A polymorphism in the promoter region of the human interleukin-16 gene is not associated with asthma or atopy in an Australian population

Authors

  • L. S. Akesson,

    1. The Asthma and Allergy Research Institute Inc.,
    2. Cooperative Research Centre for Asthma, and
    3. Centre for Asthma, Allergy and Respiratory Research, University of Western Australia, Nedlands, WA, Australia
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  • D. L. Duffy,

    1. Genetic Epidemiology Laboratory, Queensland Institute of Medical Research, Brisbane, Australia
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  • S. C. Phelps,

    1. The Asthma and Allergy Research Institute Inc.,
    2. Cooperative Research Centre for Asthma, and
    3. Centre for Asthma, Allergy and Respiratory Research, University of Western Australia, Nedlands, WA, Australia
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  • P. J. Thompson,

    1. The Asthma and Allergy Research Institute Inc.,
    2. Cooperative Research Centre for Asthma, and
    3. Centre for Asthma, Allergy and Respiratory Research, University of Western Australia, Nedlands, WA, Australia
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  • M.-A. Kedda

    1. The Asthma and Allergy Research Institute Inc.,
    2. Cooperative Research Centre for Asthma, and
    3. Centre for Asthma, Allergy and Respiratory Research, University of Western Australia, Nedlands, WA, Australia
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Prof. Philip Thompson, Asthma and Allergy Research Institute, Ground Floor E Block, Sir Charles Gairdner Hospital, Nedlands, WA 6009, Australia.
E-mail: aari@aari.uwa.edu.au

Summary

Background IL-16 is an immunomodulatory cytokine whose expression is increased in the bronchial mucosa, bronchoalveolar lavage fluid and induced sputum of asthmatic patients. It has been suggested that IL-16 has a regulatory role in the pathophysiology of asthma. A single-nucleotide polymorphism (T−295C) has been described in the promoter region of the gene and it has been hypothesized that this polymorphism may be associated with altered levels of IL-16 expression, and account for the increased levels of IL-16 seen in the asthmatic airway.

Objective To determine the association between the T−295C promoter polymorphism and asthma, disease severity and atopy in a large Australian Caucasian population.

Methods We used PCR and restriction fragment length polymorphism analysis to establish the allele frequency of the T−295C promoter polymorphism in a random Australian Caucasian population (n=176) and to characterize the polymorphism in a large Australian Caucasian population of mild (n=273), moderate (n=230) and severe (n=77) asthmatic patients, and non-asthmatic controls (n=455). Genotype association analyses were performed using χ2 tests.

Results The polymorphic C allele was present in 19% of the asthmatic population and 21% of the non-asthmatic population. There was no association between the polymorphism and asthma (P=0.153) nor with asthma severity (P=0.417) or atopy (P=0.157) in this population.

Conclusion Although it has been hypothesized that the T−295C promoter polymorphism may be associated with increased IL-16 gene expression, it is not associated with asthma, disease severity or atopy in this Australian population.

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