Kawasaki disease is a kind of self-limited systemic vasculitis involving middle and small arteries, which usually occurs in children under 5 years old. Excessive inflammatory response caused by activation of monocytes is one of the important mechanisms of Kawasaki disease. Activated monocytes secrete large amounts of inflammatory mediators such as TNF-α and IL-1β. Activin A, a member of transforming growth factor-β superfamily, is a multifunctional growth and transforming factor. Several experimental evidences pinpoint that Activin A can regulate multiple biological function of the immune system. However, whether Activin A is involved in regulation of activation of monocytes in Kawasaki disease was not well characterized. Here, this study showed that the expression of Activin A in serum decreased in acute-phase Kawasaki disease. Furthermore, Activin A inhibits activin type IIA receptor, activin type IB receptor, CD86 and CD80 expression in over-activated monocytes. In addition, Activin A inhibited Smad3 expression and NF-κB signaling pathways. Specific function and mechanism of Activin A in acute-phase Kawasaki disease need further study.
Keywords: Activin A; Kawasaki disease; Monocytes; NF-κB signaling pathways.