Lack of association between CD58 genetic variations and aspirin-exacerbated respiratory disease in a Korean population.

摘要

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 FEV(1) 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.