Analysis of autophagy in Nod1 ligand-induced coronary arteritis like Kawasaki disease

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461623
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pediatrics
• Research Institution: Kyushu University
• Principal Investigator: Nishio Hisanori 九州大学, 大学病院, 助教 (00507783)
• Co-Investigator(Kenkyū-buntansha): YAMAMURA Kennichirou 九州大学, 大学病院, 助教 (30532858) ; NANISHI Etsuro 九州大学, 大学病院, 医員 (40624937)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 川崎病 / 自然免疫 / オートファジー

Outline of Final Research Achievements

We analysed the mechanisms of autophagy in Nod1 ligand-induced coronary arteritis, one of the mice models of Kawasaki disease we reported previously. First, we found that rapamycin, autophagy incducer, improved coronary arteritis in the mice. Furthermore, in human coronary artery endothelial cells, rapamycin decreased production of inflammatory cytokines such as IL-6 and IL-8. Rapamycin is one of the mTOR (mammalian target of rapamycin) inhibitors, so we did the same experiments in vivo and in vitro by using other mTOR inhibitors. They revealed that other mTOR inhibitors also induced improvement of coronary arteritis and inhibition of cytokine production. These results showed that mTOR inihibitors, autophagy inducers, are possible new treatment with Kawasaki disease.

Free Research Field

小児感染免疫