Lack of Association between CD58 Genetic Variations and Aspirin-Exacerbated Respiratory Disease in a Korean Population

Background. Exacerbation of asthma symptoms due to aspirin ingestion may lead to life-threatening lung failure. The adhesion molecule CD58 gene may play a crucial role in aspirin-exacerbated respiratory disease (AERD) pathogenesis by mediating the biological functions of asthma-inducing mechanisms including T helper cells, proinflammatory cytokines, and natural killer T cells. Objective. This study aimed to investigate the association of CD58 variations with aspirin-induced bronchospasm in Korean asthma patients. Methods. Seven single-nucleotide polymorphisms were selected for genotyping based on previously reported polymorphisms in the International HapMap database. Genotyping was carried out using TaqMan assay and 2 major haplotypes were obtained in 163 AERD cases and 429 aspirin-tolerant asthma controls. Frequency distributions of CD58 variations were analyzed using logistic and regression models. Results. Results showed that none of the analyzed CD58 single-nucleotide polymorphisms and haplotypes was significantly associated with AERD development and fall rate of FEV1 by aspirin provocation, an important diagnostic marker of aspirin hypersensitivity. Conclusions. This preliminary study suggests that CD58 does not affect AERD susceptibility in a Korean population, and may provide a new direction for future disease etiology.

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