Lactobacillus acidophilus suppresses colitis-associated activation of the IL-23/Th17 axis

J Immunol Res. 2015;2015:909514. doi: 10.1155/2015/909514. Epub 2015 Apr 20.

Abstract

The aim of this paper is to determine the modulatory effects of Lactobacillus acidophilus on the IL-23/Th17 immune axis in experimental colitis. DSS-induced mouse models of UC were to be saline, hormones, and different concentrations of Lactobacillus acidophilus intervention. The expression of interleukin- (IL-) 17, tumor necrosis factor α (TNFα), IL-23, transforming growth factor β1 (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 of L. acidophilus suppressed Th17 cell-mediated secretion of proinflammatory cytokine IL-17 through downregulation of IL-23 and TGFβ1 expression and downstream phosphorylation of p-STAT3.

MeSH terms

  • Animals
  • Colitis / chemically induced
  • Colitis / immunology*
  • Colitis / therapy
  • Down-Regulation
  • Female
  • Interleukin-17 / biosynthesis*
  • Interleukin-23 Subunit p19 / biosynthesis
  • Interleukin-23 Subunit p19 / immunology
  • Lactobacillus acidophilus / metabolism*
  • Mice
  • Mice, Inbred BALB C
  • Probiotics / pharmacology*
  • STAT3 Transcription Factor / biosynthesis
  • Th17 Cells / immunology
  • Transforming Growth Factor beta1 / biosynthesis
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • Il17a protein, mouse
  • Il23a protein, mouse
  • Interleukin-17
  • Interleukin-23 Subunit p19
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Transforming Growth Factor beta1
  • Tumor Necrosis Factor-alpha