Korean J Med.  2002 Feb;62(2):142-152.

Cyclooxygenase-2 expression and apoptosis in Helicobacter pylori-infected human gastric epithelial cells

Affiliations
  • 1Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea.
  • 2Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea. hyunchae@plaza.snu.ac.kr.

Abstract

BACKGROUND
Helicobacter pylori induces apoptosis and alters the proliferation of gastric mucosal epithelial cells. Cyclooxygenase-2 (COX-2) is an inducible form of COX for prostaglandin (PG) synthesis, which has been known to cause alteration in epithelial cell growth. In this study, we examined whether COX-2 gene expression by H. pylori infection could influence gastric epithelial cell apoptosis.
METHODS
Human gastric epithelial cells were infected with H. pylori, after which COX-2 gene expression was evaluated using quantitative reverse transcription polymerase chain reaction (RT-PCR). The level of PGE2 was determined in culture supernatants by radioimmunoassay. Apoptosis and caspase-3 activation were also measured in H. pylori-infected gastric epithelial cells.
RESULTS
Expression of COX-2 mRNA and proteins was upregulated in Hs746T gastric epithelial cell lines infected with H. pylori, when assessed by quantitative RT-PCR and Western blot. However, COX-1 mRNA expression in H. pylori-infected Hs746T cells did not change. The extent of COX-2 mRNA expression and PGE2 production was similar in cagA-positive and cagA-negative strains and was not correlated with the presence of vacuolating cytotoxin. H. pylori infection resulted in apoptosis of gastric epithelial cell lines such as Hs746T. However, inhibition of COX-2 expression by NS-398, a specific COX-2 inhibitor, showed a significant increase of apoptosis and caspase-3 activation in Hs746T cells infected with H. pylori compared with H. pylori-infected cells without NS-398 treatment. In contrast, valerylsalicylate, an inhibitor that is relatively specific to COX-1, did not change the apoptosis levels of H. pylori-infected gastric epithelial cells.
CONCLUSION
These results suggest that upregulated COX-2 expression by H. pylori infection can inhibit apoptosis of gastric epithelial cells.

Keyword

Apoptosis; Cyclooxygenase-2; Epithelial cell; Helicobacter pylori; Prostaglandin; Stomach

MeSH Terms

Apoptosis*
Blotting, Western
Caspase 3
Cyclooxygenase 2*
Dinoprostone
Epithelial Cells*
Gene Expression
Helicobacter pylori
Helicobacter*
Humans*
Polymerase Chain Reaction
Radioimmunoassay
Reverse Transcription
RNA, Messenger
Stomach
Caspase 3
Cyclooxygenase 2
Dinoprostone
RNA, Messenger
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