JNK is critical for the development of Candida albicans-induced vascular lesions in a mouse model of Kawasaki Disease

摘要: Abstract Background Kawasaki disease (KD) is the most common systemic vasculitis of unknown etiology in children, and can cause life-threatening complication coronary artery aneurysm. Although a novel treatment strategy for patients with KD-caused vascular lesions eagerly awaited, their molecular pathogenesis remains largely unknown. c-Jun N-terminal kinase (JNK) signaling molecule known to have roles inflammation tissue remodeling. The aim this study was elucidate significant involvement JNK development mouse model KD. Methods results We injected Candida albicans cell wall extract (CAWE) into 4-week-old C57BL/6 mice. Macroscopically, we found that CAWE caused bulging at artery, carotid celiac iliac abdominal aorta. Histological examination aorta CAWE-treated mice showed marked inflammatory infiltration, destruction elastic lamellae, loss medial smooth muscle cells intimal thickening, which are similar histological features To find role lesion formation, evaluated effects inhibitor, SP600125, on aortic induced by CAWE. Interestingly, SP600125 significantly decreased incidence also protected against histologically, compared placebo treatment. Conclusions Our findings suggest crucial CAWE-induced mice, potentially represents therapeutic target