Asthma and pregnancy: emerging evidence of epigenetic interactions in utero

Purpose of reviewPregnancy is arguably the most critical period of developmental programming. Here, weparticularly focus on the emerging paradigm that disease propensity is epigeneticallydetermined by maternal exposures that have the capacity to activate or silence fetalgenes through alterations in DNA and histone methylation, histone acetylation, andchromatin structure.Recent findingsThe most notable recent candidate to emerge in this role has been dietary folate, amethyl donor clearly associated with changes in gene expression and diseasesusceptibility through gene hypermethylation. Animal studies also provide the firstevidence that the allergy protective effects of microbial exposure in pregnancy may bemediated by changes in methylation of Th1 genes of the offspring. There is alsoemerging evidence that perinatal differences in immune function of allergy-pronenewborns extend beyond previously recognized differences in effector T cell (Th1/Th2)function, to also include differences in neonatal regulatory T cell (Treg) and Th17function, and moreover, that these pathways are also epigenetically regulated.SummaryNew studies reinforce the importance of in-utero exposures (including dietary nutrients,microbial products, cigarette smoking, and certain maternal mediations) in fetal immunedevelopment and in programming the susceptibility to asthma and allergic disease.