Dog Exposure Affects Genetic Risk in Eczema, Study Finds
METHODOLOGY:
Researchers analyzed 16 European cohorts (n = 25,339) and replicated findings in 10 more (n = 254,532).
They tested for an interaction between 24 atopic eczema-associated genetic loci and 18 early-life environmental exposures.
In vitro experiments assessed IL-7R expression in keratinocytes of known rs10214237 genotype after exposure to dog allergen using cells from multiple donors.
TAKEAWAY:
The discovery analysis revealed 14 significant interactions ( P < .05 for all) between at least one gene variant for eczema and seven environmental factors (antibiotic use, cat ownership, dog ownership, breastfeeding, elder sibling, smoking, and washing practices).
< .05 for all) between at least one gene variant for eczema and seven environmental factors (antibiotic use, cat ownership, dog ownership, breastfeeding, elder sibling, smoking, and washing practices). The interaction between dog exposure and rs10214237 was confirmed in the replication analysis (odds ratio [OR], 0.91; P = .025).
= .025). The T allele of rs10214237 increased the risk for atopic eczema only in individuals not exposed to dogs (OR, 1.14; 95% CI, 1.08-1.22) but not in those with dog exposure (OR, 0.99; 95% CI, 0.93-1.05).
Keratinocytes with the T:T genotype demonstrated higher IL-7R mRNA expression than those with the C:C genotype.
mRNA expression than those with the C:C genotype. Dog allergen exposure downregulated IL-33 and TSLP but upregulated CXCL8 , CSF2 , CCL2 , and TNF , suggesting enhanced IL-10 signaling, which plays a suppressive role in atopic eczema.
IN PRACTICE:
'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,' study author Sara J. Brown, MD, PhD, of the Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, Scotland, said in a press release from Wiley, the publisher of Allergy . 'More work is needed, but our findings mean we have a chance to intervene in the rise of allergic disease, to protect future generations.'
SOURCE:
The study was led by Marie Standl, Institute of Epidemiology, Helmholtz Zentrum München — German Research Center for Environmental Health, Neuherberg, Germany, and was published online on June 4 in Allergy .
LIMITATIONS:
Genome-wide interaction analysis was not conducted. Replication samples sizes were not powered for some interactions. Detailed data on environmental factors were not available. The inclusion of predominantly White population may limit generalizability of findings.
DISCLOSURES:
The study received funding from the Innovative Medicines Initiative 2 Joint Undertaking, which was supported by the European Union's Horizon 2020 research and innovation programme and the European Federation of Pharmaceutical Industries and Associations. Many authors reported receiving research funding, honoraria, grants, and compensations for lectures and consulting from various organizations and pharmaceutical companies, including Wellcome Trust, UK Research and Innovation, Medical Research Council, Unilever, Pfizer, and AbbVie.
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