Abstract
Maintaining intestinal health requires clear segregation between epithelial cells and luminal microbes. The intestinal mucus layer, produced by goblet cells (GCs), is a key element in maintaining the functional protection of the epithelium. The importance of the gut mucus barrier is highlighted in mice lacking Muc2, the major form of secreted mucins. These mice show closer bacterial residence to epithelial cells, develop spontaneous colitis and became moribund when infected with the attaching and effacing pathogen, Citrobacter rodentium. Furthermore, numerous observations have associated GCs and mucus layer dysfunction to the pathogenesis of inflammatory bowel disease (IBD). However, the molecular mechanisms that regulate the physiology of GCs and the mucus layer remain obscured. In this review, we consider novel findings describing divergent functionality and expression profiles of GCs subtypes within intestinal crypts. We also discuss internal (host) and external (diets and bacteria) factors that modulate different aspects of the mucus layer as well as the contribution of an altered mucus barrier to the onset of IBD.
Highlights
The epithelial surface of our gastrointestinal tract (GI) is formed by a single layer of active cells that separates immune cells from an enormous source of stimuli
Along with changes in gene expression, glycosylation or genetic polymorphisms associated with inflammatory bowel disease (IBD), several cellular processes have been shown to be involved in the modulation of mucin secretion and to play a key role in the pathogenesis of IBD
The mucus layer actively contributes to the host–microbiota mutualism
Summary
The epithelial surface of our gastrointestinal tract (GI) is formed by a single layer of active cells that separates immune cells from an enormous source of stimuli These include gut commensal bacteria, pathogens and food antigens [1]. Differences in terms of thickness and type of mucins exist within the different segments of the GI tract Numerous factors, such as cytokines, dietary, bacteria-derived factors and toxins, have been shown to modulate mucin turnover, including production, secretion and degradation processes, affecting the mucus barrier [5,6]. Heterogeneous Population distributed under the terms and Within the intestinal epithelium reside GCs, the primary secretory cells of the GI tract They are recognized by their apical accumulation of mucin containing granules (Figure 1A) and they display positive staining to PAS Alcian Blue stain (Figure 1B).
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