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  1. 20 医学系研究科・医学部
  2. 20A 学術誌論文
  3. 20A1 雑誌掲載論文

G-Protein-Coupled Estrogen Receptor Agonist Suppresses Airway Inflammation in a Mouse Model of Asthma through IL-10

http://hdl.handle.net/10295/00006323
http://hdl.handle.net/10295/00006323
430d5491-7b66-490f-baa5-43e4d4afc6c6
名前 / ファイル ライセンス アクション
iA_2022_130.pdf iA_2022_130.pdf (1.4 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2023-02-25
タイトル
タイトル G-Protein-Coupled Estrogen Receptor Agonist Suppresses Airway Inflammation in a Mouse Model of Asthma through IL-10
言語 en
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
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
作成者 Itoga, Masamichi

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en Itoga, Masamichi

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Konno, Yasunori

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Moritoki, Yuki

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Saito, Yukiko

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Ito, Wataru

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Tamaki, Mami

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Kobayashi, Yoshiki

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Kayaba, Hiroyuki

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Kikuchi, Yuta

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Chihara, Junichi

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Takeda, Masahide

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Ueki, Shigeharu

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Hirokawa, Makoto

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内容記述
内容記述タイプ Abstract
内容記述 Estrogen influences the disease severity and sexual dimorphism in asthma, which is caused by complex mechanisms. Besides classical nuclear estrogen receptors (ER alpha beta), G-protein-coupled estrogen receptor (GPER) was recently established as an estrogen receptor on the cell membrane. Although GPER is associated with immunoregulatory functions of estrogen, the pathophysiological role of GPER in allergic inflammatory lung disease has not been examined. We investigated the effect of GPER-specific agonist G-1 in asthmatic mice. GPER expression in asthmatic lung was confirmed by immunofluorescent staining. OVA-sensitized BALB/c and C57BL/6 mice were treated with G-1 by daily subcutaneous injections during an airway challenge phase, followed by histological and biochemical examination. Strikingly, administration of G-1 attenuated airway hyperresponsiveness, accumulation of inflammatory cells, and levels of Th2 cytokines (IL-5 and IL-13) in BAL fluid. G-1 treatment also decreased serum levels of anti-OVA IgE antibodies. The frequency of splenic Foxp3(+) CD4(+) regulatory T cells and IL-10-producing GPER(+) CD4(+) T cells was significantly increased in G-1-treated mice. Additionally, splenocytes isolated from G-1-treated mice showed greater IL-10 production. G-1-induced amelioration of airway inflammation and IgE production were abolished in IL-10-deficient mice. Taken together, these results indicate that extended GPER activation negatively regulates the acute asthmatic condition by altering the IL-10-producing lymphocyte population. The current results have potential importance for understanding the mechanistic aspects of function of estrogen in allergic inflammatory response.
言語 en
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
書誌情報 en : PLOS ONE

巻 10, 号 3, 発行日 2015
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 1932-6203
出版者
出版者 Public Library of Science
言語 en
関連情報
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 https://doi.org/10.1371/journal.pone.0123210
権利情報
権利情報 © 2015 Itoga et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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