Cyclooxygenase-2 expression and apoptosis in Helicobacter pylori-infected human gastric epithelial cells.
- Author:
Jung Mogg KIM
1
;
Joo Sung KIM
;
Hyun Chae JUNG
;
In Sung SONG
;
Chung Yong KIM
Author Information
1. Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Apoptosis;
Cyclooxygenase-2;
Epithelial cell;
Helicobacter pylori;
Prostaglandin;
Stomach
- MeSH:
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
- From:Korean Journal of Medicine
2002;62(2):142-152
- CountryRepublic of Korea
- Language:Korean
-
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.
