Helicobater pylori에 의한 위암세포주 사멸 ; Helicobacter pylori-induced Apoptosis in Gastric Cancer Cell Lines

Background/Aims: Helicobacter pylori (H. pylori) is associated with active gastritis and peptic ulcer disease. Mechanism for H. pylori-induced gastric epithelial damage is still incompletely understood. However, the increase of apoptotic cells in H. pylori-infected mucosa suggested that apoptosis could be a major mechanism for cellular damage. As an effort to clarify the mechanism, we investigated whether H. pylori directly induce apoptosis in gastric cancer cells in vitro. Methods: Cultured H. pylori (ATCC 43504) were suspended as 109/mL. IL (interleukin)-8 was measured by enzyme linked immunosorbent assay. Cell survival was assessed by MTT [3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. Apoptosis was detected and confirmed by demonstration of DNA fragmentation and morphologic changes. Results: H. pylori induced IL-8 production as well as decrease of cell survival in gastric cancer cell lines in a time- and concentration-dependen way. Addition of H. pylori to gastric cancer cells induced apoptosis. Such induction was not organ specific. Heat or formalin treatment of H. pylori almost completely inhibited IL-8 production but only partially blocked apoptosis. H. pylori- induced apoptosis was potentiated by interferon-γ pretreatment in HT-29 but not in AGS and KATO III. Conclusions: These results suggest that H. pylori affects on gastric epithelial cell growth by direct induction of apoptosis. ; open