NF-κB and Bcl-2 in Helicobacter pylori - Induced Apoptosis in Gastric Epithelial Cells

Sang Hui Chu, Joo Weon Lim, Kyung Hwan Kim, Hyeyoung Kim

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Abstract

Helicobacter pylori (H. pylori) has been considered as an important pathogen of gastroduodenal inflammation and gastric carcinogenesis. However, the pathogenic mechanisms including H. pylori-induced apoptosis and subsequent molecular mechanisms have not been clarified yet. The present study examined the role of Bcl-2 and its relation to NF-κB in H. pylori-induced apoptosis in human gastric epithelial AGS cells. AGS cells were cultured in the presence of H. pylori, at a bacterium/cell ratio of 300:1, for the determination of apoptosis, NF-κB activation with IκBα degradation, and Bcl-2 level. AGS cells were transfected with a control vector (pCMV cells) or a full-length human Bcl-2 expression vector (Bcl-2 cells). H. pylori-induced apoptosis and NF-κB activation were compared in the wild-type cells and the transfected cells. As a result, H. pylori increased apoptotic cells with chromatin condensation and reduced Bcl-2 levels, which were accompanied with NF-κB activation. H. pylori induced sixfold increase in the number of apoptotic cells in wild-type cells and pCMV cells. H. pylori-induced increment of apoptotic cells were relatively lower in Bcl-2 cells than pCMV cells. H. pylori-induced NF-κB activation and IκBα degradation were not different in the wild-type cells, pCMV cells, and Bcl-2 cells. In conclusion, the reduced gastric Bcl-2 level may be the main pathogenic mechanism of H. pylori-induced apoptosis in gastric epithelial cells.

Original languageEnglish
Pages (from-to)568-572
Number of pages5
JournalAnnals of the New York Academy of Sciences
Volume1010
DOIs
Publication statusPublished - 2003 Jan 1

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All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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