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1,2,3Departments of Bacteriology1, Dermatology2 and Medicine and Medical Science3, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan 4Division of Bacteriology, Department of Infection and Immunity, Jichi Medical School, 3311-1 Yakushiji, Minami-Kawauchi-cho, Kouchi-Gun, Tochigi 329-0498, Japan 5Gastroenterology, Hiroshima City Hospital, 7-33 Moto-cho, Naka-ku, Hiroshima 730-8518, Japan 6National Research Institute of Police Science, 6-3-1 Kashiwanoha, Kashiwa 277-0882, Japan
Correspondence Kenji Yokota yokochan{at}md.okayama-u.ac.jp
Received August 18, 2004
Accepted October 25, 2004
Interleukin 8 (IL8) is usually produced in both epithelial and monocytic cells during bacterial infections, causing inflammation. Helicobacter pylori induces production of IL8 from gastric epithelial cells via its cag pathogenicity island (cag PAI) system, LPS and outer-membrane protein. In some bacteria, heat-shock protein 60 (HSP60) also elicits a strong pro-inflammatory response in cells of the innate immune system. Three recombinant H. pylori HSP60 (rHSP60) proteins of different sizes were produced and one of these was used to raise two monoclonal antibodies (2E7 and 7B5). IL8 production was found to be induced in cultured monocytic cells treated with H. pylori cells or rHSP60 proteins, as measured by ELISA, and the amount of IL8 produced was dose-dependent. Pre-incubation of H. pylori cells or rHSP60 preparations with the antibody 2E7 significantly inhibited IL8 production from monocytic cells. These results indicated that HSP60 is closely associated with IL8 production in monocytic cells.
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