Open AccessPlasma Prostaglandin E2 Levels Correlated with the Prevention of Intravenous Immunoglobulin Resistance and Coronary Artery Lesions Formation via CD40L in Kawasaki Disease
Author(s) -
Ho-Chang Kuo,
ChihLu Wang,
Kuender D. Yang,
MaoHung Lo,
KaiSheng Hsieh,
SungChou Li,
YingHsien Huang
Publication year - 2016
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0161265
Subject(s) - kawasaki disease , coronary artery disease , antibody , medicine , immunoglobulin a , immunoglobulin g , cardiology , cd40 , artery , immunology , chemistry , in vitro , biochemistry , cytotoxic t cell
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.