Legionella pneumophilaは、マクロファージ様U937細胞に感染するとmiR-218を介してRICTORを制御する

Material type: 博士論文

Author: 郡山, 豊泰

Publisher: Elsevier Inc.

Publication date: 2018

Material Format: Digital

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Name of awarding university/degree: 鹿児島大学,博士(医学),Doctor of Philosophy in Medical Science

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Note (General)：: 博士論文全文, 博士論文要旨, 最終試験結果の要旨, 論文審査の要旨Background: Inhalation of aerosolized Legionella pneumophila, a Gram-negative bacterium, can cause severe pneumonia....

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Material Type: 博士論文
Title: Legionella pneumophilaは、マクロファージ様U937細胞に感染するとmiR-218を介してRICTORを制御する
Author/Editor: 郡山, 豊泰
Author Heading: 郡山, 豊泰コオリヤマ, トヨヤス
Publication, Distribution, etc.: Elsevier Inc.
Publication Date: 2018
Publication Date (W3CDTF): 2018
Alternative Title: Legionella pneumophila infection-mediated regulation of RICTOR via miR-218 in U937 macrophage cells
Periodical title: Biochemical and Biophysical Research Communications
No. or year of volume/issue: 508 2
Volume: 508
Issue: 2
Pages: 608-613
Degree grantor/type: 鹿児島大学
Date Granted: 2019-03-19
Dissertation Number: 甲総研第493号
Degree Type: 博士(医学)
Doctor of Philosophy in Medical Science
Text Language Code: eng
Subject Heading: microRNA
Legionella
Rictor
macrophage
Target Audience: 一般
Note (General): 博士論文全文, 博士論文要旨, 最終試験結果の要旨, 論文審査の要旨
Background: Inhalation of aerosolized Legionella pneumophila, a Gram-negative bacterium, can cause severe pneumonia. During infection, L. pneumophila replicates intracellularly in macrophages. The involvement of host micro RNAs (miRNAs) in L. pneumophila infection is not fully understood. Methods: The human macrophage-like cell line U937 was infected with L. pneumophila. The levels of miRNA and messenger RNA (mRNAs) were measured using reverse transcriptase polymerase chain reaction. Release of lactate dehydrogenase was used to evaluate cytotoxicity The expression of RICTOR and related proteins was examined by western blotting of cell lysates. Results: L. pneumophila infection upregulated the expression of miR-218 and the host genes SLIT2 and SLIT3 in U937 cells. The expression of RICTOR, a component of the mechanistic target of rapamycin complex 2 (mTORC2), decreased during L. pneumophila infection. RICTOR protein expression was inhibited by the overexpression of miR-218, whereas knockdown of miR-218 restored the downregulation of RICTOR by L. pneumophila . L. pneumophila infection induced the expression of the proinflammatory cytokines IL-6 and TNF alpha, which was modulated by knockdown of miR-218 or RICTOR. Conclusions: Our study revealed the involvement of miR-218 in regulating the inflammatory response of macrophages against L. pneumophila infection. These findings suggest potential novel roles for miR-218 and RICTOR as therapeutic targets of L. pneumophila infection.
Format (IMT): application/pdf
Source: Diss_郡山_豊泰_ISK493_2018 （fulltext）
https://ir.kagoshima-u.ac.jp/record/14628/files/Diss_%E9%83%A1%E5%B1%B1_%E8%B1%8A%E6%B3%B0_ISK493_2018%EF%BC%88%E8%91%97%E8%80%85%E6%9C%80%E7%B5%82%E7%A8%BF%EF%BC%89.pdf
Access Restrictions: インターネット公開
Related Material: Biochemical and Biophysical Research Communications
https://www.sciencedirect.com/journal/biochemical-and-biophysical-research-communications
Related Material (DOI): 10.1016/j.bbrc.2018.11.093
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 鹿児島大学 : 鹿児島大学リポジトリ