Lactobacillus plantarum CS24.2 prevents Escherichia coli adhesion to HT-29 cells and also down-regulates enteropathogen-induced tumor necrosis factor-α and interleukin-8 expression

Microbiol Immunol. 2013 Apr;57(4):309-15. doi: 10.1111/1348-0421.12038.

Abstract

The aim of the present study was to evaluate the potential of Lactobacillus plantarum CS24.2 to antagonize Escherichia coli adhesion and modulate expression of the responses by HT-29 cells of inflammatory molecules to E. coli adhesion. Experiments were performed under different adhesion conditions and findings compared with the responses of Lactobacillus rhamnosus GG. Tests of competitive adhesion, adhesion inhibition and displacement assays were performed for lactobacilli (L. rhamnosus GG and L. plantarum CS24.2) and E. coli O26:H11 to HT-29 cells. Both the lactobacilli significantly reduced E. coli adhesion to HT-29 cells (P < 0.05). The ability of lactobacilli to modulate tumor necrosis factor-α and interleukin-8 expression was analyzed in HT-29 cells stimulated with E. coli using qRT-PCR. L. plantarum CS24.2 significantly down regulated expression of both the genes induced by E. coli in HT-29 cells at 6 hr as well as 24 hr, which was more significant than the corresponding findings for L. rhamnosus GG. The present findings suggest that L. plantarum CS24.2 inhibits pathogen adhesion to a similar extent as does the established probiotic strain L. rhamnosus GG. It may also attenuate tumor necrosis factor-α and interleukin-8 expression in HT-29 cells stimulated with E. coli.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibiosis*
  • Bacterial Adhesion*
  • Down-Regulation / genetics
  • Escherichia coli / immunology
  • Escherichia coli / metabolism*
  • Gene Expression
  • HT29 Cells
  • Humans
  • Interleukin-8 / genetics
  • Interleukin-8 / metabolism*
  • Lactobacillus plantarum / immunology
  • Lactobacillus plantarum / metabolism*
  • Lactobacillus plantarum / pathogenicity
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Interleukin-8
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha