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Infection and Immunity, March 2006, p. 1452-1461, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1452-1461.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Helicobacter pylori Induces IB Kinase Nuclear Translocation and Chemokine Production in Gastric Epithelial Cells

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

Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

Received 14 September 2005/ Returned for modification 3 November 2005/ Accepted 21 December 2005

NF-B is an important transcriptional factor that is involved in multiple cellular responses, such as inflammation and antiapoptosis. IB kinase (IKK) and IKKß, which are critical regulators of NF-B activity, possess various mechanisms for NF-B activation. This variability in NF-B signaling may be associated with distinct inflammatory responses in specific cell types. The gastric pathogen Helicobacter pylori is known to activate NF-B. However, the role of IKK in H. pylori infection remains unclear. In this report, we show that H. pylori activates both IKK and IKKß in gastric cancer cells and enhances NF-B signaling in distinct manners. We found that IKKß acted as an IB kinase during H. pylori infection, whereas IKK did not. H. pylori induced IKK nuclear translocation in time-, multiplicity of infection-, and cag pathogenicity island-dependent manners. In contrast, p100 processing, which is a known IKK activity induced by several cytokines, was not induced by H. pylori. Both IKKs were responsible for chemokine secretion by infected cells. However, the antiapoptotic effect of H. pylori was merely transduced by IKKß. Microarray analysis and real-time PCR indicated that both IKKs were involved in the transcriptional activation of genes associated with inflammation, antiapoptosis, and signal transduction. Our results indicate that H. pylori activates NF-B via both IKK and IKKß using distinct mechanisms. IKK nuclear translocation induced by H. pylori is indispensable for appropriate inflammatory responses but not for antiapoptosis, which suggests a critical role for IKK in gastritis development.

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* Corresponding author. Mailing address: Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Phone: 81-3-3815-5411. Fax: 81-3-3814-0021. E-mail: yohirata-tky{at}umin.ac.jp.

Editor: J. B. Bliska

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Infection and Immunity, March 2006, p. 1452-1461, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1452-1461.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

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