Abstract
Recently, numerous studies have shown that disruption of the mucus barrier plays an important role in the exacerbation of inflammatory bowel disease, particularly in ulcerative colitis. Alterations in the mucus barrier are well supported by published data and are widely accepted. The use of fluorescence in situ hybridization and Carnoy’s fixation has revealed the importance of the mucus barrier in maintaining a mutualistic relationship between host and bacteria. Studies have raised the possibility that modulation of the mucus barrier may provide therapies for the disease, using agents such as short-chain fatty acids, prebiotics and probiotics. This review describes changes in the mucus barrier of patients with inflammatory bowel disease and in animal models of the disease. We also review the involvement of the mucus barrier in the exacerbation of the disease and explore the therapeutic potential of modifying the mucus barrier with short-chain fatty acids, prebiotics, probiotics, fatty acid synthase, H2S, neutrophil elastase inhibitor and phophatidyl choline.
Highlights
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic relapsing disorder characterized by inflammation and mucosal tissue damage of the gastrointestinal tract
Il10 ́{ ́ mice kept in a special pathogen free (SPF) environment, which display only minor signs of histological inflammation, still have a mucus layer that can be penetrated by both beads and bacteria
Some are(2): capable binding the mucus layer and and in docommensal so act as antagonists to thecommensal binding ofbacteria pathogen; Whenofthe mucustolayer mucus layer andpathogenic in do so act as antagonists themucus binding of pathogen; (2): When the mucus was destroyed, bacteria penetratetothe layer and bind to the epithelium and layer exert was destroyed, penetrate the mucus layer(SCFA)/prebiotics/probiotics/H
Summary
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic relapsing disorder characterized by inflammation and mucosal tissue damage of the gastrointestinal tract. Fluorescence in situ hybridization result of normal and colitis colon mucus layers in mice. 1. Fluorescence in situ hybridization result of normal colon mucus layers in mice. With implementation of new as fluorescence in situ hybridization and Carnoy’s the fixation, the composition and technologies, function of thesuch mucus barrier between the intestinal microbiota. The contact of microorganism surface [11] Colonic mucus of this twomechanism, layers: an inner adherent mucus layer with formsthe thecell physical barrier against bacteria, consists of two layers: an inner “firmly”. The secretion of mucin from the apical important maintaining this inner mucus layer free from. ItGoblet was reported that mucin secretion was markedly increased in mice during infection compared to cells in the upper crypt do not seem to synthesize enough mucin to meet a constant stimulus uninfected controls [6]. Increased sulfation sulfation and of mucin was found yield gelresistance with a higher viscosity, which is predicted to be more resistant to physical erosion [21]
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