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Associations between antibiotic exposure during pregnancy, birth weight and aberrant methylation at imprinted genes

A C Vidal1, S K Murphy, A P Murtha

  • 1Division of Epidemiology, Department of Obstetrics and Gynecology, Duke University School of Medicine, Durham, NC 27710, USA.

International Journal of Obesity (2005)
|April 24, 2013
PubMed

Insights

Maternal antibiotic use during pregnancy is linked to lower birth weight in infants. This study provides evidence for epigenetic mechanisms, specifically imprinted gene methylation, playing a role in this association.

Area of Science:

  • Reproductive biology and epigenetics
  • Perinatal health and developmental origins of disease

Background:

  • Low birth weight (LBW) is a risk factor for adult chronic diseases.
  • Antibiotic exposure during pregnancy is a potential, understudied contributor to LBW.
  • Epigenetic mechanisms are hypothesized to mediate the link between antibiotic use and LBW.

Purpose of the Study:

  • To investigate the association between maternal antibiotic use and LBW.
  • To explore the role of DNA methylation in imprinted genes in this relationship.

Main Methods:

  • Prospective cohort study of 397 pregnant women.
  • Ascertainment of prenatal antibiotic use via self-report.
  • Measurement of DNA methylation at imprinted gene differentially methylated regions (DMRs) using bisulfite pyrosequencing.
  • Statistical analysis using generalized linear models.

Main Results:

  • Maternal antibiotic use was associated with a 138g reduction in birth weight, after adjusting for multiple confounders.
  • The association was more pronounced with non-penicillin antibiotics.
  • Maternal antibiotic use correlated with altered methylation at several imprinted gene DMRs (IGF2, H19, PLAGL1, MEG3, PEG3).
  • Methylation at the PLAGL1 DMR was specifically associated with birth weight.

Conclusions:

  • An inverse association exists between in utero antibiotic exposure and infant birth weight.
  • This study offers the first empirical support for imprinted gene plasticity in response to prenatal antibiotic exposure.
Abstract

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