D1.239 - Are Maternal Epidermal Lipid Profiles Associated with Atopic Dermatitis Development in Early Childhood?
Background
Early-life epidermal barrier impairment contributes to the development of atopic dermatitis (AD). While infant skin lipid composition has been studied, little is known about whether maternal stratum corneum (SC) lipid profiles in early infancy are associated with subsequent AD development in offspring.
Method
This birth cohort study included 106 mother–child pairs, with children followed prospectively until 3 years of age. Maternal and infant forearm SC samples were collected at 2 months postpartum using skin tape stripping. Lipidomic analyses were performed using liquid chromatography–electrospray ionization tandem mass spectrometry.
Results
By age 3, children were classified as AD-positive (n=34) or AD-negative (n=72) based on physician diagnosis. Mothers of children who developed AD had significantly higher levels of multiple ultra–long-chain esterified ω-hydroxy ceramides (EOS-CER), particularly EO30–EO34 species across C18, C20, and C22 sphingoid bases (P<0.05). Total maternal EOS-CER levels were higher in the AD group than in the non-AD group (median 1205.2 vs 971.9, P=0.039). In addition, several maternal ceramide subclass ratios reflecting the balance between non-hydroxy fatty acid–sphingosine ceramides (NS-CER) and non-hydroxy fatty acid–phytosphingosine ceramides (NP-CER), including C20S/C20P and C22S/C22P, were elevated in mothers of children who developed AD (P<0.05). Ratios of EOS-CER to corresponding protein-bound ceramides were also higher in the AD group. Spearman correlation analyses demonstrated overall positive correlation patterns between maternal and infant SC ceramide profiles, particularly for EOS-CER, NS-CER, and NP-CER.
Conclusion
Maternal SC ceramide profiles at 2 months postpartum are associated with the subsequent development of AD in children up to 3 years of age, suggesting that maternal skin barrier lipid characteristics may reflect early-life biological contexts relevant to offspring AD risk.
