Plasma Prostaglandin E(2) Levels Correlated with the Prevention of Intravenous Immunoglobulin Resistance and Coronary Artery Lesions Formation via CD40L in Kawasaki Disease

BACKGROUND: A form of systemic vasculitis, Kawasaki disease (KD) occurs most frequently in children under the age of five years old. Previous studies have found that Prostaglandin E(2) (PGE(2)) correlates with KD, although the related mechanisms are still unknown. CD40L may also be a marker of vasculitis in KD, so this study focuses on PGE(2) and CD40L expression in KD. MATERIALS AND METHODS: This study consisted of a total of 144 KD patients, whose intravenous immunoglobulin (IVIG)/coronary arterial lesion (CAL) formation resistance was evaluated. PGE(2) levels were evaluated in vitro to study the effect of CD40L on CD4+ T lymphocytes. RESULTS: PGE(2) levels significantly increased after IVIG treatment (p<0.05), especially in patients who responded to initial IVIG treatment (p = 0.004) and for patients without CAL formation (p = 0.016). Furthermore, an in vitro study revealed that IVIG acted as a trigger for PGE(2) expression in the acute-stage mononuclear cells of KD patients. According to our findings, both IVIG and PGE(2) can impede surface CD40L expressions on CD4+ T lymphocytes (p<0.05). CONCLUSIONS: The results of this study are among the first to find that plasma PGE(2) is correlated with the prevention of IVIG resistance and CAL formation through CD40L in KD.