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

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タイトル: Effect of the steroid receptor antagonist RU486 (mifepristone) on an IFNγ-induced persistent Chlamydophila pneumoniae infection model in epithelial HEp-2 cells
著者: Ishida, Kasumi 著作を一覧する
Yamazaki, Tomohiro 著作を一覧する
Motohashi, Kazuki 著作を一覧する
Kobayashi, Miho 著作を一覧する
Matsuo, Junji 著作を一覧する
Osaki, Takako 著作を一覧する
Hanawa, Tomoko 著作を一覧する
Kamiya, Shigeru 著作を一覧する
Yamamoto, Yoshimasa 著作を一覧する
Yamaguchi, Hiroyuki 著作を一覧する
キーワード: Chlamydophila pneumoniae
Mifepristone
Steroid receptor antagonist
RU486
HEp-2
IFNγ
Persistent infection
発行日: 2012年 2月
出版者: 日本化学療法学会・日本感染症学会
誌名: Journal of Infection and Chemotherapy
巻: 18
号: 1
開始ページ: 22
終了ページ: 29
出版社 DOI: 10.1007/s10156-011-0274-6
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.
Rights: The original publication is available at www.springerlink.com
資料タイプ: article (author version)
URI: http://hdl.handle.net/2115/48266
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 山口 博之

 

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