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Changes in Gene Expression Related to Atopic Dermatitis in Mothers and Infants Following VOC Exposure
Seung Hwan Kim1, So Yeon Yu2, Jeong Hyeop Choo3
1Department of Bio-Nanotechnology, Hanyang University, Sangnok-gu, Ansan 15588, Gyeonggi-do, Republic of Korea.
Abstract:
Environmental pollutants, particularly volatile organic compounds (VOCs), are associated with various diseases, including atopic dermatitis (AD). However, despite numerous studies on AD, there is a lack of research on the impact of various environmental exposures on mothers and infants. This study, therefore, investigated the effects of maternal exposure to specific VOCs (toluene, xylene, and benzene) on the expression of AD-related genes in mothers and their infants. RNA expression levels and DNA methylation patterns were analyzed to examine the correlation between environmental exposures and AD. A multi-omics approach integrating gene expression and methylation data was additionally employed to gain a broader understanding of the genetic impact of VOC exposure. Network analysis revealed significant changes in gene expression associated with AD. For example, maternal exposure to toluene resulted in the upregulation of AQP10, which is linked to keratinocyte dysfunction, and in infants, the genes IL31RA and CCL20 were notably affected, both of which play critical roles in immune response and skin barrier function. In mothers exposed to xylene, the histamine receptor gene HRH1 was identified as a key player in influencing AD through its role in skin barrier recovery, while infants exhibited consistent network responses with upregulation of IL31RA and downregulation of TIGIT, reflecting a shared response across different xylene isomers. Interestingly, infants exposed to xylene isomers displayed nearly identical gene network patterns, suggesting developmental resistance to diverse environmental factors. No significant gene changes were identified in the benzene-exposed group. These findings suggest that exposure to specific VOCs may have different effects on gene expression related to AD, highlighting the complexity of how environmental factors contribute to disease development.
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