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Association of β 2 ‐adrenergic receptor polymorphisms with severe asthma
Author(s) -
John W. Holloway,
P. Rod Dunbar,
Greta Riley,
Gillian Sawyer,
Penny Fitzharris,
Neil Pearce,
Graham Le Gros,
Richard Beasley
Publication year - 2000
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.2000.00929.x
Subject(s) - asthma , odds ratio , pathogenesis , medicine , allele , polymorphism (computer science) , allele frequency , endocrinology , immunology , restriction fragment length polymorphism , genotype , gene , genetics , biology
Background There is considerable interest in the role of different candidate loci in the development of asthma. This study investigates the association between asthma severity and previously identified polymorphisms at two sites within the β 2 ‐adrenergic receptor (β 2 AR) gene: the Arg16→Gly16 and Gln27→Glu27 alleles. Methods Restriction enzyme analysis of amplified β 2 AR gene products (PCR‐RFLP) was used to analyse the frequency of the Arg16→Gly16 and Gln27→Glu27 polymorphisms within the β 2 AR gene in 95 severe asthmatic patients (with a markedly increased risk of death from asthma), 59 mild asthmatic patients, and a control group of 92 nonasthmatic subjects. Results The Gly16 polymorphism was significantly associated with asthma severity with odds ratios (95% CI) for the Gly16 allele being 1.56 (1.02–2.40, P = 0.04) and 0.98 (0.61–1.57, P = 0.92) for the severe and mild asthma groups, respectively. The corresponding odds ratios (95% CI) for Gly16 homozygotes were 1.91 (0.82–4.41, P = 0.13) and 0.82 (0.35–1.92, P = 0.65) for the severe and mild asthma groups, respectively. There was no significant association between either polymorphism at amino acid 27 and asthma or asthma severity. Conclusions We conclude that the polymorphisms of amino acids 16 and 27 of the β 2 AR gene are not associated with the development of asthma per se , but that the Gly16 polymorphism may play a role in the pathogenesis of asthma severity.