Korean J Med.
2000 Aug;59(2):161-173.
Increase of apoptosis in human gastric epithelial cells infected with Helicobacter pylori and possible involvement of neutrophils
- Affiliations
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- 1Department of Microbiology, Hanyang University College of Medicine, Seoul, Korea.
- 2Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea.
- 3Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
- 4Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Abstract
- BACKGROUND
Infection with Helicobacter pylori activates a proinflammatory gene program in human gastric epithelial cells and is associated with significant epithelial cell damage. We evaluated whether immune mediators produced by neutrophils could modulate gastric epithelial cell apoptosis in response to H. pylori infection.
METHODS
After human gastric epithelial cells were infected with H. pylori in the presence of immune mediators, including tumor necrosis factor (TNT)alpha and Fas ligand (FasL), apoptosis and caspase-3 activity were assessed. The neutrophils were obtained from healthy volunteers, and Western blot analysis for FasL and quantitative reverse transcription polymerase chain reaction for TNFalpha transcripts were performed. Fas expression in gastric epithelial cells was explored by flow cytometric analysis.
RESULTS
Activation of caspase-3 was first apparent 12 hours after H. pylori infection, and the phenotypic expression of apoptosis was first apparent 18 hours after infection. The extent of apoptosis was similar in cases of cagA+cytotoxin+, cagA+cytotoxin-, cagA-cytotoxin- H. pylori- infected gastric epithelial cells. Approximately 20% of the Hs746T cells expressed Fas within 24 hours after H. pylori infection. The soluble FasL was upregulated in neutrophils after treatment with H. pylori-soluble proteins for 24 and 48 hours. The addition of TNFalpha and the soluble form of FasL, produced by neutrophils, significantly increased H. pylori-infected cell apoptosis and caspase-3 activation. However, the combination of these two immune mediators showed only an additive increase.
CONCLUSION
These results suggest that H. pylori-induced gastric epithelial cell apoptosis and caspase-3 activation can be modulated by the immune response of neutrophils.
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