DNA methylation at imprint regulatory regions in preterm birth and infection

Ying Liu1, Cathrine Hoyo, Susan Murphy

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

Insights

Intrauterine infections in preterm birth may alter DNA methylation at the PLAGL1 gene, potentially increasing chronic disease risk. This epigenetic change was observed in infants with chorioamnionitis and funisitis.

Area of Science:

  • Epigenetics
  • Developmental Biology
  • Perinatal Medicine

Background:

  • Intrauterine infections are linked to preterm birth and potential long-term health issues.
  • Epigenetic modifications, such as DNA methylation, play a crucial role in gene regulation and development.
  • Understanding the impact of infection on fetal epigenetics is vital for predicting future health outcomes.

Purpose of the Study:

  • To investigate DNA methylation patterns in preterm infants based on birth type and intrauterine infection status.
  • To examine methylation at 9 differentially methylated regions regulating imprinted genes.
  • To determine if infection (chorioamnionitis or funisitis) influences DNA methylation in preterm infants.

Main Methods:

  • Prospective cohort study of 73 mother-infant dyads.
  • Cord blood DNA methylation measured using bisulfite pyrosequencing at 9 imprinted gene regions.
  • Statistical analyses (ANOVA, logistic regression) to compare methylation by preterm birth type and infection status.

Main Results:

  • No significant differences in DNA methylation were found across different types of preterm birth.
  • Increased PLAGL1 DNA methylation was observed in infants with chorioamnionitis compared to those without (P < .01).
  • PLAGL1 DNA methylation was also elevated in infants with funisitis versus those without (P < .05).

Conclusions:

  • Intrauterine infections, specifically chorioamnionitis and funisitis, are associated with altered PLAGL1 DNA methylation in preterm infants.
  • Dysregulation of PLAGL1 is linked to abnormal development and cancer, suggesting potential long-term risks.
  • Early-life infection/inflammation may induce epigenetic changes that predispose individuals to chronic diseases later in life.
Abstract

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