Abstract
BackgroundA 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 E2 (PGE2) 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 PGE2 and CD40L expression in KD.Materials and MethodsThis study consisted of a total of 144 KD patients, whose intravenous immunoglobulin (IVIG)/coronary arterial lesion (CAL) formation resistance was evaluated. PGE2 levels were evaluated in vitro to study the effect of CD40L on CD4+ T lymphocytes.ResultsPGE2 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 PGE2 expression in the acute-stage mononuclear cells of KD patients. According to our findings, both IVIG and PGE2 can impede surface CD40L expressions on CD4+ T lymphocytes (p<0.05).ConclusionsThe results of this study are among the first to find that plasma PGE2 is correlated with the prevention of IVIG resistance and CAL formation through CD40L in KD.
Highlights
Kawasaki disease (KD) is a form of systemic vasculitis that was initially described by Tomisaki Kawasaki in 1974[1] and later reported in English
Prostaglandin E2 (PGE2) levels significantly increased after intravenous immunoglobulin (IVIG) treatment (p
The results of this study are among the first to find that plasma PGE2 is correlated with the prevention of IVIG resistance and CAL formation through CD40 Ligand (CD40L) in KD
Summary
Kawasaki disease (KD) is a form of systemic vasculitis that was initially described by Tomisaki Kawasaki in 1974[1] and later reported in English. Another study found that PGE2 could activate β1-integrins through the PGE2 receptor in human coronary arterial endothelial cells [14]. Single nucleotide polymorphisms of an ATP-binding cassette, subfamily C, member 4, which is a mediator of prostaglandin efflux, are correlated with KD susceptibility [17]. These findings piqued our interest in the influence of PGE2 on the pathogenesis of KD, and this study aims to determine the specific role of PGE2 in both KD’s pathophysiology and its treatment outcomes. A form of systemic vasculitis, Kawasaki disease (KD) occurs most frequently in children under the age of five years old. CD40L may be a marker of vasculitis in KD, so this study focuses on PGE2 and CD40L expression in KD
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