促炎因子CD147、DcR3和IL33在川崎病发病机制中的网络关系

The Network of Pro-Inflammatory Factors CD147, DcR3, and IL33 in the Development of Kawasaki Disease.

作者信息

Qi Yanqi, Xu Jiawen, Lin Zhe, Tao Yijing, Zheng Fenglei, Wang Yujia, Sun Yameng, Fu Songling, Wang Wei, Xie Chunhong, Zhang Yiying, Gong Fangqi

机构信息

Department of Cardiology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, 310052, People's Republic of China.

出版信息

J Inflamm Res. 2021 Nov 19;14:6043-6053. doi: 10.2147/JIR.S338763. eCollection 2021.

DOI:10.2147/JIR.S338763

PMID:34824540

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8610753/

Abstract

INTRODUCTION

Kawasaki disease (KD) is an acute febrile systemic vasculitis, but the etiology remains unknown. We studied serum levels of CD147, DcR3, and IL33 in different stages of KD to explore the value of CD147, DcR3, and IL33 in the pathophysiology of KD.

METHODS

We measured serum levels of CD147, DcR3, and IL33 by enzyme-linked immunosorbent assay (ELISA) at different stages with 71 KD patients and 66 healthy control children. We apply for network tools GeneMANIA and Cytoscape APP to analyze the functions of these pro-inflammatory factors at the gene and protein level.

RESULTS

Serum levels of CD147, DcR3, and IL33 were significantly increased in KD patients before IVIG treatment. Serum levels of CD147, DcR3, and IL33 gradually decreased over time after the treatment of IVIG. Eight cases were IVIG non-responders, while nine KD patients got CALs, but they did not overlap. And there were no statistical differences between group IVIG responders and IVIG non-responders or between groups without CALs and with CALs. We explored the functions of CD147, DcR3, and IL33 from GeneMANIA and Cytoscape APP and found these third pro-inflammatory factors were coexpressed, physical interactions, genetic interactions with other KD-related factors.

CONCLUSION

CD147, DcR3, and IL33 are involved in the pathophysiology of KD, which provides novel evidence for diagnosing and treating KD with their inhibitors.

摘要

引言

川崎病（KD）是一种急性发热性全身性血管炎，但其病因仍不清楚。我们研究了KD不同阶段血清中CD147、DcR3和IL33的水平，以探讨CD147、DcR3和IL33在KD病理生理学中的价值。

方法

我们采用酶联免疫吸附测定（ELISA）法，对71例KD患者和66例健康对照儿童在不同阶段的血清CD147、DcR3和IL33水平进行了检测。我们应用网络工具GeneMANIA和Cytoscape APP在基因和蛋白质水平分析这些促炎因子的功能。

结果

KD患者在静脉注射免疫球蛋白（IVIG）治疗前血清CD147、DcR3和IL33水平显著升高。IVIG治疗后，血清CD147、DcR3和IL33水平随时间逐渐下降。8例为IVIG无反应者，9例KD患者发生冠状动脉瘤（CALs），但两者无重叠。IVIG反应者与IVIG无反应者之间或无CALs组与有CALs组之间无统计学差异。我们通过GeneMANIA和Cytoscape APP探索了CD147、DcR3和IL33的功能，发现这三种促炎因子与其他KD相关因子共表达、存在物理相互作用和遗传相互作用。