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Cyclooxygenase-1 gene polymorphisms in patients with different asthma phenotypes and atopy

¹ Cooperative Research Centre for Asthma, ² Asthma and Allergy Research Institute (Inc.) and Centre for Asthma, Allergy and Respiratory Research, ³ Western Australian Institute for Medical Research and Centre for Medical Research, The University of Western Australia, Perth, and ⁴ Genetic Epidemiology Laboratory, Queensland Institute of Medical Research, Brisbane, Australia.

CORRESPONDENCE: P. J. Thompson, Asthma and Allergy Research Institute, Ground Floor, E Block, Sir Charles Gairdner Hospital, Nedlands, WA 6009, Australia. Fax: 61 893464159. E-mail: aari@aari.uwa.edu.au

Keywords: Aspirin-induced asthma, asthma, atopy, cyclooxygenase-1, haplotypes, polymorphism

Received: December 9, 2004
Accepted April 23, 2005

Cyclooxygenase-1 (COX-1) regulates the biosynthesis of prostaglandins, which are important mediators in asthma. The possible association of COX-1 gene polymorphisms with asthma has not been investigated.

The allele frequencies of 20 COX-1 polymorphisms were determined in a random Australian Caucasian population using MassARRAY technology. Informative and potentially functional promoter (c.8592C>T, c.1676C>T) and coding region (c.22C>T, c.50C>T) polymorphisms were investigated in carefully phenotyped patients with mild (n = 316), moderate (n = 241), severe (n = 86) or aspirin-intolerant asthma (AIA) (n = 58), and in nonasthmatic subjects (n = 477).

There were no allelic, genotypic or haplotypic associations between these four polymorphisms and asthma or asthma severity. Over-representation of the c.50TT genotype among AIA patients (3.4%) compared with aspirin-tolerant patients (0.8%), and a global haplotype association with AIA did not reach statistical significance. The c.22TT genotype was less frequent among atopic (0.1%) rather than nonatopic individuals (1.2%; odds ratio = 9.05, 95% confidence interval 1.01–81.29).

In conclusion, the present investigation of cyclooxygenase-1 polymorphisms in asthma indicates that they do not appear to play a substantial role in genetic pre-disposition for asthma or asthma severity. However, the c.22TT genotype confers a small protective effect against atopy. Potential associations with aspirin-intolerant asthma were identified and warrant further investigation in a larger population of aspirin-intolerant asthma patients.

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