The contribution of toll-like receptor 2 on Helicobacter pylori activation of the nuclear factor-kappa B signaling pathway in gastric epithelial cells

Shu Li, Mei Cao, Liju Song, Panpan Qi, Chong Chen, Xuege Wang, Ningzhe Li, Jingshan Peng, Daoyan Wu, Guoku Hu, Jian Zhao

Research output: Contribution to journalArticle

9 Scopus citations


Helicobacter pylori (H. pylori) is a spiral shaped gram-negative bacterium that induces immune responses in the gastric mucosa. Toll-like receptors (TLRs) play important roles in mediating inflammatory cytokines by recognition of conserved molecular patterns on bacteria. Changes in the expression of toll-like receptor (TLR) 2, TLR4 and the relative inflammatory cytokines were analyzed in normal gastric epithelial GES-1 cells following treatment with H. pylori or Escherichia coli lipopolysaccharide (E. coli LPS) in order to investigate the contribution of TLRs in recognizing and mediating the inflammatory response to H. pylori, and study the differences in TLRs’ performance between H. pylori and E. coli. Specific inhibitors for the declines in TLR2 and TLR4 were also employed. The results showed that H. pylori infection increased TLR2 expression in GES-1 cells, but TLR4 remained unchanged regardless of H. pylori or TLR2 small interfering RNA treatment. Furthermore, the secretion of cyclooxygenase-2 (COX-2) induced by H. pylori was inhibited by declines in TLR2, but not in TLR4. In conclusion, TLR2 plays an even more important role than TLR4 not only in recognizing H. pylori, but also in the induction of inflammatory cytokines initiated by H. pylori. However, both TLR2 and TLR4 are necessary in mediating the inflammatory response to E. coli LPS.

Original languageEnglish (US)
Pages (from-to)63-68
Number of pages6
JournalMicrobial Pathogenesis
Publication statusPublished - Sep 1 2016



  • Cyclooxygenase-2
  • Escherichia coli lipopolysaccharide
  • Helicobacter pylori
  • Toll-like receptor 2
  • Toll-like receptor 4

ASJC Scopus subject areas

  • Microbiology
  • Infectious Diseases

Cite this