The Caveolin-1/nuclear factor kappa-B signalling pathway is involved in Kawasaki disease vasculitis induced by...

Kawasaki disease (KD) is an acute vasculitis and its pathogenesis is complex. Caveolin-1 (Cav-1) is the main structural protein of caveolae and is involved in the pathogenesis of many vascular diseases. A clinical study revealed that the Cav-1 serum level in children significantly increases in the acute phase of KD, but the role of Cav-1 in KD is still unclear. We aimed to explore whether and how Cav-1 is involved in the KD pathogenesis.

KD vasculitis was induced by Lactobacillus casei cell wall extract intraperitoneal injection in mice, and Cav-1 expression was inhibited by adeno-associated viruses (AAV)-Cav-1 shRNA. Cardiovascular lesions was assessed via haematoxylin and eosin staining. Proinflammatory cytokine and matrix metalloproteinase-9 levels were measured via quantitative real-time polymerase chain reaction. Endothelial cell adhesion molecule expression was evaluated by immunohistochemistry. Cav-1 expression and nuclear factor kappa-B pathway activation were evaluated by Western blotting.

Mice with Lactobacillus casei cell wall extract-induced KD vasculitis exhibited severe heart vessel inflammation and increased Cav-1, proinflammatory cytokine, matrix metalloproteinase-9, and endothelial cell adhesion molecule expression, which were reversed after Cav-1 inhibition. Moreover, nuclear factor kappa-B activation of KD vasculitis model mice was suppressed after Cav-1 inhibition.

Cav-1 participates in KD vasculitis pathogenesis by regulating the nuclear factor kappa-B signalling pathway.