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