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Clinical & Experimental Allergy

Prenatal smoke exposure, DNA methylation, and childhood atopic dermatitis

Authors

  • I.-J. Wang,

    1. Department of Pediatrics, Taipei Hospital Department of Health, Taipei, Taiwan
    2. College of Public Health, China Medical University, Taichung, Taiwan
    3. College of Medicine, National Yang-Ming University, Taipei, Taiwan
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  • S.-L. Chen,

    1. Genomics, BioSci & Tech, Taipei, Taiwan
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  • T.-P. Lu,

    1. YongLin Biomedical Engineering Center, National Taiwan University, Taipei, Taiwan
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  • E. Y. Chuang,

    1. YongLin Biomedical Engineering Center, National Taiwan University, Taipei, Taiwan
    2. Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University, Taipei, Taiwan
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  • P.-C. Chen

    Corresponding author
    1. Institute of Occupational Medicine and Industrial Hygiene, National Taiwan University College of Public Health, Taipei, Taiwan
    2. Department of Public Health, National Taiwan University College of Public Health, Taipei, Taiwan
    3. Department of Environmental and Occupational Medicine, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan
    • Department of Pediatrics, Taipei Hospital Department of Health, Taipei, Taiwan
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Correspondence:

Pau-Chung Chen, Institute of Occupational Medicine and Industrial Hygiene, National Taiwan University College of Public Health, Room 733, 17 Syujhou Road, Taipei 10055, Taiwan.

E-mail:pchen@ntu.edu.tw

Summary

Background

The biological mechanisms of how prenatal smoke exposure leading to atopic disorders remain to be addressed. Whether prenatal smoke exposure affects DNA methylation leading to atopic disorders is not clear.

Objective

As most children suffering from atopic dermatitis (AD) continue to develop asthma later in life, we explored whether prenatal smoke exposure induces cord blood DNA methylation.

Methods

Methylation differences associated with smoke exposure were screened by Illumina Infinium 27K methylation arrays for 14 children from the Taiwan birth panel study cohort initially. Information about development of atopic dermatitis (AD) and risk factors was collected. Cord blood cotinine levels were measured to represent prenatal smoke exposure. CpG loci that demonstrated a statistically significant difference in methylation were validated by methylation-dependent fragment separation (MDFS). Differential methylation in three genes (TSLP, GSTT1, and CYB5R3) was identified through the screen.

Results

Among these, only thymic stromal lymphopoietin (TSLP) gene displayed significant difference in promoter methylation percentage after being validated by MDFS (= 0.018). TSLP gene was further investigated in a larger sample of 150 children from the cohort who completed the follow-up study. Methylation status of the TSLP 5′-CpG island (CGI) was found to be significantly associated with prenatal smoke exposure (OR=3.17, 95% CI=1.63–6.19) and with AD (OR=2.32, 95% CI=1.06–5.11). The degree of TSLP 5′CGI methylation inversely correlated with TSLP protein expression levels (r = −0.45, = 0.001).

Conclusions & Clinical Relevance

The effect of prenatal tobacco smoke exposure on the risk for AD may be mediated through DNA methylation.

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