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Helicobacter pylori Activates NF-B via the Alternative Pathway in B Lymphocytes

Tomoya Ohmae^1,*, Yoshihiro Hirata^*, Shin Maeda^*,, Wataru Shibata^*, Ayako Yanai^*,, Keiji Ogura^*, Haruhiko Yoshida^*, Takao Kawabe^* and Masao Omata^*

^* Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan and Division of Gastroenterology, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan

Helicobacter pylori causes various gastroduodenal diseases including gastric MALT lymphoma, but the mechanism underlying H. pylori-induced carcinogenesis is not known. The alternative pathway for NF-B activation, which involves the processing of NF-B2/p100 to p52, has been implicated in lymphocyte survival, attenuated apoptosis, and secondary lymphoid tissue development. In this study, we investigated H. pylori-induced activation of NF-B through the alternative pathway in B lymphocytes. In immunoblot and EMSA, H. pylori induced NF-B2/p100 processing to p52 and subsequent nuclear accumulation in IM-9 (human B cell line) cells and human peripheral blood B cells, but not in AGS (human gastric cancer cell line) cells. The activation of the alternative pathway was LPS-dependent but not cag pathogenicity island-dependent. Alternative pathway activation by H. pylori was associated with attenuated apoptosis. The expression levels of B lymphocyte chemoattractant, EBI-1 ligand chemokine, and stromal cell-derived factor-1 mRNAs were up-regulated in cocultured human B cells and in infected human gastric mucosa. In the infected mucosa, NF-B2/p100 and p52 were detected immunohistochemically in the cytoplasm and nuclear compartments of lymphocytes, but not in epithelial cells. In summary, H. pylori activates the alternative NF-B pathway in B lymphocytes. The effects on chemokine production and antiapoptosis mediated by H. pylori-induced processing of NF-B2/p100 to p52 may drive lymphocytes to acquire malignant potential.

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