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Interleukin-1R antagonist gene and pre-natal smoke exposure are associated with childhood asthma

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

CORRESPONDENCE: S. L. Ewart, G-100 Veterinary Medical Center, Michigan State University, East Lansing, MI 48823, USA, Fax: 1 5174321037. E-mail: ewart{at}cvm.msu.edu

Keywords: Asthma, genetic association, interleukin-1 receptor antagonist, interleukin-1 receptor antagonist gene, maternal smoking, smoking

Received: February 27, 2006
Accepted November 3, 2006

The interleukin-1 receptor antagonist (IL1RN) is a potent anti-inflammatory cytokine. In the present study, association of the human IL1RN gene polymorphisms with asthma, bronchial hyperresponsiveness and forced expiratory volume in one second/forced vital capacity ratio was tested and the data was stratified by environmental tobacco smoke exposure in order to investigate a gene-smoking interaction.

In an unselected subset (n = 921) of the Isle of Wight birth (UK) cohort, which has previously been evaluated for asthma and related manifestations at ages 1, 2, 4 and 10 yrs, three IL1RN single nucleotide polymorphisms (SNP) were genotyped. Logistic regression and repeated measurement models for tests of association using a representative SNP rs2234678 were used, as all SNPs 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 and persistent asthma.

In conclusion, the present results show that in the first decade of life, the gene–environment interaction of the interleukin-1 receptor antagonist gene polymorphism rs2234678 and maternal smoking during pregnancy increased the risk for childhood asthma.

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