating inflammatory diseases by understanding the interactions between adaptive immunity and the microbiota. This discussion will explore the connection between adaptive immunity and microbiota.

Retraction Note: Application of optical medical equipment imaging detection and fire needle therapy for intestinal mucosal barrier function in patients with intestinal diseases

Retraction Note: Application of optical medical equipment imaging detection and fire needle therapy for intestinal mucosal barrier function in patients with intestinal diseases

GZMA suppressed GPX4-mediated ferroptosis to improve intestinal mucosal barrier function in inflammatory bowel disease

BackgroundOur previous study has demonstrated a decreased colonic CD8+CD39+ T cells, enrichment of granzyme A (GZMA), was found in pediatric-onset colitis and inflammatory bowel disease (IBD) characterized by impaired intestinal barrier function. However, the influence of GZMA on intestinal barrier function remains unknown.MethodsWestern blotting(WB), real-time PCR (qPCR), immunofluorescence (IF) and in vitro permeability assay combined with intestinal organoid culture were used to detect the effect of GZMA on intestinal epithelial barrier function in vivo and in vitro. Luciferase, immunoprecipitation (IP) and subcellular fractionation isolation were performed to identify the mechanism through which GZMA modulated intestinal epithelial barrier function.ResultsHerein, we, for the first time, demonstrated that CD8+CD39+ T cells promoted intestinal epithelial barrier function through GZMA, leading to induce Occludin(OCLN) and Zonula Occludens-1(ZO-1) expression, which was attributed to enhanced CDX2-mediated cell differentiation caused by increased glutathione peroxidase 4(GPX4)-induced ferroptosis inhibition in vivo and in vitro. Mechanically, GZMA inhibited intestinal epithelial cellular PDE4B activation to trigger cAMP/PKA/CREB cascade signaling to increase CREB nuclear translocation, initiating GPX4 transactivity. In addition, endogenous PKA interacted with CREB, and this interaction was enhanced in response to GZMA. Most importantly, administration of GZMA could alleviate DSS-induced colitis in vivo.ConclusionThese findings extended the novel insight of GZMA contributed to intestinal epithelial cell differentiation to improve barrier function, and enhacement of GZMA could be a promising strategy to patients with IBD.

Dietary astragalin confers protection against lipopolysaccharide-induced intestinal mucosal barrier damage through mitigating inflammation and modulating intestinal microbiota.

The intestinal mucosal barrier (IMB) damage is intricately linked with the onset of numerous intestinal diseases. Astragalin (AS), a flavonoid present in numerous edible plants, exhibits notable antioxidant and anti-inflammatory properties, demonstrating a promising impact on certain intestinal ailments. In this study, our objective was to investigate the protective effects of AS and elucidate the underlying mechanisms by which it mitigates lipopolysaccharide (LPS)-induced damage to the IMB in mice. During the experimental period, mice were subjected to a 7-day regimen of AS treatment, followed by LPS injection to induce IMB damage. Subsequently, a comprehensive evaluation of relevant biological indicators was conducted, including intestinal pathological analysis, serum inflammatory factors, intestinal tight junction proteins, and intestinal microbiota composition. Our results suggested that AS treatment significantly bolstered IMB function. This was evidenced by the enhanced morphology of the small intestine and the elevated expression of tight junction proteins, including ZO-1 and Claudin-1, in addition to increased levels of MUC2 mucin. Moreover, the administration of AS demonstrated a mitigating effect on intestinal inflammation, as indicated by the reduced plasma concentrations of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α. Furthermore, AS treatment exerted a positive influence on the composition of the gut microbiota, primarily by augmenting the relative abundance of beneficial bacteria (including Lachnospiracea and Lactobacillus murinus), while simultaneously reducing the prevalence of the harmful bacterium Mucispirillum schaedleri. AS mitigates LPS-induced IMB damage via mitigating inflammation and modulating intestinal microbiota.

Differential intestinal microbes and metabolites between Behcet's uveitis and Fuchs syndrome

ObjectiveBehcet's uveitis (BU) is a type of uveitis with a high rate of blindness, characterized by anterior segment inflammation, vitreous opacity, and retinal vasculitis. Its pathogenesis is still unclear. Fuchs syndrome (Fuchs) is another common type of uveitis, which clinically presents with anterior segment inflammation and vitreous opacity, but rarely causes blindness. This study aims to compare the gut microbiota and metabolites of two different types of uveitis to clarify whether the differences in clinical manifestations are relevant to the alterations in gut microbiota. MethodsFaecal samples were collected from new-onset BU (n = 11) patients without systemic treatment and other diseases. 16S rRNA and liquid chromatography-tandem mass spectrometry (LC-MS/MS) were performed to analyze gut microbes and metabolites. Fuchs (n = 15) was used as the disease control, and healthy controls (n = 18) without autoimmune diseases and systemic medication were included. ResultsMicrobial composition and metabolite profiles differed significantly among the three groups. Compared to controls, Fusicatenibacter and eight metabolites were specifically altered in BU patients, and Pantoea and five metabolites in Fuchs. Pathways involving delta-tocopherol, palmitic acid, and serotonin are significantly disrupted in BU patients. Pathways involving linoleic acid are dysregulated considerably in Fuchs. Microbial markers consisting of 4 genera and 7 metabolites can respectively distinguish BU patients from controls. AUC values of metabolite markers were greater than those of microbial markers. Furthermore, serum zonulin levels were significantly elevated in both types of uveitis, with no difference between them. Correlation analysis revealed correlations between zonulin levels and multiple microbes. ConclusionsPatients with BU and Fuchs syndrome showed significant differences in gut microbiota and metabolites. Disruption of the intestinal mucosal barrier was observed in both types of uveitis. However, the mechanism of different intestinal microbiota causing different clinical manifestations needs to be studied in the future.

Multi-platform analysis revealed the substance basis and mechanism of Wei-Tong-Xin in ameliorating ENS dysfunction for dyspepsia treatment

Ethnopharmacological relevanceDuodenal motility disorder is a contributing factor to dyspepsia. The traditional Chinese medicine (TCM) formula Wei-Tong-Xin (WTX), originated from the famous ancient Chinese formula “Wan Ying Yuan”, has been demonstrated efficacy in alleviating dyspepsia. Aim of the studyThe current study aims to elucidate the chemical composition of WTX to establish the pharmacodynamic material basis. On the basis of component, in depth to illuminate the mechanism by which WTX treats dyspepsia via constructing the comprehensive analysis of multi-platform. Materials and methodsThe chemical constituents of WTX were systematically analyzed by UHPLC-Q-TOF-MS/MS data processing methods. Based on this, network pharmacology was employed to predict the mechanism by which WTX improved dyspepsia. The dyspepsia mouse model was constructed, and histopathology as well as intestinal permeability were assessed using H&E staining, PAS staining and FITC-dextran assay. Protein expression was detected using Western blot, immunofluorescence, immunohistochemistry and ELISA kits. ResultsA total of 100 chemical components of WTX were preliminarily identified. Network pharmacological analysis indicated that the therapeutic mechanism of WTX in treating dyspepsia may be related to the regulation of inflammation and oxidative stress-related signaling pathways. In vivo studies showed that WTX mitigated duodenal inflammation and oxidative stress responses, repairing the intestinal mucosal barrier damaged by cisplatin (CIS). Additionally, WTX restored the number of glial cells diminished by inflammatory damage, and ameliorated the serotoninergic neuronal dysfunction caused by insufficient secretion of glia-derived neurotrophic factor (GDNF), and enhanced intestinal transit. ConclusionsIn this study, a total of 100 components of the WTX extract were identified through literature review and mass spectrometry database search. Utilizing computer technology, in conjunction with pharmacodynamic and mechanistic studies, WTX has been found to restore serotoninergic neuronal function by reducing intestinal mucosal inflammatory and oxidative damage, ultimately promoting intestinal transport and treating dyspepsia.

Enhancing sepsis therapy: the evolving role of enteral nutrition.

Sepsis is a life-threatening organ dysfunction syndrome caused by a dysregulated response to infection in the body. Effective treatment of sepsis poses a significant challenge in today's clinical field. In recent years, enteral nutrition has garnered significant attention as an essential supportive therapeutic strategy. Serving as a means to provide ample nutritional support directly through the gastrointestinal tract, enteral nutrition not only addresses the nutritional depletion caused by the disease but also holds potential advantages in regulating immune function, maintaining intestinal mucosal barrier integrity, and promoting tissue repair. This article delves into the latest advancements of enteral nutrition in the treatment of sepsis, with a particular focus on its application effectiveness in clinical practice, potential mechanisms, and challenges faced. By examining relevant basic and clinical research, the aim is to provide a deeper understanding of nutritional therapy for sepsis patients and offer valuable insights for future research and clinical practice.

Expert consensus on the clinical application of bifidobacterium tetravaccine tablets for digestive diseases

Based on the fact that the human gut microbiota dysbiosis can cause various diseases, probiotics have a regulatory effect on human microecological imbalance and can be used to alleviate symptoms of some diseases and/or preventing and treating certain diseases. Probiotics have been widely applied in digestive diseases in both children and adults. Bifidobacterium tetravaccine tablets as a probiotic product contains Bifidobacterium infantis (CGMCC 0460.1), Lactobacillus acidophilus (CGMCC 0460.2), Enterococcus faecalis (CGMCC 0460.3), and Bacillus cereus (CGMCC 0460.4). By combining the unique characteristics of different strains, it exerts therapeutic effects through enhancing intestinal colonization resistance, improving intestinal mucosal barrier function, and modulating immune function, thereby maintaining gut and overall health. Bifidobacterium tetravaccine tablets have been widely used for digestive diseases, with a large number of fundamental and clinical research findings accumulated in the past years, a unified clinical guideline has yet to be achieved. To standardize and guide the rational clinical use of bifidobacterium tetravaccine tablets, this expert consensus have been formulated based on the summary and update of evidence-based medical data, providing a reference for its clinical application.

Mucosal Healing Research Advances of Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) refers to a group of chronic intestinal diseases, including Crohn's disease (CD) andulcerative colitis (UC). These diseases cause chronic inflammation of the intestinal mucosa and wall, leading to symptoms such as diarrhea, abdominal pain, constipation, fatigue, etc. Intestinal mucosal barrier can prevent microbial and other antigens enter the intestinal wall, maintain its healthy function. However, Immune system dysregulation, dysbiosis of the gut microbiome, and dysfunction of the intestinal epithelial barrier are key pathogenic mechanisms of IBD. The treatment of IBD remains an important medical challenge, the current treatment mainly by inhibiting immune activity, blocking certain inflammatory molecules. Although these methods can induce mucosal healing (MH), but infection and tumor adverse reactions associated with immunosuppression still need to solve. Therefore, researchers are exploring new treatments, to promote the healing of the intestinal mucosa and maintain intestinal health. This review summarizes the traditional treatment of IBD and the application of new technologies such as hydrogels, organoids, probiotics and prebiotics, which aim to safely and effectively promote mucosal barrier healing and restore intestinal function and balance.

Mucosal Healing Research Advances of Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) refers to a group of chronic intestinal diseases, including Crohn's disease (CD) and ulcerative colitis (UC). These diseases cause chronic inflammation of the intestinal mucosa and wall, leading to symptoms such as diarrhea, abdominal pain, constipation, fatigue, etc. Intestinal mucosal barrier can prevent microbial and other antigens enter the intestinal wall, maintain its healthy function. However, Immune system dysregulation, dysbiosis of the gut microbiome, and dysfunction of the intestinal epithelial barrier are key pathogenic mechanisms of IBD. The treatment of IBD remains an important medical challenge, the current treatment mainly by inhibiting immune activity, blocking certain inflammatory molecules. Although these methods can induce mucosal healing (MH), but infection and tumor adverse reactions associated with immunosuppression still need to solve. Therefore, researchers are exploring new treatments, to promote the healing of the intestinal mucosa and maintain intestinal health. This review summarizes the traditional treatment of IBD and the application of new technologies such as hydrogels, organoids, probiotics and prebiotics, which aim to safely and effectively promote mucosal barrier healing and restore intestinal function and balance.

Effects of cardamonin on the growth performance, intestinal barrier function and intestinal microbiota of Danzhou chickens under heat stress

The aim of this study was to investigate the effects of cardamonin (CDN) on the growth performance, intestinal mucosal barrier function and intestinal microbiota of Danzhou chickens under heat stress. A total of 200 one-day-old female Danzhou chickens were randomly divided into 5 groups. The daytime temperature of heat stress (HS) was set at 36 ± 2°C, and the nighttime temperature was kept the same as in the control (CON) group at 25 ± 2°C. The formal experiment lasted for 21 d. The CON and HS groups were fed a basal diet, whereas the L-CDN, M-CDN, and H-CDN groups received a basal diet supplemented with 50, 100, and 200 mg/kg CDN, respectively. Compared with the HS group, the CDN group presented a significantly greater average daily gain (ADG) (P < 0.001) but a significantly lower feed-to-gain ratio (F/G) (P = 0.007). CDN supplementation also increased the villus height (VH) and the ratio of the villus height to crypt depth (V/C) (P < 0.001) and reduced intestinal permeability by increasing expression of the ZO-1 (P < 0.001), Occludin (P < 0.001), and Claudin-1 (P = 0.034) proteins and decreasing the content of D-lactic acid (D-LA) and the activity of diamine oxidase (DAO) in serum (P < 0.001). Additionally, CDN reduced the levels of the intestinal mucosal inflammatory factors (IL-1β (P = 0.031), IL-6 (P = 0.003), and TNF-α (P = 0.014)) while upregulating IL-10 (P < 0.001). Furthermore, it increased the total antioxidant capacity (T-AOC) (P = 0.004) and catalase (CAT) activity (P < 0.001) and reduced the malondialdehyde (MDA) content (P = 0.017), effectively reducing intestinal oxidative stress and inflammatory reactions. Expression of the Nrf2 pathway-related proteins Nrf2 (P = 0.012), HO-1 (P = 0.008), and NQO1 (P = 0.003) was also increased by CDN. Moreover, feeding CDN increased the proportion of beneficial bacteria such as Firmicutes and Bacteroidetes but decreased the proportion of harmful bacteria such as Proteobacteria, thus protecting the intestinal barrier. In summary, 200 mg/kg CDN in the diet improved growth performance, enhanced intestinal barrier function and improved intestinal flora disorders in heat stress-induced Danzhou chickens, which may be related to the Nrf2/NQO1 signaling pathway.