Experimental pathological study on mannose binding lectin in Kawasaki disease

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461628
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pediatrics
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: Hamaoka Kenji 京都府立医科大学, 医学(系)研究科(研究院), 教授 (60189602)
• Co-Investigator(Kenkyū-buntansha): NAKAMURA Akihiro 京都府立医科大学, 大学院医学(系)研究科(研究院), 博士研究員 (50313854)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: mannose binding lectin / vasculitis / Kawasaki disease / mouse model / complement

Outline of Final Research Achievements

Kawasaki disease (KD) is an idiopathic vasculitis. Its etiology is not clear, some clinical genetic studies have indicated involvement of genetic polymorphisms of mannose binding lectin (MBL) gene in the disease. Using an animal model for KD, in this study, we explored the roles of MBL in KD. Deposition of MBL-A, MBL-C and complement were observed in the aortic root including coronary arteries in the model mice. Plasma MBL-A lebel was gradually increased with development of the vasculitis, whereas plasma MBL-C level was rapidly decreased. Employing proteomics , forthermore, we revealed that MBL-A and -C interact with some specific endogenous proteins to activate lecin pathway in vitro weakly but significantly.
Taken together, these results suggest that MBLs involve in exacerbration of KD-like murine vasculitis through interacting with intracellular proteins released from damaged tissues.

Free Research Field

小児科学