IL-17A Activated by Toll-Like Receptor 9 Contributes to Development of Septic Acute Kidney Injury 1

• Material Type: 博士論文
• Title: IL-17A Activated by Toll-Like Receptor 9 Contributes to Development of Septic Acute Kidney Injury
• Volume: 318 1
• Author/Editor: 内藤, 善隆
• Author Heading: 内藤, 善隆
• Publication, Distribution, etc.: American Physiological Society
• Publication Date: 2020-01-09
• Publication Date (W3CDTF): 2020-01-09
• Alternative Title: Toll様受容体9によるインターロイキン-17Aの活性化は敗血症性急性腎障害の進展に寄与する
• Periodical title: American journal of physiology. Renal physiology
• Degree grantor/type: 浜松医科大学
• Date Granted: 2020-03-16
• Date Granted (W3CDTF): 2020-03-16
• Dissertation Number: 甲第838号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第838号
• Text Language Code: eng
• Subject Heading: Acute kidney injury; sepsis; interleukin-17A; Toll-like receptor 9
• Target Audience: 一般
• Note (General): doctoral; 医学系研究科; Toll-like receptor 9 (TLR9) activated by endogenously released mitochondrial DNA during sepsis contributes to the development of polymicrobial septic acute kidney injury (AKI). However, downstream factors of TLR9 to AKI remain unknown. We hypothesized that IL-17A activated by TLR9 may play a critical role in septic AKI development. To determine the effects of TLR9 on IL-17A production in septic AKI, we used a cecal ligation and puncture (CLP) model in Tlr9-knockout (Tlr9KO) mice and wild-type (WT) littermates. We also investigated the pathway from TLR9 activation in dendritic cells (DCs) to IL-17A production by γδT cells in vitro. To elucidate the effects of IL-17A on septic AKI, Il-17a-knockout (Il-17aKO) mice and WT littermates were subjected to CLP. We further investigated the relationship between the TLR9/IL-17A axis and septic AKI by intravenously administering recombinant IL-17A or vehicle into Tlr9KO mice and assessing kidney function. IL-17A levels in both plasma and the peritoneal cavity and mRNA levels of IL-23 in the spleen were significantly higher in WT mice after CLP than in Tlr9KO mice. Bone marrow-derived DCs activated by TLR9 induced IL-23, and consequently promoted IL-17A production in γδT cells in vitro. Knockout of Il-17a improved survival, functional and morphological aspects of AKI, and splenic apoptosis after CLP. Exogenous IL-17A administration aggravated CLP-induced AKI attenuated by knockout of Tlr9. TLR9 in DCs mediated IL-17A production in γδT cells during sepsis and contributed to the development of septic AKI.
• DOI: info:doi/10.1152/ajprenal.00313.2019; https://doi.org/info:doi/10.1152/ajprenal.00313.2019
• Persistent ID (NDL): info:ndljp/pid/11644953; https://dl.ndl.go.jp/pid/11644953
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2021-03-07T02:10:05+09:00
• Date Created (W3CDTF): 2021-02-17
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10271/00003785; https://hama-med.repo.nii.ac.jp/records/3653
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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2023-12-06 再収集