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Published online before print November 15, 2006
Eur Respir J 2006, doi:10.1183/09031936.00029506
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ORIGINAL ARTICLE

IL-1R antagonist gene and prenatal smoke exposure are associated with childhood asthma

R.A. Ramadas 1, A. Sadeghnejad 2, W. Karmaus 2, S.H. Arshad 3, S. Matthews 3, M. Huebner 4, D-Y. Kim 4, S.L. Ewart 5*

1 Comparative Medicine and Integrative Biology Graduate Program and
2 Arnold School of Public Health, University of South Carolina, Columbia, South Carolina; and
3 David Hide Asthma and Allergy Research Centre, St Mary's Hospital, Newport, Isle of Wight, UK
4 Dept of Statistics and Probability, Michigan State University, East Lansing, Michigan
5 Dept of Large Animal Clinical Sciences, College of Veterinary Medicine and

* To whom correspondence should be addressed. E-mail: ewart{at}cvm.msu.edu.


  Abstract

Interleukin-1 receptor antagonist is a potent anti-inflammatory cytokine. We tested for the association of human IL1RN gene polymorphisms with asthma, bronchial hyperresponsiveness (BHR) and forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) ratio. To investigate a gene-smoking interaction, we stratified by environmental tobacco smoke exposure (ETS).

We completely genotyped three IL1RN single nucleotide polymorphisms (SNPs) in an unselected subset (n=921) of the Isle of Wight birth cohort, which has previously been evaluated for asthma and related manifestations at ages 1, 2, 4 and 10 years. We used logistic regression and repeated measurement models for tests of association using a representative SNP rs2234678, as all the SNPs we tested were in strong linkage disequilibrium.

In the overall analysis, the SNP rs2234678 was not associated with asthma. However, in the stratum with maternal smoking during pregnancy the rs2234678 GG genotype significantly increased the relative risk of asthma in children, both in analyses of repeated asthma occurrences (OR 4.43, CI 1.62-12.1, p=0.0037) and persistent asthma (OR 4.53, CI 1.69-12.1, p=0.0025).

In conclusion, our results show that in the first decade of life, the gene-environment interaction of the IL1RN SNP rs2234678 and maternal smoking during pregnancy increased the risk for childhood asthma.

Keywords:  Asthma, genetic association, IL-1 receptor antagonist, IL1RN, maternal smoking, smoking




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