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Infection and Immunity, April 2000, p. 1806-1814, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Activation of Intercellular Adhesion Molecule 1 Expression by Helicobacter pylori Is Regulated by NF-kappa B in Gastric Epithelial Cancer Cells

Naoki Mori,1,* Akihiro Wada,2 Toshiya Hirayama,2 Thomas P. Parks,3 Christian Stratowa,4 and Naoki Yamamoto1

Department of Preventive Medicine and AIDS Research1 and Department of Bacteriology,2 Institute of Tropical Medicine, Nagasaki University, Nagasaki, Japan; Department of Inflammatory Diseases, Boehringer Ingelheim Pharmaceuticals, Incorporated, Ridgefield, Connecticut3; and Ernst Boehringer Institut, Vienna, Austria4

Received 22 September 1999/Returned for modification 19 November 1999/Accepted 28 December 1999

Interactions between leukocytes and epithelial cells may play a key role in Helicobacter pylori-associated gastric mucosal inflammation. This process is mediated by various cell adhesion molecules. The present study examined the molecular mechanisms leading to H. pylori-induced epithelial cell intercellular adhesion molecule-1 (ICAM-1; also called CD54) expression. Coculture of epithelial cells with cytotoxin-associated gene pathogenicity island-positive (cag PAI+) H. pylori strains, but not with a cag PAI- strain or H. pylori culture supernatants, resulted in upregulation of steady-state mRNA levels and cell surface expression of ICAM-1. Coculture with H. pylori induced an increase in luciferase activity in cells which were transfected with a luciferase reporter gene linked to the 5'-flanking region of the ICAM-1 gene. H. pylori activated the ICAM-1 promoter via the NF-kappa B binding site. An inducible nuclear protein complex bound to the ICAM-1 NF-kappa B site and was identified as the NF-kappa B p50-p65 heterodimer. H. pylori induced the degradation of Ikappa B-alpha , a major cytoplasmic inhibitor of NF-kappa B, and stimulated the expression of Ikappa B-alpha mRNA. Pretreatment of epithelial cells with pyrrolidine dithiocarbamate, which blocks NF-kappa B activation, inhibited H. pylori-induced ICAM-1 expression. THP-1 macrophagic cells, peripheral blood mononuclear cells, and purified neutrophils adhered to H. pylori-infected epithelial cells to a greater extent than to uninfected cells. These results show that H. pylori directly induces expression of ICAM-1 on gastric epithelial cells in an NF-kappa B-dependent manner that may support leukocyte attachment during inflammation.

* Corresponding author. Mailing address: Department of Preventive Medicine and AIDS Research, Institute of Tropical Medicine, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan. Phone: 81-95-849-7846. Fax: 81-95-849-7805. E-mail: n-mori{at}net.nagasaki-u.ac.jp.

Infection and Immunity, April 2000, p. 1806-1814, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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