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Induction of monocyte chemoattractant protein 1 by Helicobacter pylori involves NF-kappa B

  1. Author:
    Mori, N.
    Ueda, A.
    Geleziunas, R.
    Wada, A.
    Hirayama, T.
    Yoshimura, T.
    Yamamoto, N.

  2. Author Address

    Nagasaki Univ, Inst Trop Med, Dept Prevent Med & AIDS Res, 1- 12-4 Sakamoto, Nagasaki 8528523, Japan. Nagasaki Univ, Inst Trop Med, Dept Prevent Med & AIDS Res, Nagasaki 8528523, Japan. Nagasaki Univ, Inst Trop Med, Dept Bacteriol, Nagasaki 8528523, Japan. Yokohama City Univ, Sch Med, Dept Internal Med 1, Yokohama, Kanagawa 232, Japan. Gladstone Inst Virol & Immunol, San Francisco, CA USA. NCI, Frederick Canc Res & Dev Ctr, Immunobiol Lab, Immunopathol Sect, Frederick, MD 21701 USA. Mori N Nagasaki Univ, Inst Trop Med, Dept Prevent Med & AIDS Res, 1-12-4 Sakamoto, Nagasaki 8528523, Japan.
    1. Year: 2001
  2. Journal: Infection and Immunity
    1. 69
    2. 3
    3. Pages: 1280-1286
  4. Type of Article: Article
  1. Abstract:

    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-kappaB-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-kappaB complexes containing p50 and p65. Kinase-deficient mutants of NF-kappaB- inducing kinase (NIK) and I kappaB kinases (IKK) caused suppression of MCP-1 distal enhancer-dependent reporter activity following H. pylori infection. H. pylori infection induces the activation of NF-kappaB via the NIK-IKK signaling complex, leading to MCP-1 gene transcription in gastric epithelial cells.

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