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Interleukin 13, CD14, pet and tobacco smoke influence atopy in three Dutch cohorts: the allergenic study

Depts of ¹ Pulmonology, and ³ Epidemiology, University Medical Center Groningen, Depts of ² Paediatrics, and ⁴ Paediatric Pulmonology, Beatrix Children's Hospital, University Medical Center Groningen, University of Groningen, Groningen, ⁵ Dept of Medical Microbiology, University Hospital Maastricht, ⁶ Dept of Epidemiology, Care and Public Health Research Institute, and Nutrition and Toxicology Research Institute Maastricht, ⁹ Dept of General Practice and Care and Public Health Research Institute, Maastricht University, Maastricht, ⁷ Institute for Risk Assessment Sciences, University of Utrecht, and ⁸ Julius Center for Health Sciences and Primary Care, University Medical Centre Utrecht, Utrecht, The Netherlands.

CORRESPONDENCE: D. S. Postma, Dept of Pulmonology, University Medical Center Groningen, P.O. Box 196, 9700 AD Groningen, The Netherlands, . Fax: 31 503619320. E-mail: d.s.postma{at}int.umcg.nl

Keywords: Atopy, CD14, environmental tobacco smoke, interleukin 13, pets

Received: December 3, 2007
Accepted April 5, 2008

Studying gene–environment interactions may elucidate the complex origins of atopic diseases but requires large study populations. Pooling data from several cohort studies may help but may also obscure findings. Gene–environment interactions in atopy development were studied and the benefits of pooling data were evaluated.

Haplotype-tagging polymorphisms in the genes interleukin (IL)13 and CD14 were genotyped in 3,062 children from the following birth cohorts: the Prevention and Incidence of Asthma and Mite Allergy (PIAMA) study; the Prevention of Asthma in Children (PREVASC) study; and the Child, Parent, Health, Focus on Lifestyle and Predisposition (KOALA) study, and tested for association with total and specific immunoglobulin (Ig)E and interaction with tobacco smoke and pet exposure at ages 1, 2, 4 and 8 yrs by analysis of variance, Chi-squared tests and regression analyses.

At all ages, in IL13, minor alleles of rs1295685 and rs20541 were significantly associated with elevated IgE levels in pooled analyses. In CD14, the rs2569190-TT and rs2569191-CC genotypes associated with lower IgE and decreased risk of sensitisation at 4 and 8 yrs in children exposed to pets, with an opposite effect in nonexposed children. Findings for IL13 and CD14 were comparable in separate cohorts.

The present study indicates that atopy is importantly influenced by interleukin 13 at age 1–8 yrs and by CD14 in interaction with pet exposure at ages 4 and 8 yrs. Additionally, pooled data improved effect estimates and genetic effects could be detected in interaction with important environmental factors.

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