4.4 Article

Collectin Kidney 1 Plays an Important Role in Innate Immunity against Streptococcus pneumoniae Infection

期刊

JOURNAL OF INNATE IMMUNITY
卷 9, 期 2, 页码 217-228

出版社

KARGER
DOI: 10.1159/000453316

关键词

Collectin; Complement; Innate immunity; Knockout mice; Pneumonia

资金

  1. JSPS KAKENHI [22390113, 26293124]
  2. Northern Advancement Center for Science & Technology (Sapporo, Japan)
  3. Smoking Research Foundation
  4. Mizutani Foundation [120136]
  5. Grants-in-Aid for Scientific Research [26670489, 22390113, 26293124, 16K19045] Funding Source: KAKEN

向作者/读者索取更多资源

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. (C) 2017 S. Karger AG, Basel

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.4
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据