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IL-17A Activated by Toll-Like Receptor 9 Contributes to Development of Septic Acute Kidney Injury
http://hdl.handle.net/10271/00003785
http://hdl.handle.net/10271/000037858a82c7ac-6026-4ea5-bb1d-0c4328f7b81a
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
論文本文 (18.1 MB)
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| Item type | 学位論文 / Thesis or Dissertation(1) | |||||||
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| 公開日 | 2021-02-18 | |||||||
| タイトル | ||||||||
| タイトル | IL-17A Activated by Toll-Like Receptor 9 Contributes to Development of Septic Acute Kidney Injury | |||||||
| 言語 | en | |||||||
| 言語 | ||||||||
| 言語 | eng | |||||||
| キーワード | ||||||||
| 主題 | Acute kidney injury | |||||||
| キーワード | ||||||||
| 主題 | sepsis | |||||||
| キーワード | ||||||||
| 主題 | interleukin-17A | |||||||
| キーワード | ||||||||
| 主題 | Toll-like receptor 9 | |||||||
| 資源タイプ | ||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_db06 | |||||||
| 資源タイプ | doctoral thesis | |||||||
| アクセス権 | ||||||||
| アクセス権 | open access | |||||||
| アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||||
| その他のタイトル | ||||||||
| その他のタイトル | 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 | |||||||
| 著者 |
内藤, 善隆
× 内藤, 善隆
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| 書誌情報 |
en : American journal of physiology. Renal physiology 巻 318, 号 1, p. F238-F247, 発行日 2020-01-09 |
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| 出版者 | ||||||||
| 出版者 | American Physiological Society | |||||||
| 言語 | en | |||||||
| 抄録 | ||||||||
| 内容記述タイプ | Abstract | |||||||
| 内容記述 | 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. | |||||||
| 言語 | en | |||||||
| 学位名 | ||||||||
| 学位名 | 博士（医学） | |||||||
| 学位の区分 | ||||||||
| 内容記述 | doctoral | |||||||
| 学位の分野 | ||||||||
| 内容記述 | 医学系研究科 | |||||||
| 学位授与機関 | ||||||||
| 学位授与機関識別子Scheme | kakenhi | |||||||
| 学位授与機関識別子 | 13802 | |||||||
| 学位授与機関名 | 浜松医科大学 | |||||||
| 学位授与年月日 | ||||||||
| 学位授与年月日 | 2020-03-16 | |||||||
| 学位授与番号 | ||||||||
| 学位授与番号 | 甲第838号 | |||||||
| ISSN | ||||||||
| 収録物識別子タイプ | EISSN | |||||||
| 収録物識別子 | 1931-857X | |||||||
| EISSN | ||||||||
| 収録物識別子タイプ | PISSN | |||||||
| 収録物識別子 | 1522-1466 | |||||||
| PubMed番号 | ||||||||
| 識別子タイプ | PMID | |||||||
| 関連識別子 | 31760767 | |||||||
| 出版社DOI | ||||||||
| 識別子タイプ | DOI | |||||||
| 関連識別子 | https://doi.org/10.1152/ajprenal.00313.2019 | |||||||
| 著者版フラグ | ||||||||
| 出版タイプ | AM | |||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||
