Abstract

The corneocyte layers forming the upper surface of mammalian skin are embedded in a lamellar-membrane matrix which repels harmful molecules while retaining solutes from subcutaneous tissues. Only certain bacterial and fungal taxa colonize skin surfaces. They have ways to use epidermal lipids as nutrients while resisting antimicrobial fatty acids. Skin microorganisms release lipophilic microbe-associated molecular pattern (MAMP) molecules which are largely retained by the epidermal lipid barrier. Skin barrier defects, as in atopic dermatitis, impair lamellar-membrane integrity, resulting in altered skin microbiomes, which then include the pathogen Staphylococcus aureus. The resulting increased penetration of MAMPs and toxins promotes skin inflammation. Elucidating how microorganisms manipulate the epidermal lipid barrier will be key for better ways of preventing inflammatory skin disorders.

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