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Prenatal smoke exposure, DNA methylation, and childhood atopic dermatitis

I-J Wang1, S-L Chen, T-P Lu

  • 1Department of Pediatrics, Taipei Hospital Department of Health, Taipei, Taiwan.

Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology
|April 23, 2013
PubMed

Insights

Prenatal smoke exposure may increase the risk of atopic dermatitis (AD) by altering DNA methylation in the thymic stromal lymphopoietin (TSLP) gene. This epigenetic change in TSLP is linked to both smoke exposure and AD development in children.

Area of Science:

  • Epigenetics
  • Environmental Health
  • Pediatrics

Background:

  • Biological mechanisms linking prenatal smoke exposure to atopic disorders are not fully understood.
  • The role of DNA methylation in mediating the effects of prenatal smoke exposure on atopic diseases requires further investigation.

Purpose of the Study:

  • To investigate whether prenatal smoke exposure induces DNA methylation changes in cord blood.
  • To explore the association between prenatal smoke exposure, DNA methylation, and the development of atopic dermatitis (AD).

Main Methods:

  • Screening of methylation differences using Illumina Infinium 27K arrays in a cohort of 14 infants.
  • Validation of differentially methylated CpG loci using methylation-dependent fragment separation (MDFS).
  • Measurement of cord blood cotinine levels to quantify prenatal smoke exposure.

Main Results:

  • Significant promoter methylation differences were identified in the thymic stromal lymphopoietin (TSLP) gene.
  • TSLP 5'-CpG island (CGI) methylation was significantly associated with prenatal smoke exposure (OR=3.17) and AD (OR=2.32) in a larger cohort.
  • Increased TSLP 5'CGI methylation inversely correlated with TSLP protein expression (r=-0.45).

Conclusions:

  • Prenatal tobacco smoke exposure may increase the risk of atopic dermatitis (AD) through epigenetic modifications, specifically DNA methylation.
  • The TSLP gene's methylation status serves as a potential biomarker linking prenatal smoke exposure to AD development.
Abstract

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