Lactobacillus acidophilusSuppresses Colitis-Associated Activation of the IL-23/Th17 Axis

Abstract

The aim of this paper is to determine the modulatory effects ofLactobacillus acidophiluson the IL-23/Th17 immune axis in experimental colitis. DSS-induced mouse models of UC were to be saline, hormones, and different concentrations ofLactobacillus acidophilusintervention. The expression of interleukin- (IL-) 17, tumor necrosis factorα(TNFα), IL-23, transforming growth factorβ1 (TGFβ1), signal transducer and activator of transcription 3 (STAT3), and phosphorylated (p)-STAT3 was examined by RT-PCR, Western blotting, and immunohistochemical analysis. And the results showed that administration ofL. acidophilussuppressed Th17 cell-mediated secretion of proinflammatory cytokine IL-17 through downregulation of IL-23 and TGFβ1 expression and downstream phosphorylation of p-STAT3.