Asthma is a chronic inflammatory disorder of the airways which affects nearly 300 million people worldwide. Although the etiology of asthma is unknown, many candidate genes were identified or suspected to be involved in pathogenesis of asthma. This study examines both main effects of single loci and multilocus interactions to test the hypothesis that these candidate genes may contribute to the etiology of pediatric asthma independently and/or through complex interactions amongst Taiwanese individuals. We genotyped 13 single nucleotide polymorphisms (SNPs) for seven candidate genes including beta-2-adrenergic receptor surface (ADRB2), CD14 molecule (CD14), interleukin 4 (IL4), interleukin 4 receptor (IL4R), interleukin 13 (IL13), membrane-spanning 4-domains subfamily A member 2 (MS4A2), and tumor necrosis factor (TNF). There were 961 subjects, including 449 asthmatic children and 512 non-asthma children. Single locus analyses showed significant main effects of the CD14 rs2569190 and MS4A2 rs569108 polymorphisms on the risk of pediatric asthma (P = 0.032, 0.014, respectively). Furthermore, interactions involving CD14 rs2569190, IL4 rs2070874, and IL4R rs1805010 were suggested using the generalized multifactor dimensionality reduction (GMDR) method (P = 0.011). The results suggest that the SNPs from some of these candidate genes may contribute to the risk of pediatric asthma independently and/or in an interactive manner.
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