Dog exposure may lower genetic risk of eczema in children

New research published in Allergy indicates that certain environmental exposures may affect a child's risk of developing atopic eczema, a condition characterized by dry, itchy, and inflamed skin. In other words, although some people may be genetically predisposed to eczema, certain environmental factors may increase or decrease that risk.

For the study, investigators analyzed data from 16 European studies to test for interactions between the 24 most significant eczema-associated genetic variants and 18 early-life environmental factors. They applied their findings to an additional 10 studies and used lab modelling tests to assess their results.

The first analysis (including 25,339 individuals) showed suggestive evidence for interaction between 7 environmental factors (antibiotic use, cat ownership, dog ownership, breastfeeding, elder sibling, smoking, and washing practices) and at least one established genetic variant for eczema, with 14 interactions in total.

In the additional analysis (254,532 individuals), dog exposure interacted with a particular genetic risk variant on chromosome 5, near the gene that codes for the interleukin-7 receptor, a protein involved in immune cell function. Lab modelling tests showed that this variant affects expression of interleukin-7 receptor in human skin cells and that dog exposure modifies the genetic effect of this variant on the development of eczema, essentially providing a protective effect by suppressing skin inflammation.

Additional studies are needed to explore these lab findings and the other potential interactions identified in the first analysis.

Our research aims to answer some of the most difficult questions that I am asked in clinic: 'Why does my child have eczema?' and 'What can I do to help protect my baby?' We know that genetic make-up affects a child's risk of developing eczema and previous studies have shown that owning a pet dog may be protective, but this is the first study to show how this may occur at a molecular level. More work is needed, but our findings mean we have a chance to intervene in the rise of allergic disease, to protect future generations."

Sara J. Brown, MD, PhD, FRCPE, corresponding author of the University of Edinburgh