Journal
MICROBIAL PATHOGENESIS
Volume 98, Issue -, Pages 63-68Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.micpath.2016.06.028
Keywords
Helicobacter pylori; Escherichia coli lipopolysaccharide; Toll-like receptor 2; Toll-like receptor 4; Cyclooxygenase-2
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Funding
- National Natural Science Foundation of China [31270175, 81301872]
- Program for New Century Excellent Talents in University
- Fundamental Research Funds for the Central Universities
- High Technology Research and Development Programs of Sichuan Province [NCET-13-0397, 2013SCU04B14, 2013GZX0161]
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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. (C) 2016 Elsevier Ltd. All rights reserved.
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