Wucheng Qi

Lactic acid bacteria (LAB) and their exopolysaccharides (EPS) are recognized to promote intestinal barrier function by mechanisms that remain incompletely understood. Herein, we sought to identify the roles of exopolysaccharides from Lactobacillus plantarum NCU116 (EPS116) in intestinal barrier function. Our data showed that EPS116 attenuated dextran sodium sulfate (DSS) induced colitis and promoted epithelial barrier function and the expression of tight junction (TJ) proteins in vivo and in vitro. Moreover, chromatin immunoprecipitation data showed that EPS116 facilitated STAT3 (signal transducer and activator of transcription 3) binding to the promoter of occludin and ZO-1. Furthermore, knockdown of STAT3 in Caco-2 cell with EPS116 treatment led to decreased expression of occludin and ZO-1 and increased intestinal permeability, suggesting that the regulation of epithelial barrier function by EPS116 should be STAT3 dependent. Thus, our data revealed a novel mechanism that EPS116 inhibited intestinal inflammation via regulating intestinal epithelial barrier function.

NCU116 (EPS116) regulated the barrier function and homeostasis of the intestine; however, the relevant mechanisms remain obscure. Therefore, we sought to explore the role of EPS116 in promoting intestinal epithelial regeneration. Our data showed that the administration of EPS116 markedly ameliorated inflammatory bowel disease-related phenotypes and promoted the regeneration of crypts in the colon of colitis mice. The results of immunofluorescence and reverse transcription-quantitative polymerase chain reaction experiments indicated that EPS116 strikingly increased the number of intestinal stem cells (ISCs) and the expression of differentiation markers for goblet cells, enterocytes, and enteroendocrine cells in the mouse colon. Intestinal microbiota analysis showed that EPS116 increased microbial populations associated with intestinal regeneration and glycan metabolism. Therefore, the present study revealed a novel model that EPS116 promoted the intestinal homeostasis through modulating the proliferation and differentiation of ISCs and altering the gut microbiota profile.