Interleukin (IL)-13, which is essential for IgE synthesis, mediates its effects by binding with a receptor composed of IL-4Ra and IL-13Ra1. We investigated the effects of IL-13 and IL-13Ra1 polymorphisms in Korean children with asthma, and whether these have been associated with IgE production. We enrolled 358 atopic asthmatic, 111 non-atopic asthmatic, and 146 non-atopic healthy children. IL-13 and IL-13Ra1 genotypes were identified using the PCR-RFLP method. There was an association between the asthma susceptibility and homozygosity for risk allele of IL-13 G+2044A. In children with atopic asthma, risk alleles in IL-13 (A-1512C and C-1112T) and IL-13Ra1 (A+1398G) showed increased total IgE (P=0.012, 0.015 and 0.017, respectively). Three-loci haplotype analysis for IL-13 showed that the haplotype composed of -1512C, -1112T and +2044A was associated with higher total IgE than other tested haplotypes in children with atopic asthma (P=0.003). The genegene interaction between risk alleles of each IL-13 promoter polymorphism and IL-13Ra1 polymorphism was associated with higher total IgE in children with atopic asthma (P=0.002, 0.010). These findings indicate that the IL-13 G+2044A is associated with asthma development and the IL-13 and IL-13Ra1 polymorphisms may interact to enhance IgE production.

Kawasaki disease (KD) is an acute febrile vasculitic syndrome of unknown etiology that preferentially affects the coronary artery. Interleukin-10 (IL-10) is a key proinflammatory cytokine, and a polymorphism near the major transcriptional start site of the IL-10 gene was shown to influence IL-10 production in vitro. This study investigated the association of the IL-10 promoter polymorphism with KD and its clinical parameters in Korean children. A total of 194 children with congenital heart disease (CHD) and 95 children with KD were included in this study. IL-10 (-627 A/C) polymorphism genotypes were determined using the single-base extension method. There was no difference in the allele frequencies of IL-10 (-627 A/C) polymorphism between CHD children and KD children. KD children with one or two copies of the IL-10 (-627C) allele showed significantly lower albumin levels (p ϭ 0.020) and higher frequencies of early coronary artery aneurysm [62.22% versus 37.78%, adjusted odds ratio (aOR) ϭ 3.50, 95% confidence interval (CI): 1.50 -8.16] compared with KD children with the common IL-10 (-627A) allele. These findings suggest that the IL-10 (-627 A/C) promoter polymorphism might be a genetic marker for the risk of early coronary artery complication in KD. (Pediatr Res 61: 584-587, 2007) K D is an acute, self-limiting vasculitis of unknown etiology that occurs predominantly in infants and young children. KD is characterized by widespread vascular inflammation of the coronary artery and other medium-sized arteries (1,2). Coronary artery lesions, including coronary artery dilatation or aneurysm, are the most common complications and develop in approximately 20%-25% of untreated children with KD (3). Even after high-dose intravenous immunoglobulin (IVIG) therapy, coronary artery lesions occur in a small percentage of KD patients, occasionally leading to lifethreatening complications (e.g. myocardial infarction) and/or acquired heart diseases such as myocardial dysfunction, valvular diseases, and arrhythmias (4,5).

The risk of AHR development was closely linked with allergen sensitization itself, and the number or types of sensitized allergens such as indoor and fungal allergens in Korean young adolescents.