The Caveolin-1/NF-κB signalling pathway is involved in Kawasaki disease vasculitis induced by Lactobacillus casei cell wall extract.

Abstract

Objectives: 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.

Methods: KD vasculitis was induced by Lactobacillus casei cell wall extract (LCWE) intraperitoneal injection in mice, and Cav-1 expression was inhibited by AAV-Cav-1 shRNA. Cardiovascular lesions was assessed via haematoxylin & eosin (HE) staining. Proinflammatory cytokine and MMP-9 levels were measured via quantitative real-time polymerase chain reaction (qRT-PCR). Endothelial cell adhesion molecule expression was evaluated by immunohistochemistry. Cav-1 expression and NF-κB pathway activation were evaluated by Western blotting (WB).

Results: Mice with LCWE-induced KD vasculitis exhibited severe heart vessel inflammation and increased Cav-1, proinflammatory cytokine, MMP-9, and endothelial cell adhesion molecule expression, which were reversed after Cav-1 inhibition. Moreover, NF-κB activation of KD vasculitis model mice was suppressed after Cav-1 inhibition.

Conclusion: Cav-1 participates in KD vasculitis pathogenesis by regulating the NF-κB signalling pathway.