Helicobacter pylori-induced Apoptosis in Gastric Cancer Cell Lines

Kim, Won Ho; Yeo, Marie; Lee, Kkot Sil; Lee, Yong Chan; Park, In Suh; Lee, Kyong Won

Abstract

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-gamma 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.