Interaction between mucus layer and gut microbiota in non-alcoholic fatty liver disease: Soil and seeds / 中华医学杂志(英文版)

The intestinal mucus layer is a barrier that separates intestinal contents and epithelial cells, as well as acts as the "mucus layer-soil" for intestinal flora adhesion and colonization. Its structural and functional integrity is crucial to human health. Intestinal mucus is regulated by factors such as diet, living habits, hormones, neurotransmitters, cytokines, and intestinal flora. The mucus layer's thickness, viscosity, porosity, growth rate, and glycosylation status affect the structure of the gut flora colonized on it. The interaction between "mucus layer-soil" and "gut bacteria-seed" is an important factor leading to the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Probiotics, prebiotics, fecal microbiota transplantation (FMT), and wash microbial transplantation are efficient methods for managing NAFLD, but their long-term efficacy is poor. FMT is focused on achieving the goal of treating diseases by enhancing the "gut bacteria-seed". However, a lack of effective repair and management of the "mucus layer-soil" may be a reason why "seeds" cannot be well colonized and grow in the host gut, as the thinning and destruction of the "mucus layer-soil" is an early symptom of NAFLD. This review summarizes the existing correlation between intestinal mucus and gut microbiota, as well as the pathogenesis of NAFLD, and proposes a new perspective that "mucus layer-soil" restoration combined with "gut bacteria-seed" FMT may be one of the most effective future strategies for enhancing the long-term efficacy of NAFLD treatment.

Reduced expression of intestinal epithelial tight junction protein claudin-1 in mice with fulminant hepatic failure / 中国医师杂志

Objective To explore the expression change of intestinal epithelial tight junction (IJ)protein claudin-1 in mice with fulminant hepatic failure (FHF).Methods FHF was induced with a method that combined intraperitoneal injection of lipopolysaccharide (LPS,10 mg/kg) and D-galactosamine (GalN,800 mg/kg).Control saline (2 ml/kg,ip),LPS (10 mg/kg,ip) and GaIN (800 mg/kg,ip) were also detected.The effect of administration of anti-tumor necrosis factor alpha (TNF-α) IgG antibody (anti-TNF-α IgG,100 μg/per) on the level of TNF-α was assessed before administration of D-galactosamine/lipopolysaccharide.At the 2nd h,6th h,9th h,12th h,24th h after injection in FHF group,the 9th h after injection in control groups and 9th h after injection in anti-TNF-α IgG group,the mice were killed for the collection of large intestine specimens.Claudin-1 was analyzed with immunohistochemistry,Western blotting,and real-time quantitative PCR.Results Tight junction protein claudin-1 was localized along the apical region of the lateral plasma membrane representing the region of tight junctions in surface and crypt epithelial cells.Weakly distributed density of claudin-1 in intestinal mucosa was found in mice with FHF from the 9th h after injection.Compared to saline group,Western blotting analysis demonstrated markedly reduced claudin-1 expression in mice with FHF at the 6th h and 9th h after injection (6th h:0.8600±0.0208 vs 1.0,P ＜0.05; 9th h:0.6633 ±0.0328 vs 1.0,P ＜0.01).Furthermore,the expression of claudin-1 mRNA was markedly reduced at the 6th h,9th h,and 12th h after injection in mice with FHF (6th h:0.3067 ±0.1291 vs 1.0,P ＜0.05; 9th h:0.2233 ±0.1155 vs 1.0,P ＜0.01 ; 12th h:0.5275 ±0.1222 vs 1.0,P ＜0.05).Compared to saline group,no significant difference in claudin-1 expression was found with prophylactic treatment with anti-TNF-α-IgG antibody in mice with FHF at the 9th h after injection (protein:0.9533 ±0.0186 vs 1.0,P ＞0.05; mRNA:0.85 ±0.1437 vs 1.0,P ＞0.05).Conclusions The expression of tight junction protein claudin-1 was reduced at both protein and mRNA levels in intestinal epithelial cells that were induced by TNF-α in mice model of FHF.