Adhesion of H. pylori to gastric epithelial cells is
recognized as one of the essential steps in the develop-
ment of gastritis, which leads to injection of the
definitive virulence factor, cytotoxin-associated antigen
A (CagA), through type-IV secretion systems.6,7) Several
reports have suggested that H. pylori inoculates CagA
into gastric epithelial cells inducing phosphorylations
of MEK, Src, and SHP-2, thereby promoting the
production of IL-8, IL-1, and tumor necrosis factor-