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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-
B
Naoki
Mori,1,*
Atsuhisa
Ueda,2
Romas
Geleziunas,3,
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-
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-
B complexes
containing p50 and p65. Kinase-deficient mutants of NF-
B-inducing
kinase (NIK) and I
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-
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.

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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