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.
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