Epigenetics and prenatal influences on asthma and allergic airways disease

Abstract

Epigenetics and prenatal influences on asthma and allergic airways disease IntroductionAsthma is a complex, heritable disease that has been increasing in prevalence, incidence and severity [1], although recent evidence suggests that the prevalence of asthma and allergies may have come to a plateau in developed countries [2]. Several separate lines of evidence support a role for epigenetics in asthma. First, asthma, like epigenetic mechanisms, is heritable. While asthma is a strongly familial condition (36-79% heritability) with a non-Mendelian pattern of inheritance and polymorphisms in more than 100 genes [3-6], these associations have infrequently been replicated and genetics has explained only a small portion of the aetiology of this disease [4]. Second, asthma, like epigenetic mechanisms, shows a parentof-origin transmission of inheritance with an affected mother significantly more likely to transmit the disease than an affected father [7]. These parent-of-origin effects may result from immune interactions between the fetus and the mother [8]. Alternatively, the maternal effect may be the result of epigenetically regulated genomic imprinting [9]. Several known genes show parent-of-origin effects on allergic disease; these genes include the FceRI-b locus [10], and the Spink5 gene [11]. Third, asthma, like epigenetic mechanisms [12,13], is affected by in utero exposures HERMES syllabus link: modules A.1, B.6 Statement of InterestNone declared.