MRNAs in skin surface lipids unveiled atopic dermatitis at one month.

Abstract

The molecular pathogenesis of atopic dermatitis (AD), presenting skin barrier dysfunction and abnormal inflammations around 1-2 months is unreported. We aimed to examine the molecular pathogenesis of very early-onset AD by skin surface lipid-RNA (SSL-RNA) using a non-invasive technology in infants aged 1 and 2 months from a prospective cohort. We collected sebum by oil-blotting film of infants aged 1 and 2 months and analyzed RNAs in their sebum. We diagnosed AD according to the United Kingdom Working Party's criteria. Infants with AD aged one month showed lower expression of genes related to various lipid metabolism and synthesis, antimicrobial peptides, tight junctions, desmosomes, and keratinization. They also had higher expression of several genes involved in Th2-, Th17-, and Th22-type immune responses and lower expression of negative regulators of inflammation. In addition, gene expressions related to innate immunity were higher in AD infants. Infants aged one month with neonatal acne and diagnosed with AD aged two months already had gene expression patterns similar to AD aged one month in terms of redox, lipid synthesis, metabolism, and barrier-related gene expression. We identified molecular changes in barrier function and inflammatory markers that characterize the pathophysiology of AD in infants aged one month. We also revealed that neonatal acne at one month could predict the subsequent development of AD by sebum transcriptome data.