Association of lower eosinophil‐related T helper 2 (Th2) cytokines with coronary artery lesions in Kawasaki disease

Abstract

Kawasaki disease (KD) is a systemic febrile vasculitis particular coronary artery involvement. Eosinophilia has been found in our and other studies in KD. This study further investigates whether eosinophil-related T helper 2 (Th2) cytokines or the activation marker (eosinophil cationic protein - ECP) is involved in KD with coronary artery lesions (CAL). A total of 95 KD patients were enrolled for this study. Plasma samples were subjected to the measurement of interleukin (IL)-4, IL-5, and eotaxin by Luminex-Bedalyte multiplex beadmates system and to the measurement of ECP by fluoroimmunoassay. Patients with KD had higher eosinophils than controls. Eosinophil-related mediators: IL-4, IL-5, eotaxin, and ECP levels were also higher in KD patients than controls before intravenous immunoglobulin (IVIG) treatment. After IVIG treatment, ECP decreased but IL-4, IL-5, and eotaxin increased significantly. The higher the IL-5 and eosinophil levels after IVIG treatment, the lower rate of CAL was found. Changes of eosinophils after IVIG treatment were positively correlated to changes of IL-5 levels but not ECP levels. An increase of eosinophils and IL-5, but not ECP levels after IVIG treatment, was inversely correlated with CAL formation in KD.

TARC/CCL17 gene polymorphisms and expression associated with susceptibility and coronary artery aneurysm formation in Kawasaki disease

“…Furthermore, they can be objective parameters for disease severity-specific atopic dermatitis and treatment monitoring. In our KD patients, we found that significantly high levels of TARC/CCL17 have also been observed than those in the controls, which was compatible with our previous findings of increased IL-4/IL-5 expression in patients with KD (13). Moreover, our previous study showed that IL-4, IL-5, and eotaxin increased significantly after IVIG treatment (13).…”

“…TARC/CCL17 has been suggested as a candidate gene for conferring susceptibility to Th2 associated with allergy diseases and is highly implicated in the pathogenesis of atopic dermatitis (10,11) and bronchial asthma (12). There are several lines of evidence pointing out an abnormal Th1/Th2 balance in KD patients (13). Recently, it has been shown that the incidence of atopic dermatitis and bronchial asthma among children with KD was nine times and three times greater than that of controls (14,15), respectively.…”

CASP3 gene single-nucleotide polymorphism (rs72689236) and Kawasaki disease in Taiwanese children

“…All patients were treated with a single high dose of IVIG (2 g/kg) over a 12 h period. 7,10,23 This study was approved by the Institutional Review Board of Chang Gung Memorial Hospital. Blood samples were collected after informed consent was obtained from parents or guardians.…”

“…7 The most serious complication of KD is coronary artery lesions (CALs), including myocardial infarction, coronary artery fistula, 8 coronary artery dilatation and coronary artery aneurysm. 9,10 Studies conducted have either failed to identify certain pathogens responsible for KD or have reported discrepant results. [11][12][13] Therefore, the genetic background may have a more important role in the pathogenesis of KD.…”

Genetic polymorphisms in Kawasaki disease

“…Indeed, genetic polymorphisms of the TGF-β pathway, including TGFB2, TGFBR2, and SMAD3, are associated with susceptibility to KD and development of CAL in the European and US populations [12] . In the Asian population, we reported that monocytosis, eosinophilia, and eosinophilrelated Th2 immune response (especially, plasma level of IL-5) are associated with CAL formation and/or initial intravenous immunoglobulin (IVIG) treatment response [13][14][15][16] . Immunerelated genes, such as CTLA-4, CASP3 and ITPKC, have also been suggested to influence the susceptibility to and the clinical status of KD [14,15,[17][18][19][20][21] .…”