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Collectin kidney 1 (CL-K1) plays an important role in innate immunity against Streptococcus pneumoniae infection
https://asahikawa-med.repo.nii.ac.jp/records/5659
https://asahikawa-med.repo.nii.ac.jp/records/565917fd3f22-7994-44f2-b2fd-6a2ff410e1a5
名前 / ファイル | ライセンス | アクション |
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Item type | 学位論文 / Thesis or Dissertation_02(1) | |||||||
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公開日 | 2017-04-26 | |||||||
タイトル | ||||||||
言語 | en | |||||||
タイトル | Collectin kidney 1 (CL-K1) plays an important role in innate immunity against Streptococcus pneumoniae infection | |||||||
言語 | ||||||||
言語 | jpn | |||||||
資源タイプ | ||||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_46ec | |||||||
資源タイプ | thesis | |||||||
著者 |
黄, 仁秀
× 黄, 仁秀
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著者 ローマ字 | ||||||||
Hwang, Insu | ||||||||
書誌情報 |
Journal of innate immunity 巻 9, 号 2, p. 217-228, 発行日 2017-01-01 |
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ISSN | ||||||||
収録物識別子タイプ | ISSN | |||||||
収録物識別子 | 1662-811X | |||||||
DOI | ||||||||
識別子タイプ | DOI | |||||||
関連識別子 | 10.1159/000453316 | |||||||
識別番号 その他 | ||||||||
内容記述タイプ | Other | |||||||
内容記述 | PMID:28068663 | |||||||
学位授与番号 | ||||||||
学位授与番号 | 10107A507 | |||||||
学位授与年月日 | ||||||||
学位授与年月日 | 2017-03-24 | |||||||
学位名 | ||||||||
学位名 | 博士(医学) | |||||||
学位授与機関 | ||||||||
学位授与機関名 | 旭川医科大学 | |||||||
抄録 | ||||||||
内容記述タイプ | Abstract | |||||||
内容記述 | Collectins are C-type lectins that are involved in innate immunity as pattern recognition molecules. Recently, collectin kidney 1 (CL-K1) has been discovered, and in vitro studies have shown that CL-K1 binds to microbes and activates the lectin complement pathway. However, in vivo functions of CL-K1 against microbes have not been elucidated. To investigate the biological functions of CL-K1, we generated CL-K1 knockout (CL-K1-/-) mice and then performed a Streptococcus pneumoniae infection analysis. First, we found that recombinant human CL-K1 bound to S. pneumoniae in a calcium-dependent manner, and induced complement activation. CL-K1-/- mice sera formed less C3 deposition on S. pneumoniae. Furthermore, immunofluorescence analysis in the wild-type (WT) mice demonstrated that CL-K1 and C3 were localized on S. pneumoniae in infected lungs. CL-K1-/- mice revealed decreased phagocytosis of S. pneumoniae. Consequently, less S. pneumoniae clearance was observed in their lungs. CL-K1-/- mice showed severe pulmonary inflammation and weight loss in comparison with WT mice. Finally, the decreased clearance and severe pulmonary inflammation caused by S. pneumoniae infection might cause higher CL-K1-/- mice lethality. Our results suggest that CL-K1 might play an important role in host protection against S. pneumoniae infection through the activation of the lectin complement pathway. | |||||||
資源タイプ | ||||||||
内容記述タイプ | Other | |||||||
内容記述 | application/pdf | |||||||
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内容記述タイプ | Other | |||||||
内容記述 | application/pdf |