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Nicotinic acetylcholine receptor agonist reduces acute lung injury after renal ischemia-reperfusion injury by acting on splenic macrophages in mice
http://hdl.handle.net/10271/00004268
http://hdl.handle.net/10271/000042685e21303d-91da-4e94-adc8-839e29cf022d
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
論文本文 (4.1 MB)
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| Item type | 学位論文 / Thesis or Dissertation(1) | |||||
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| 公開日 | 2023-02-15 | |||||
| タイトル | ||||||
| タイトル | Nicotinic acetylcholine receptor agonist reduces acute lung injury after renal ischemia-reperfusion injury by acting on splenic macrophages in mice | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | acute kidney injury | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | acute lung injury | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | macrophage | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | nicotinic acetylcholine receptor agonist | |||||
| 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 | ニコチン性アセチルコリン受容体作動薬はマウスにおいて脾臓マクロファージに作用することにより腎虚血再灌流障害後の急性肺障害を軽減する | |||||
| 言語 | ja | |||||
| 著者 |
後藤, 大樹
× 後藤, 大樹 |
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| 書誌情報 |
en : American Journal of Physiology-Renal Physiology 巻 322, 号 5, p. F540-F552, 発行日 2022-05-01 |
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| 出版者 | ||||||
| 出版者 | The American Physiological Society | |||||
| 言語 | en | |||||
| 権利 | ||||||
| 言語 | en | |||||
| 権利情報 | Copyright 2022 the American Physiological Society. | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Acute kidney injury (AKI) contributes to the development of acute lung injury (ALI) via proinflammatory responses. We hypothesized that activation of a nicotinic acetylcholine receptor (nAChR), which exerts cholinergic anti-inflammatory effects on macrophages, could reduce ALI after AKI. We aimed to determine whether nAChR agonists could reduce ALI after AKI and which macrophages in the lung or spleen contribute to the improvement of ALI by nAChR agonists. We induced AKI in male mice by unilateral ischemia-reperfusion injury (IRI) with contralateral nephrectomy and administered nAChR agonists in three experimental settings: 1) splenectomy, 2) deletion of splenic macrophages and systemic mononuclear phagocytes via intravenous administration of clodronate liposomes, and 3) alveolar macrophage deletion via intratracheal administration of clodronate liposomes. Treatment with GTS-21, an a7nAChR-selective agonist, significantly reduced the levels of circulating IL-6, a key proinflammatory cytokine, and lung chemokine (C-X-C motif) ligand (CXCL)1 and CXCL2 and neutrophil infiltration, and Evans blue dye (EBD) vascular leakage increased after renal IRI. In splenectomized mice, GTS-21 did not reduce circulating IL-6 and lung CXCL1 and CXCL2 levels and neutrophil infiltration, and EBD vascular leakage increased after renal IRI. In mice depleted of splenic macrophages and systemic mononuclear phagocytes, GTS-21 treatment did not reduce lung neutrophil infiltration, and EBD vascular leakage increased after renal IRI. In mice depleted of alveolar macrophages, GTS-21 treatment significantly reduced lung neutrophi infiltration, and EBD vascular leakage increased after renal IRI. Our findings show that nAChR agonist reduces circulating IL-6 levels and acute lung injury after renal IRI by acting on splenic macrophages. | |||||
| 言語 | en | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | NEW & NOTEWORTHY Acute lung injury associated with acute kidney injury contributes to high mortality. This study showed, for the first time, that nicotinic acetylcholine receptor agonists reduced circulating IL-6 and ALI after renal ischemia-reperfusion injury in mice. These effects of a7nAChR agonist were eliminated in both splenectomized and splenic macrophage (including systemic mononuclear phagocyte)-depleted mice but not alveolar macrophage-depleted mice. nAChR agonist could reduce ALI after AKI via splenic macrophages and provide a novel strategy in AKI. | |||||
| 言語 | en | |||||
| 学位名 | ||||||
| 言語 | ja | |||||
| 学位名 | 博士（医学） | |||||
| 学位の区分 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | doctoral | |||||
| 言語 | en | |||||
| 学位の分野 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 医学系研究科 | |||||
| 言語 | ja | |||||
| 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 | |||||
| 言語 | ja | |||||
| 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 | 2022-09-16 | |||||
| 学位授与番号 | ||||||
| 学位授与番号 | 甲第914号 | |||||
| ISSN | ||||||
| 収録物識別子タイプ | PISSN | |||||
| 収録物識別子 | 1931-857X | |||||
| EISSN | ||||||
| 収録物識別子タイプ | EISSN | |||||
| 収録物識別子 | 1522-1466 | |||||
| NII書誌ID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA12070596 | |||||
| PubMed番号 | ||||||
| 識別子タイプ | PMID | |||||
| 関連識別子 | 35311383 | |||||
| 出版社DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.1152/ajprenal.00334.2021 | |||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
