Journal
CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY
Volume 7, Issue 1, Pages 75-82Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/ACI.0b013e328012ce39
Keywords
asthma; environmental exposure; experimental model; genetic predisposition to disease; research design
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Purpose of review Asthma is likely to result from the effects of environmental stimuli in genetically susceptible individuals. This review summarizes recent studies of gene-environmental interaction in the pathogenesis of asthma, focusing on study designs. Recent findings Studies using genetic epidemiology, in-vitro and ex-vivo models and in-vivo model; organisms demonstrate that gene-environmental interaction in involved in the development of asthma. Genetic association studies show a reduced risk of asthma and atopy with early life exposure to farming environments and house dust endotoxin, and increased risk with environmental tobacco smoke: These associations are modified, by CD14 genotype. In people with a specific genotype, high environmental exposure may have the opposite effect of low exposure, possibly explaining some of the inconsistencies in previous studies. In-vitro and ex-vivo cell culture experiments show gene - environmental interactions with Toll-like receptor agonists virus and tobacco smoke. Interactions between innate immunity genes and exposure to endotoxin and air pollution have been observed in-vivo mouse models. Summary The expanding evidence for gene - environmental interaction in asthma indicates the importance of measuring environmental factors in genetic studies of asthma. Understanding gene - environmental interaction would facilitate risk prognostication, improve preventive strategies and develop targeted interactions in people with asthma.
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