Epigenetics, Asthma, and Allergic Diseases: A Review of the Latest Advancements

Abstract

Environmental epigenetic regulation in asthma and allergic disease is an exciting area that has gained a great deal of scientific momentum in recent years. Environmental exposures, including prenatal maternal smoking, have been associated with asthma-related outcomes that may be explained by epigenetic regulation. In addition, several known allergy and asthma genes have been found to be susceptible to epigenetic regulation. We review the latest experimental and translational studies that have been published this past year in several areas, including 1) characterization of environmental asthma triggers that induce epigenetic changes, 2) characterization of allergic immune and regulatory pathways important to asthma that undergo epigenetic regulation, 3) evidence of active epigenetic regulation in asthma experimental models and the production of asthma biomarkers, 4) evidence of transmission of an asthma-related phenotype across multiple generations, and 5) “pharmaco-epigenetics.” The field has certainly advanced significantly in the past year.

The ‘golden age’ of DNA methylation in neurodegenerative diseases

“…Strictly linked to the immune systems disorders, allergic disorders appear to be linked to epigenetic changes due to the role of environmental factors in early life [ 49 ]. According to emerging theories, in utero exposure to specific factors may be associated with epigenetic aberrations affecting the expression of genes involved in immune programming, thus resulting in the development of allergic disorders in the offspring and, maybe, [ 50 ] in future generations.…”

DNA methylation in lung cells is associated with asthma endotypes and genetic risk

“…It is likely, therefore, that additional genetic variants remain to be discovered, including those involved in gene-environment interactions that may not reach criteria for significance in GWAS (5-7). Many asthma-promoting environmental exposures alter epigenetic profiles in airway cells (8)(9)(10), suggesting that changes in DNA methylation may be a mechanism through which environmental exposures modify asthma risk or contribute to phenotypic heterogeneity. Given the combined importance of environmental exposures and genetic variation on disease risk, a comprehensive understanding of the molecular architecture of asthma requires approaches that integrate genetic, epigenetic, and transcriptional variation with phenotypic measures of specific asthma endotypes (5).…”

Folate and Asthma

“…For example, maternal levels of folate (a methyl donor) could alter the risk of asthma by causing hypo-or hypermethylation (and thus increased or decreased expression) of disease-susceptibility genes in relevant fetal tissues (6,7).…”