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Helicobacter pylori infection activates NF-B signaling pathway to induce iNOS and protect human gastric epithelial cells from apoptosis

¹Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul 133-791; ²Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul 110-744; ³Department of Microbiology, Pochon CHA University College of Medicine, Kyunggi-do 487-800; and ⁴Department of Medical Genetics, Hanyang University College of Medicine, Seoul 133-791, Korea

Submitted 25 November 2002 ; accepted in final form 24 June 2003

Helicobacter pylori infection induces apoptosis and inducible nitric oxide synthase (iNOS) expression in gastric epithelial cells. In this study, we investigated the effects of NF-B activation and iNOS expression on apoptosis in H. pylori-infected gastric epithelial cells. The suppression of NF-B significantly increased caspase-3 activity and apoptosis in H. pylori-infected MKN-45 and Hs746T gastric epithelial cell lines as well as primary gastric epithelial cells. An NF-B signaling pathway via NF-B-inducing kinase and IB kinase- activation was found to be involved in the inhibition of apoptosis in H. pylori-infected gastric epithelial cells. In gastric epithelial cells transfected with retrovirus containing IB superrepressor, iNOS mRNA and protein levels were reduced, indicating that H. pylori infection induced the expression of iNOS by activating NF-B. Moreover, a NO donor, S-nitroso-N-acetylpenicillamine (100 µM), decreased caspase-3 activity and apoptosis in NF-B-suppressed cells infected with H. pylori. These results suggest that NF-B activation may play a role in protecting gastric epithelial cells from H. pylori-induced apoptosis by upregulating endogenous iNOS.

IB kinase; NF-B-inducing kinase; nitric oxide; superrepressor

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