Abstract

G A A b st ra ct s a significant increase in PELI1 mRNA expression. PELI1 knock-down inhibited TLR2mediated activation of NF-κB and the IL-8 promoter in response to Pam2CSK4 and H. pylori LPS. Conversely, TRIB3 knock-down enhanced NF-κB and IL-8 promoter activity in response to Pam2CSK4 and H. pylori LPS. Furthermore, over-expression of TRIB3 resulted in a dose dependent inhibition of the activating properties Pam2CSK4 and H. pylori LPS. Conclusions: PELI1 positively regulates TLR2-mediated signaling in response to H. pylori LPS, while TRIB3 has a negative effect. Further studies are required to investigate the expression of these proteins in gastric epithelial cells from H. pylori-infected patients. By identifying new regulators of H. pylori-induced cell signaling events, potential therapeutic targets to treat H. pylori-associated disease may be revealed.

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