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

Yujie Wang,Chen Zhang,Rong Wen,Zhuo A Wang,Dongdong Liu,Yuguang Du

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.

Highlights

Inflammatory bowel disease (IBD) is becoming a public health challenge worldwide with its increasing incidence and prevalence [1,2]
We introduced 2% of dextran sulfate sodium (DSS) to HT-29 and Caco-2 cells to recreate DSS-induced intestinal mucus and epithelium tight junction disruption and investigated the effect of chitosan oligosaccharide (COS) on the expression of MUC2 and occludin in cells
After incubation with 200 μg/mL COS for 24 h, we found that COS significantly alleviated DSS-induced damage on mucus by promoting MUC2 expression of HT-29 cells and increased the occludin expression of Caco-2 cells

Summary

Introduction

Inflammatory bowel disease (IBD) is becoming a public health challenge worldwide with its increasing incidence and prevalence [1,2]. Several IBD patients display severe intestinal barrier dysfunction followed by enhanced antigen and bacterial invasion [5]. Several studies have found that mice lacking MUC2 displayed severe impaired intestinal barrier and colitis [9,10]. The intestinal epithelium is composed of monolayer cells and acts as a physical barrier against harmful antigens permeation that aggravates intestinal inflammation [11]. The defection of the intestinal epithelium, such as a lack of the tight junction protein occludin, will increase intestinal permeability and bacterial translocation, followed by gut inflammation [12]. It has become another pathogenic factor of IBD [7]

Results

Discussion

Conclusion