Adhesion of H. pylori to gastric epithelial cells is
recognized as one of the essential steps in the development 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-