Volume 120, Issue 1 , Pages 84-90, July 2007
Polymorphisms in IL13, total IgE, eosinophilia, and asthma exacerbations in childhood
Background
It is unclear whether single nucleotide polymorphisms (SNPs) in the gene for IL-13 (IL13) influence asthma severity and/or asthma morbidity.
Objectives
To examine the relation between IL13 SNPs and asthma-related phenotypes in 2 independent populations.
Methods
We used family-based methods to test for association between SNPs in IL13 and asthma-related phenotypes in Costa Rican children with asthma. We attempted to reproduce significant findings in white (non-Hispanic) children with asthma in the Childhood Asthma Management Program (CAMP).
Results
In Costa Rica and in CAMP, the A allele (Gln) of IL13 coding SNP (rs20541) was significantly associated with increased eosinophil count (P < .011 in both studies) and increased serum total IgE (P < .054 in both studies). The T allele of IL13 promoter SNP (rs1800925) was inversely associated with asthma exacerbations in Costa Rica (P = .069). Although this SNP (rs1800925) was not associated with asthma exacerbations among all white children in CAMP, it was associated with increased risk of asthma exacerbations among children on inhaled corticosteroids (P = .02).
Conclusion
Polymorphisms in IL13 were significantly associated with serum total IgE and eosinophil count in 2 populations. IL13 polymorphisms may also be associated with asthma exacerbations, and this effect may be dependent on medication use. Our study is the first to report a potential negative interaction between a genetic polymorphism and response to inhaled corticosteroids.
Clinical implications
Polymorphisms in IL13 are associated with serum total IgE and eosinophil count and may be associated with asthma exacerbations.
Key words: IL13, asthma, IgE, eosinophil, severity, exacerbations, Costa Rica, CAMP
Abbreviations used: CAMP, Childhood Asthma Management Program, FBAT, Family-based association test, FVC, Forced vital capacity, SNP, Single nucleotide polymorphism
Supported by grants HL04370 and HL66289 from the National Institutes of Health. The CAMP Genetics Ancillary Study is supported by the National Heart, Lung, and Blood Institute, N01-HR-16049. Additional support for this research came from grants P50 HL67664 and T32 HL07427 from the National Institutes of Health and the National Heart, Lung, and Blood Institute.Disclosure of potential conflict of interest: E. K. Silverman has consulting arrangements with GlaxoSmithKline; has received grant support from GlaxoSmithKline; has received money for a talk on chronic obstructive pulmonary disease genetics from Wyeth; and has received honoraria from Bayer. The rest of the authors have declared that they have no conflict of interest.
PII: S0091-6749(07)00858-5
doi:10.1016/j.jaci.2007.04.032
© 2007 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Volume 120, Issue 1 , Pages 84-90, July 2007
