Involvement of mannose-binding lectin in the pathogenesis of Kawasaki disease-like murine vasculitis
Involvement of mannose-binding lectin in the pathogenesis of Kawasaki disease-like murine vasculitis
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DOI：
10.1016/j.clim.2014.03.019
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发表时间：
2014-07-01
影响因子：
8.6
通讯作者：
Hamaoka, Kenji
中科院分区：
文献类型：
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作者：
Nakamura, Akihiro;Okigaki, Mitsuhiko;Hamaoka, Kenji
川崎是一种儿童特发性血管炎。在这项研究中，使用一个已建立的动物模型KD的研究的基础上，我们报告甘露糖结合凝集素（MBL）参与疾病的发病机制。通过腹腔注射白色念珠菌水溶性提取物（CAWS）诱导KD样实验性小鼠血管炎。模型组小鼠血清MBL-A水平逐渐升高。MBL-A和MBL-C沉积在主动脉根部，包括冠状动脉，这是实验性血管炎的好发部位。对应于MBL的分布模式，还观察到C3/C3衍生肽的显著沉积。关于MBLs的自身反应性，我们观察到MBLs与核心组蛋白相互作用以激活凝集素途径。这些结果表明，某些类型的病原体引起MBL依赖性补体途径（凝集素途径），导致和/或加重KD样血管炎。(C)2014爱思唯尔公司All rights reserved.
Kawasaki disease (KD) is a paediatric idiopathic vasculitis. In this study, on the basis of studies using an established animal model for KD, we report that mannose-binding lectin (MBL) is involved in the pathogenesis of the disease. KD-like experimental murine vasculitis was induced by intraperitoneally administering a Candida albicans water-soluble extract (CAWS). MBL-A gradually increased in the serum of the model mice treated with CAWS. Deposition of MBL-A and MBL-C was observed in the aortic root, including the coronary arteries, which is a predilection site in experimental vasculitis. Corresponding to the distribution patterns of MBLs, marked deposition of C3/C3-derived peptides was also observed. Regarding the self-reactivity of MBLs, we observed that MBLs interacted with core histones to activate the lectin pathway. These results suggest that some types of pathogens provoke the MBL-dependent complement pathway (lectin pathway) to cause and/or exacerbate KD-like vasculitis. (C) 2014 Elsevier Inc. All rights reserved.