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Infection and Immunity, April 2000, p. 1806-1814, Vol. 68, No. 4
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
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-
B in
Gastric Epithelial Cancer Cells
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-
B
binding site. An inducible nuclear protein complex bound to the ICAM-1
NF-B site and was identified as the NF-B p50-p65 heterodimer.
H. pylori induced the degradation of IB-
, a major
cytoplasmic inhibitor of NF-B, and stimulated the expression of
IB- mRNA. Pretreatment of epithelial cells with pyrrolidine
dithiocarbamate, which blocks NF-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-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.
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