4.7 Article

Mucins Dynamics in Physiological and Pathological Conditions

Journal

Publisher

MDPI
DOI: 10.3390/ijms222413642

Keywords

goblet cell; mucus barrier; Muc2 mucin; glycan; microbiota; inflammatory bowel diseases

Funding

  1. SNSF [310030_175548]
  2. Swiss National Science Foundation (SNF) [310030_175548] Funding Source: Swiss National Science Foundation (SNF)

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Maintaining intestinal health requires a clear segregation between epithelial cells and luminal microbes, which is achieved by the intestinal mucus layer produced by goblet cells. Disruption of goblet cells and mucus layer dysfunction are closely related to the pathogenesis of inflammatory bowel disease (IBD), but the molecular mechanisms regulating goblet cell physiology and the mucus layer remain unclear. Further research is needed to understand how internal (host) and external (diets and bacteria) factors modulate the mucus layer and its impact on the onset of IBD.
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.

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