The role of epigenetics in the developmental origins of allergic disease

Ann Allergy Asthma Immunol. 2011 May;106(5):355-61; quiz 362. doi: 10.1016/j.anai.2011.02.008. Epub 2011 Mar 16.

Abstract

Objective: To review current research findings in the field of epigenetics pertaining to the developmental origins of allergic disease.

Data sources: We examined original research and review articles identified from MEDLINE, OVID, and PubMed that addressed the topic of interest, using the search terms atopy, allergy, asthma, development, IgE, origins, and cord blood paired with epigenetic(s). Relevant references from each article were also procured for review.

Study selection: Articles were selected based on their relevance to the contributory role of epigenetic modifications in asthma and other atopic diseases.

Results: There is increasing evidence pointing to the influence of prenatal and early life exposures on the development of allergic disease. A growing body of literature supports the theory that transient environmental pressures can have permanent effects on gene regulation and expression through epigenetic mechanisms. Histone modifications have been associated with degree of bronchial hyperresponsiveness and corticosteroid resistance in asthma. Epigenetic mechanisms can operate independently in various cell types; recent studies have suggested a role in the differentiation of human T cells. Murine studies have revealed that a maternal diet rich in methyl donors can enhance susceptibility to allergic inflammation in the offspring, mediated through increased DNA methylation. Murine studies have also implicated epigenetically modified dendritic cells in the transmission of allergic risk from mothers to offspring.

Conclusion: The current literature offers exciting data to support a role for epigenetics in the development and persistence of asthma and allergic rhinitis. However, further human studies are necessary to explore these mechanisms and assess future clinical applicability.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Epigenesis, Genetic / physiology*
  • Genomic Imprinting / physiology
  • Humans
  • Hypersensitivity / drug therapy
  • Hypersensitivity / etiology*
  • Hypersensitivity / genetics
  • Hypersensitivity / metabolism