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Exogenous Lipids Influence Permeability Barrier Recovery in Acetone-Treated Murine Skin
Mao-Qiang Man, MD;
Kenneth R. Feingold, MD;
Peter M. Elias, MD
Arch Dermatol. 1993;129(6):728-738.
Abstract
• Background and Design.—
When the epidermal permeability barrier is perturbed with acetone, transcutaneous water loss returns to normal over 24 hours in parallel with the reappearance of stratum corneum lipids, derived from secreted lamellar bodies and accelerated lipid synthesis. Prior studies have demonstrated a separate requirement for cholesterol, fatty acid, and ceramide synthesis for barrier homeostasis, but the requirement for these lipids individually or together for barrier function is not known. We therefore applied these lipids alone or in various mixtures to acetonetreated hairless mouse skin and assessed barrier recovery.
Results.—
Ceramide and fatty acid alone, and their complex derivatives (cholesterol esters and cerebrosides), and two-component mixtures of fatty acid plus ceramide, cholesterol plus fatty acid, or cholesterol plus ceramide delayed barrier recovery. In contrast, complete mixtures of ceramide, fatty acid, and cholesterol allowed normal barrier recovery. Moreover, fluorescent-labeled cholesterol, fatty acid, and ceramide rapidly traversed the stratum corneum with uptake into the epidermal nucleated layers. Finally, incomplete, but not complete mixtures produce abnormal lamellar bodies, leading to abnormal stratum corneum intercellular membrane bilayers.
Conclusions.—
(1) Topical applications of individual lipids or incomplete mixtures of lipids interfere with barrier Conclusions.—(1) ery, while complete mixtures of cholesterol, fatty acid, and ceramide allow normal barrier repair; and (2) incomplete mixtures of topical lipids appear to inhibit barrier recovery at the level of the lamellar body resulting in abnormal intercellular membrane structures in the stratum corneum, abnormalities that do not occur when a complete lipid mixture is provided.
(Arch Dermatol. 1993;129:728-738)
Author Affiliations
From the Dermatology Service (190) and Metabolism Section (111F), Veterans Affairs Medical Center, and the Departments of Dermatology and Medicine, University of California School of Medicine, San Francisco.
Footnotes
Accepted for publication February 9, 1993.
Presented in part at the annual meeting of the Skin Pharmacology Society, Cleveland, Ohio, October 14-16, 1992.
Reprint requests to the Dermatology Service (190), Veterans Affairs Medical Center, 150 Clement St, San Francisco, CA 94121 (Dr Elias).
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