Plasma Prostaglandin E2 Levels Correlated with the Prevention of Intravenous Immunoglobulin Resistance and Coronary Artery Lesions Formation via CD40L in Kawasaki Disease

• Published in: PloS one Vol. 11; no. 8; p. e0161265
• Main Authors: Kuo, Ho-Chang, Wang, Chih-Lu, Yang, Kuender D, Lo, Mao-Hung, Hsieh, Kai-Sheng, Li, Sung-Chou, Huang, Ying-Hsien
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01.08.2016; Public Library of Science (PLoS)
• Subjects: Biology and Life Sciences; Biomarkers - blood; CD4 antigen; CD4-Positive T-Lymphocytes - drug effects; CD40 Ligand - metabolism; CD40L protein; Children; Coronary artery; Coronary Artery Disease - complications; Coronary Artery Disease - prevention & control; Coronary vessels; Dinoprostone - blood; Drug dosages; Drug Resistance; Female; Gene Expression Regulation - drug effects; Guillain-Barre syndrome; Hospitals; Humans; Immunoglobulins; Immunoglobulins, Intravenous - pharmacology; Immunology; Infant; Inflammation; Intravenous administration; Kawasaki disease; Lesions; Leukocytes (mononuclear); Ligands; Lymphocytes; Lymphocytes T; Medicine; Medicine and Health Sciences; Mucocutaneous lymph node syndrome; Mucocutaneous Lymph Node Syndrome - blood; Mucocutaneous Lymph Node Syndrome - complications; Mucocutaneous Lymph Node Syndrome - diagnosis; Mucocutaneous Lymph Node Syndrome - metabolism; Patients; Pediatrics; Physicians; Plasma; Prevention; Prognosis; Prostaglandin E2; Research and Analysis Methods; Systemic vasculitis; Veins & arteries
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0161265

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 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. This 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. PGE2 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). 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 CD40L in KD.