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Epigenetics and Prenatal Influences on Asthma and Allergic Airways Disease

David Martino, BSc(Hons); Susan Prescott, MD, PhD
Author and Funding Information

From the School of Paediatrics and Child Health Research, University of Western Australia, Perth, WA, Australia.

Correspondence to: Susan Prescott, MD, PhD, University of Western Australia, School Paediatrics and Child Health Research, Princess Margaret Hospital for Children, GPO Box D 184, Perth, WA, 6840, Australia; e-mail: sprescott@meddent.uwa.edu.au


Funding/Support: Dr Prescott is funded by a National Health and Medical Research Fellowship.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;139(3):640-647. doi:10.1378/chest.10-1800
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Uterine life is arguably the most critical time in developmental programming, when environmental exposures may have the greatest potential to influence evolving fetal structure and function. There has been substantial progress in understanding the epigenetic mechanisms through which environmental exposures can permanently alter the expression of fetal genes and contribute to the increasing propensity for many complex diseases. These concepts of “developmental origins” of disease are being applied across virtually all fields of medicine, and emerging epigenetic paradigms are the likely mechanism behind the environment-driven epidemic of asthma and allergic disease. Here, we examine the epigenetic regulation of immune development and the early immune profiles that contribute to allergic risk. In particular we review new evidence that key environmental exposures, such as microbial exposure, dietary changes, tobacco smoke, and pollutants, can induce epigenetic changes in gene expression and alter disease risk. Although most of these factors have already been clearly implicated in epidemiologic studies of asthma and allergic disease, new studies investigating the mechanisms of these effects may provide new avenues for using these pathways for disease prevention.

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