Background/Aims: CagA or cytotoxin-positive H. pylori may be associated with gastroduodenal diseases. However, controversies about this association also exist. Moreover, there could be geographic differences in the prevalence of virulence factors such as cagA or cytotoxin. It is also not clear whether there are substantial differences among clinical isolates which differ in bearing cagA or cytotoxin in the ability to induce IL-8 gene expression and protein secretion from the gastric epithelial cells. We performed this study 1) to determine the prevalence rate of the genes of virulence factor such as cagA and cytotoxin in H. pylori, 2) to test the ability of cagA cytotoxin', cagA cytotoxin or cagA cytotoxin H. pylori strain to evoke the proinflammatory cytokine expression in cultured gastric epithelial cells respectively. Methods: 1) The prevalence of the cagA gene in H. pylori strains isolated from Koreans was determined by PCR analysis. 2) Cytotoxin assay was performed by the concentrated broth supematants and HeLa cells(ATCC CCL2). 3) Proinflammatory cytokine gene expression was observed by RT-PCR analysis using the RNA extracted from human gastric epithelial cells such as Hs746T(ATCC HTB 135) and AGS(ATCC CRL 1739) infected with H. pylori. Cytokine proteins were also measured by ELISA. Results: 1) 96.8% of H. pylori isolates from Korean adults possessed cagA gene. And 80.6% of H. pylori strains have expressed vacuolating cytotoxicity against HeLa cells within 24 hours. 2) All cagAcytotoxin', cagAcytotoxin or cagA cytotoxin H. pylori strains could evoke the expression of cytokines such as IL-la/p, IL-8, MCP-1 and GM-CSF in the gastric epithelial cells. In case of IL-8, number of molecules of the expressed cytokine transcripts was parallel to the amounts of protein secreted from the gastric epithelial cells infected with H. pylori. Conclusions: These results suggest that H. pylori itself could give rise to express the proinflammatory cytokines in gastric epithelial cells regardless of possessing the known viru1ence factors of H. pylori. (Korean J Gastroenterol 1997;29:579-590)