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Infection and Immunity, March 2001, p. 1280-1286, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1280-1286.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Induction of Monocyte Chemoattractant Protein 1 by Helicobacter pylori Involves NF-kappa B

Naoki Mori,1,* Atsuhisa Ueda,2 Romas Geleziunas,3,dagger Akihiro Wada,4 Toshiya Hirayama,4 Teizo Yoshimura,5 and Naoki Yamamoto1

Department of Preventive Medicine and AIDS Research1 and Department of Bacteriology,4 Institute of Tropical Medicine, Nagasaki University, Nagasaki, and First Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama,2 Japan; Gladstone Institute of Virology and Immunology, San Francisco, California3; and Immunopathology Section, Laboratory of Immunobiology, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland5

Received 26 June 2000/Returned for modification 14 September 2000/Accepted 8 December 2000

Helicobacter pylori stimulates secretion of monocyte chemoattractant protein 1 (MCP-1) from gastric epithelial cells. Secretion of this chemokine may be instrumental in monocyte infiltration of the gastric epithelium that characterizes H. pylori gastritis. The aim of this study was to identify the mechanism by which H. pylori induces MCP-1 production. Induction of MCP-1 mRNA was assessed by reverse transcription-PCR. We used luciferase reporter assays to monitor activation of the MCP-1 gene promoter and electrophoretic mobility shift assays to explore binding of transcription factors to this promoter. H. pylori infection increased MCP-1 mRNA expression from gastric epithelial cells. Induction of MCP-1 mRNA relies on an intact cag pathogenicity island. We identified two closely spaced NF-kappa B-binding sites within the MCP-1 distal enhancer as required for H. pylori-induced MCP-1 gene transcription. H. pylori infection led to the specific activation of NF-kappa B complexes containing p50 and p65. Kinase-deficient mutants of NF-kappa B-inducing kinase (NIK) and Ikappa B kinases (IKK) caused suppression of MCP-1 distal enhancer-dependent reporter activity following H. pylori infection. H. pylori infection induces the activation of NF-kappa B via the NIK-IKK signaling complex, leading to MCP-1 gene transcription in gastric epithelial cells.

* 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.

dagger Present address: Dupont Pharmaceuticals Company, Wilmington, Del.

Infection and Immunity, March 2001, p. 1280-1286, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1280-1286.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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