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Abstract
Lipids are important constituents of the human epidermis. Either free and organized into broad lipid bilayers in the intercorneocytes spaces, or covalently bound to the corneocyte envelope, they play a crucial role in permeability barrier function. This article presents the structures of various human skin ceramides, their role in the maintenance of skin barrier function and homeostasis, and their qualitative and quantitative changes in some cases of dry skin or atopic xerosis. Moreover, we show that reconstructed human skin models could provide valuable tools to assess in vitro the biological interest of active compounds on epidermal lipogenesis. Based on such in vitro studies, we assume that the association of vitamin C and some exogenous sphingolipid could enhance the endogenous ceramide content deficient in some cases of atopic dry skin.
Highlights
Lipids are important components of human epidermis
It has been shown that qualitative and/or quantitative changes in stratum corneum lipids may result in defective barrier function, impaired water-retention function, and higher penetration of exogenous compounds through the skin and appearance of dry skin
We recently identify the presence of two novel types of bound ceramides, one that is composed of a sphinganine base, the second displaying a phytosphingosine (PHY) base and both supposedly linked to an a-hydroxyacid [2]
Summary
Mide multi-lamellae organization and for barrier function property of the skin. Recently, we determined a new profile of human stratum corneum ceramide including two new classes. The lamellar structure results from the accumulation and reorganization of lipid-rich organelles, lamellar bodies, which are excreted into intercellular spaces at the interface between stratum corneum and stratum granulosum This specific lipid organization has been reported to be responsible for the barrier function [3], and the loss of the lamellar structure after solvent extraction or its absence in specific skin disorders, such as free fatty acid deficiency, is associated with breakdown of the barrier properties [4,5,6]. Ceramides, which are essential for the structure and the stability of stratum corneum lipid sheets, have been shown to be reduced in atopic dermatitis and ceramide metabolism abnormalities are thought to be etiological factor for dry and barrier disrupted skin Keeping this information in mind, many attempts have been made to elucidate the biochemical mechanisms involved in the ceramide deficiency observed in atopic dermatitis. Recent studies have challenged these findings indicating that barrier alterations observed in atopic dermatitis are dependent upon the skin zone evaluated as well as the clinical characteristics of subjects being studied
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