Prenatal maternal diet affects asthma risk in offspring
Rachel L. Miller
Rachel L. Miller
Published September 18, 2008
Citation Information: J Clin Invest. 2008;118(10):3265-3268. https://doi.org/10.1172/JCI37171.
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Commentary

Prenatal maternal diet affects asthma risk in offspring

Abstract

Recently, epigenetic-mediated mechanisms — which involve heritable changes in gene expression in the absence of alterations in DNA sequences — have been proposed as contributing to asthma. In this issue of the JCI, Hollingsworth and colleagues report on the effect of prenatal maternal dietary intake of methyl donors on the risk of allergic airway disease in offspring in mice and show that these effects involve epigenetic regulation (see the related article beginning on page 3462). Supplementation of the maternal diet with methyl donors was associated with greater airway allergic inflammation and IgE production in F1 and, to some extent, F2 progeny. Site-specific differences in DNA methylation and reduced transcriptional activity were detected. If these findings are confirmed, a new paradigm for asthma pathogenesis may be emerging.

Authors

Rachel L. Miller

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Figure 1

Prenatal maternal diet affects asthma risk in offspring.

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Prenatal maternal diet affects asthma risk in offspring. Prenatal matern...
Prenatal maternal environmental exposure to diets high in folate, vitamin B12, choline, and methionine, which provide methyl donors, as well as to cigarette smoking may be associated with the covalent addition of a methyl group to cytosines in CpG dinucleotides and other epigenetic changes. These changes in turn may repress gene transcription and induce asthma phenotypes (i.e., airway allergic inflammation) in the offspring. As reported by Hollingsworth and colleagues in their study in mice in this issue of the JCI (25), prenatal methyl-rich diets may promote DNA methylation and reduce transcription of genes associated with the downregulation of allergic immune responses in the airway, such as runt-related transcription factor 3 (Runx3).