Exploring Effects of Chitosan Oligosaccharides on the DSS-Induced Intestinal Barrier Impairment In Vitro and In Vivo

Molecules. 2021 Apr 11;26(8):2199. doi: 10.3390/molecules26082199.

Abstract

Intestinal barrier dysfunction is an essential pathological change in inflammatory bowel disease (IBD). The mucus layer and the intestinal epithelial tight junction act together to maintain barrier integrity. Studies showed that chitosan oligosaccharide (COS) had a positive effect on gut health, effectively protecting the intestinal barrier in IBD. However, these studies usually focused on its impact on the intestinal epithelial tight junction. The influence of COS on the intestinal mucus layer is still poorly understood. In this study, we explored the effect of COS on intestinal mucus in vitro using human colonic mucus-secreted HT-29 cells. COS relieved DSS (dextran sulfate sodium)-induced mucus defects. Additionally, the structural characteristics of COS greatly influenced this activity. Finally, we evaluated the protective effect of COS on intestinal barrier function in mice with DSS-induced colitis. The results indicated that COS could manipulate intestinal mucus production, which likely contributed to its intestinal protective effects.

Keywords: chitosan oligosaccharide; inflammatory bowel disease; intestinal barrier; intestinal tight junction; mucus.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Body Weight / drug effects
  • Caco-2 Cells
  • Chitosan / pharmacology*
  • Colitis / chemically induced
  • Colitis / drug therapy*
  • Colitis / genetics
  • Colitis / mortality
  • Dextran Sulfate / administration & dosage
  • Disease Models, Animal
  • Gene Expression Regulation
  • HT29 Cells
  • Humans
  • Intestinal Mucosa / drug effects*
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mucin-2 / genetics
  • Mucin-2 / metabolism
  • Occludin / genetics
  • Occludin / metabolism
  • Oligosaccharides / pharmacology*
  • Permeability / drug effects
  • Signal Transduction
  • Survival Analysis
  • Tight Junctions / drug effects*
  • Tight Junctions / metabolism
  • Tight Junctions / pathology

Substances

  • Anti-Inflammatory Agents
  • MUC2 protein, human
  • Mucin-2
  • OCLN protein, human
  • Occludin
  • Oligosaccharides
  • Chitosan
  • Dextran Sulfate