State Key Laboratory of Food Science and Technology, China-Canada Joint Lab of Food Science and Technology (Nanchang) , Nanchang University , 235 Nanjing East Road , Nanchang , Jiangxi 330047 , China.
J Agric Food Chem. 2019 Sep 4;67(35):9831-9839. doi: 10.1021/acs.jafc.9b03939. Epub 2019 Aug 23.
Probiotic lactobacilli and their exopolysaccharides (EPS) are thought to modulate mucosal homeostasis; however, their mechanisms remain elusive. Thus, we tried to clarify the role of exopolysaccharides from NCU116 (EPS116) in the intestinal mucosal homeostasis. Our results indicated that EPS116 regulated the colon mucosal healing and homeostasis, enhanced the goblet cell differentiation, and promoted the expression of Muc2 gene in vivo and in vitro. Further experiments showed that EPS116 promoted the expression and phosphorylation of transcription factor c-Jun and facilitated its binding to the promoter of Muc2. Moreover, knocking down c-Jun or inhibiting its function in LS 174T cells treated with EPS116 led to decreased expression of Muc2, implying that EPS116 promoted the colonic mucosal homeostasis and Muc2 expression via c-Jun. Therefore, our study uncovered a novel model where EPS116 enhanced colon mucosal homeostasis by controlling the epithelial cell differentiation and c-Jun/Muc2 signaling.
益生菌乳杆菌及其胞外多糖（EPS）被认为可以调节黏膜稳态；然而，其机制仍不清楚。因此，我们试图阐明 NCU116（EPS116）的胞外多糖在肠道黏膜稳态中的作用。我们的结果表明，EPS116 调节结肠黏膜的愈合和稳态，增强杯状细胞的分化，并在体内和体外促进 Muc2 基因的表达。进一步的实验表明，EPS116 促进转录因子 c-Jun 的表达和磷酸化，并促进其与 Muc2 启动子的结合。此外，在 EPS116 处理的 LS 174T 细胞中敲低 c-Jun 或抑制其功能，导致 Muc2 的表达减少，表明 EPS116 通过 c-Jun 促进结肠黏膜稳态和 Muc2 的表达。因此，我们的研究揭示了一个新的模型，即 EPS116 通过控制上皮细胞分化和 c-Jun/Muc2 信号通路增强结肠黏膜稳态。
