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Infection and Immunity, February 2003, p. 830-837, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.830-837.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Effect of Inhibition of Extracellular Signal-Regulated Kinase 1 and 2 Pathway on Apoptosis and bcl-2 Expression in Helicobacter pylori-Infected AGS Cells

Il Ju Choi,1 Joo Sung Kim,2 Jung Mogg Kim,3 Hyun Chae Jung,2* and In Sung Song2

Center for Gastric Cancer, National Cancer Center, Goyang, Gyeonggi,1 Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, and Clinical Research Institute, Seoul National University Hospital,2 Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea3

Received 9 July 2002/ Returned for modification 20 September 2002/ Accepted 14 November 2002

Helicobacter pylori induces activation of mitogen-activated protein kinases (MAPKs). However, its effect on H. pylori-induced apoptosis has not been evaluated. Thus, we examined whether H. pylori-induced extracellular signal-regulated kinase 1 and 2 (ERK1/2) and p38 MAPK activation affects gastric epithelial cell apoptosis and bcl-2 family gene expression, especially in relation to the cagA status of an H. pylori strain. In flow cytometric and oligonucleosome-bound DNA enzyme-linked immunosorbent assay analyses, infection with cagA+ H. pylori strains induced gastric cancer cell apoptosis in AGS cells more prominently than infection with cagA mutants. Activation of ERK1/2 and p38 MAPKs was also more prominent in cagA+ strains. Pretreatment with a MEK inhibitor (PD98059) inhibited ERK1/2 activation and increased H. pylori-induced apoptosis significantly. This increased apoptosis was accompanied by decreased antiapoptotic bcl-2 mRNA expression among bcl-2-related genes (bcl-2, bax, bak, mcl-1, and bcl-XL/S), and the effect was also more prominent in the cagA+ strains. However, the alteration of bcl-2 gene expression was not accompanied by protein level changes. Inhibition of p38 using specific inhibitor SB203580 decreased H. pylori-induced apoptosis but resulted in little alteration of bcl-2-related gene expression. In conclusion, H. pylori-induced ERK1/2 activation, especially by the cagA+ H. pylori strain, may play a protective role against gastric epithelial cell apoptosis partially through maintenance of bcl-2 gene expression.

* Corresponding author. Mailing address: Department of Internal Medicine, Seoul National University College of Medicine, 28 Yungon-dong, Chongno-gu, 110-744 Seoul, Korea. Phone: 82 2 740 8112. Fax: 82 2 743 6701. E-mail: hyunchae{at}plaza.snu.ac.kr.

Editor: J. D. Clements

Infection and Immunity, February 2003, p. 830-837, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.830-837.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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