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Helicobacter pylori heat-shock protein 60 induces inflammatory responses through the Toll-like receptor-triggered pathway in cultured human gastric epithelial cells.

Abstract

Contact between Helicobacter pylori and gastric epithelial cells results in activation of NF-kappaB followed by secretion of interleukin (IL)-8. However, host-cell receptor(s) and their ligands involved in H. pylori-related IL-8 production have yet to be fully defined. In this study, the interaction between Toll-like receptors (TLRs), which are host receptors for pathogens involved in the innate immune response, and heat-shock protein (HSP) 60, an immune-potent antigen of H. pylori, was examined during H. pylori-induced IL-8 secretion in vitro. Recombinant H. pylori HSP60 (rHpHSP60) was prepared and added to cultured KATO III human gastric epithelial cells with or without pre-incubation with mouse monoclonal anti-TLR2 or anti-TLR4 antibodies. IL-8 mRNA expression and IL-8 protein release were analysed by Northern blotting and immunoassay. Involvement of NF-kappaB activation was analysed immunocytochemically by anti-NF-kappaB p65 antibody and ammonium pyrrolidinedithiocarbamate (PDTC), an inhibitor of NF-kappaB-mediated transcriptional activation. rHpHSP60 induced IL-8 mRNA expression and IL-8 secretion in a dose-dependent manner in KATO III cells. Anti-TLR2 antibody inhibited rHpHSP60-induced IL-8 secretion by 75 %, and anti-TLR4 antibody inhibited it by 30 %. rHpHSP60 induced nuclear translocation of NF-kappaB p65, which was inhibited by pretreatment with anti-TLR2 antibody. Treatment with PDTC significantly decreased the secretion of IL-8 induced by rHpHSP60. These findings suggest that H. pylori HSP60 activates NF-kappaB and induces IL-8 production through TLR-triggered pathways in gastric epithelial cells. Thus, it is possible that H. pylori HSP60 and TLR interaction in host cells contributes to the development of gastric inflammation caused by H. pylori infection.

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  • Authors+Show Affiliations

    ,

    Department of Medicine and Medical Science (Medicine 1), Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.

    , , , , , , , , ,

    Source

    Microbiology (Reading, England) 150:Pt 12 2004 Dec pg 3913-22

    MeSH

    Animals
    Cell Line
    Chaperonin 60
    Epithelial Cells
    Gastric Mucosa
    Helicobacter pylori
    Humans
    Immunohistochemistry
    Inflammation
    Interleukin-8
    Membrane Glycoproteins
    Mice
    NF-kappa B
    Receptors, Cell Surface
    Toll-Like Receptor 2
    Toll-Like Receptor 4
    Toll-Like Receptors

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    15583145

    Citation

    Takenaka, Ryuta, et al. "Helicobacter Pylori Heat-shock Protein 60 Induces Inflammatory Responses Through the Toll-like Receptor-triggered Pathway in Cultured Human Gastric Epithelial Cells." Microbiology (Reading, England), vol. 150, no. Pt 12, 2004, pp. 3913-22.
    Takenaka R, Yokota K, Ayada K, et al. Helicobacter pylori heat-shock protein 60 induces inflammatory responses through the Toll-like receptor-triggered pathway in cultured human gastric epithelial cells. Microbiology (Reading, Engl). 2004;150(Pt 12):3913-22.
    Takenaka, R., Yokota, K., Ayada, K., Mizuno, M., Zhao, Y., Fujinami, Y., ... Oguma, K. (2004). Helicobacter pylori heat-shock protein 60 induces inflammatory responses through the Toll-like receptor-triggered pathway in cultured human gastric epithelial cells. Microbiology (Reading, England), 150(Pt 12), pp. 3913-22.
    Takenaka R, et al. Helicobacter Pylori Heat-shock Protein 60 Induces Inflammatory Responses Through the Toll-like Receptor-triggered Pathway in Cultured Human Gastric Epithelial Cells. Microbiology (Reading, Engl). 2004;150(Pt 12):3913-22. PubMed PMID: 15583145.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Helicobacter pylori heat-shock protein 60 induces inflammatory responses through the Toll-like receptor-triggered pathway in cultured human gastric epithelial cells. AU - Takenaka,Ryuta, AU - Yokota,Kenji, AU - Ayada,Kiyoshi, AU - Mizuno,Motowo, AU - Zhao,Ying, AU - Fujinami,Yoshihito, AU - Lin,Song-Nan, AU - Toyokawa,Tatsuya, AU - Okada,Hiroyuki, AU - Shiratori,Yasushi, AU - Oguma,Keiji, PY - 2004/12/8/pubmed PY - 2005/3/8/medline PY - 2004/12/8/entrez SP - 3913 EP - 22 JF - Microbiology (Reading, England) JO - Microbiology (Reading, Engl.) VL - 150 IS - Pt 12 N2 - Contact between Helicobacter pylori and gastric epithelial cells results in activation of NF-kappaB followed by secretion of interleukin (IL)-8. However, host-cell receptor(s) and their ligands involved in H. pylori-related IL-8 production have yet to be fully defined. In this study, the interaction between Toll-like receptors (TLRs), which are host receptors for pathogens involved in the innate immune response, and heat-shock protein (HSP) 60, an immune-potent antigen of H. pylori, was examined during H. pylori-induced IL-8 secretion in vitro. Recombinant H. pylori HSP60 (rHpHSP60) was prepared and added to cultured KATO III human gastric epithelial cells with or without pre-incubation with mouse monoclonal anti-TLR2 or anti-TLR4 antibodies. IL-8 mRNA expression and IL-8 protein release were analysed by Northern blotting and immunoassay. Involvement of NF-kappaB activation was analysed immunocytochemically by anti-NF-kappaB p65 antibody and ammonium pyrrolidinedithiocarbamate (PDTC), an inhibitor of NF-kappaB-mediated transcriptional activation. rHpHSP60 induced IL-8 mRNA expression and IL-8 secretion in a dose-dependent manner in KATO III cells. Anti-TLR2 antibody inhibited rHpHSP60-induced IL-8 secretion by 75 %, and anti-TLR4 antibody inhibited it by 30 %. rHpHSP60 induced nuclear translocation of NF-kappaB p65, which was inhibited by pretreatment with anti-TLR2 antibody. Treatment with PDTC significantly decreased the secretion of IL-8 induced by rHpHSP60. These findings suggest that H. pylori HSP60 activates NF-kappaB and induces IL-8 production through TLR-triggered pathways in gastric epithelial cells. Thus, it is possible that H. pylori HSP60 and TLR interaction in host cells contributes to the development of gastric inflammation caused by H. pylori infection. SN - 1350-0872 UR - https://www.unboundmedicine.com/medline/citation/15583145/Helicobacter_pylori_heat_shock_protein_60_induces_inflammatory_responses_through_the_Toll_like_receptor_triggered_pathway_in_cultured_human_gastric_epithelial_cells_ L2 - http://mic.microbiologyresearch.org/pubmed/content/journal/micro/10.1099/mic.0.27527-0 DB - PRIME DP - Unbound Medicine ER -