TY - JOUR
T1 - The contribution of toll-like receptor 2 on Helicobacter pylori activation of the nuclear factor-kappa B signaling pathway in gastric epithelial cells
AU - Li, Shu
AU - Cao, Mei
AU - Song, Liju
AU - Qi, Panpan
AU - Chen, Chong
AU - Wang, Xuege
AU - Li, Ningzhe
AU - Peng, Jingshan
AU - Wu, Daoyan
AU - Hu, Guoku
AU - Zhao, Jian
N1 - Funding Information:
Shu Li and Mei Cao contributed equally to this work. This work was financially supported by National Natural Science Foundation of China ( 31270175 , 81301872 ). This was also supported by the Program for New Century Excellent Talents in University, the Fundamental Research Funds for the Central Universities and High Technology Research and Development Programs of Sichuan Province ( NCET-13-0397 , 2013SCU04B14 , and 2013GZX0161 ).
Publisher Copyright:
© 2016 Elsevier Ltd
PY - 2016/9/1
Y1 - 2016/9/1
N2 - 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.
AB - 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.
KW - Cyclooxygenase-2
KW - Escherichia coli lipopolysaccharide
KW - Helicobacter pylori
KW - Toll-like receptor 2
KW - Toll-like receptor 4
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U2 - 10.1016/j.micpath.2016.06.028
DO - 10.1016/j.micpath.2016.06.028
M3 - Article
C2 - 27364547
AN - SCOPUS:84976889179
SN - 0882-4010
VL - 98
SP - 63
EP - 68
JO - Microbial Pathogenesis
JF - Microbial Pathogenesis
ER -