Autor: |
Jane Dewar, Harvey Jf, J Wilkinson, Holgate St, Liggett Sb, N. S. Thomas, Pietro Liò, Morton N, Ian P. Hall, Iolo Doull, Amanda Wheatley |
Rok vydání: |
1997 |
Předmět: |
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Zdroj: |
Journal of Allergy and Clinical Immunology. 100:261-265 |
ISSN: |
0091-6749 |
DOI: |
10.1016/s0091-6749(97)70234-3 |
Popis: |
Background: The β 2 -adrenoceptor polymorphisms occurring at amino acid positions 16 (arginine to glycine) and 27 (glutamine to glutamate) are known to be functionally relevant and also disease-modifying in subjects with asthma. However, the contribution of these polymorphisms to the development of the asthmatic phenotype or other markers for allergic disease remains to be established. Objective: This large family study examines the contributions of these polymorphisms in determining the heritable component of markers for allergic disease in asthmatic families. Methods: Three hundred twenty-four individuals from 60 families multiplex for asthma selected by means of an asthmatic proband were characterized for the following markers of allergic disease: asthma, atopy, and serum IgE. The polymerase chain reaction was used to generate a 234 base pair fragment spanning the region of interest, and the β 2 -adrenoceptor polymorphism was then defined by allele-specific oligonucleotide hybridization. Segregation analysis was then performed. Results: We found a significant association ( p = 0.009) between the glutamine 27 β 2 -adrenoceptor polymorphism and elevated levels of IgE, which was supported by the observation of linkage between IgE and β 2 -adrenoceptor polymorphisms at locus 27 ( p = 0.037). However, there was no association between either the arginine-glycine 16 or the glutamine-glutamate 27 β 2 -adrenoceptor polymorphism and an increased risk of asthma or atopy per se. Conclusion: The glutamine 27 β 2 -adrenoceptor polymorphism appears to contribute to IgE variability in families with asthma. However, it seems that although both amino acid 16 and 27 β 2 -adrenoceptor polymorphisms are disease-modifying in subjects with asthma, they do not contribute markedly to the development of the asthmatic phenotype. (J Allergy Clin Immunol 1997;100:261-5.) |
Databáze: |
OpenAIRE |
Externí odkaz: |
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