Effect of the steroid receptor antagonist RU486 (mifepristone) on an IFN_γ-induced persistent Chlamydophila pneumoniae infection model in epithelial HEp-2 cells

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著者

    • ISHIDA Kasumi
    • Department of Medical Laboratory Sciences, Faculty of Health Sciences, Hokkaido University
    • YAMAZAKI Tomohiro
    • Department of Medical Laboratory Sciences, Faculty of Health Sciences, Hokkaido University
    • MOTOHASHI Kazuki
    • Department of Medical Laboratory Sciences, Faculty of Health Sciences, Hokkaido University
    • KOBAYASHI Miho
    • Department of Medical Laboratory Sciences, Faculty of Health Sciences, Hokkaido University
    • MATSUO Junji
    • Department of Medical Laboratory Sciences, Faculty of Health Sciences, Hokkaido University
    • OSAKI Takako
    • Laboratory of Molecular Microbiology, Department of Bioinformatics, Osaka University Graduate School of Medicine
    • HANAWA Tomoko
    • Laboratory of Molecular Microbiology, Department of Bioinformatics, Osaka University Graduate School of Medicine
    • KAMIYA Shigeru
    • Laboratory of Molecular Microbiology, Department of Bioinformatics, Osaka University Graduate School of Medicine
    • YAMAMOTO Yoshimasa
    • Division of Microbiology, Department of Infectious Disease, School of Medicine, Kyorin University
    • YAMAGUCHI Hiroyuki
    • Department of Medical Laboratory Sciences, Faculty of Health Sciences, Hokkaido University

抄録

We have previously demonstrated that the steroid receptor antagonist mifepristone (RU486) causes growth inhibition of Chlamydophila pneumoniae by binding to and subsequently destroying the bacteria during their normal developmental cycle in epithelial HEp-2 cells. In the present study, we assessed the efficacy of treatment with RU486 against persistent C. pneumoniae infection in interferon (IFN)γ-treated HEp-2 cells. Assessment of bacterial growth modification, the number of infectious progenies, the formation of inclusions, and the expressions of the C. pneumoniae genes 16S rRNA and hsp60 were investigated in cells with or without IFNγ stimulation in the presence of RU486, using an inclusion-forming unit (IFU) assay, fluorescence microscopic analysis, and reverse transcription polymerase chain reaction (RT-PCR), respectively. Our results indicated that RU486 treatment produced growth inhibition and an absence of C. pneumoniae gene expression in normal HEp-2 cells and that this treatment failed to inhibit C. pneumoniae growth in HEp-2 cells stimulated with IFNγ. These results indicate that treatment with RU486 had a limited effect on C. pneumoniae growth only during the active developmental stage of the bacteria, suggesting that the bacterial target molecule of RU486 is not expressed sufficiently during persistent infection in which there is an aberrant developmental cycle. Thus, our findings provide valuable insight into the complicated chlamydial biological processes involved in the recurrent cycling between normal and persistent infections.

収録刊行物

  • Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy

    Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy 18(1), 22-29, 2012-02-01

    日本化学療法学会・日本感染症学会

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