<I>H. pylori</I>-Induced Gastric Mucosal Apoptosis

대한Helicobacter 연구학회지 2001;1(1):31-35.
Published online December 30, 2001.

H. pylori-Induced Gastric Mucosal Apoptosis

Helicobacter pylori 감염과 위점막 Apoptosis

김정목

한양대학교 의과대학 미생물학교실

Abstract

Apoptosis, a programmed cell death, is an essential mechanism of eliminating damaged or aged cells and thus contributing to maintain tissue integrity. In the stomach, mucosal surface epithelial cells are constantly exfoliating into the gastric lumen by apoptotic process and completely replaced within 3∼5 days under physiological conditions. Helicobacter pylori infection induces apoptosis in the gastric epithelial cell lines. The onset of apparent apoptosis in H. pylori- infected gastric epithelial cells is a relatively late event compared with expression kinetics of chemokines such as interleukin(IL)-8. The apoptosis appears to be independent of cagA gene status and vacuolating cytotoxin production of H. pylori strains. Activation of NF-ՊB, up-regulation of cyclooxygenase(COX)-2, and inducible nitric oxide synthase(iNOS) in H. pylori-infected gastric epithelial cells appear to promote cell survival and suppress signals for cell death. The apoptotic process may be induced directly by H. pylori, and be further up- regulated by immune responses, including TNF-Ձ and the soluble form of FasL produced by neutrophils. In addition, the water-soluble surface proteins of H. pylori may prolong the life-span of neutrophil through the inhibition of the apoptosis, indicating that the gastric mucosal inflammatory response could be enhanced by H. pylori infection. In summary, increased apoptosis of gastric epithelial cells and decreased apoptosis of neutrophils by H. pylori infection may be associated with development of several gastric diseases such as atrophic gastritis and gastric cancer. However, this hypothesis and the underlying genetic mechanism need to be tested and further clarified in the future. (Korean J Helicobacter Res Prac 2001;1:31-35)

Key Words: Apoptosis, Epithelial cell, Helicobacter pylori, Neutrophil, Stomach