Abstract
The infection of Helicobacter pylori was thought to be related with human gastric diseases including peptic ulcer, lymphoma, gastric atrophy, and adenocaecinoma. Upon infection of gastric epithelial cells, Helicobacter pylori cytotoxin-associated gene A (CagA) is injected into epithelial cells via the type IV secretion system, which is dependent on cholesterol. Translocated CagA then co-localizes with the lipid raft marker GM1 and interacts with c-Src in which a tyrosine residue in the CagA Glu-Pro-Ile-Tyr-Ala (EPIYA) repeat region can be phosphorylated. In the present study, we found that CagA induction of IL-8 promoter activity in gastric epithelial cells was dependent on both of the presence of activator protein-1 (AP-1) and nuclear factor (NF)-kB binding sites, and cholesterol plays a crucial role in the pathway. Additionally, the EPIYA repeat region in the C-terminal domain was indispensable for CagA-induced interleukin (IL)-8 promoter activity, and this activity was dependent on cholesterol. Using multiple CagA truncation constructs, we showed that the C-terminal domain containing the EPIYA repeats was responsible for CagA-induced IL-8 promoter activity and for raft association. Our results suggest the importance of the EPIYA repeat region for interaction of CagA with lipid rafts and for CagA-induced pathogenesis.
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