Ceramides and the Defective Barrier in Atopic Dermatitis

Atopic dermatitis (AD) is a common remitting-relapsing inflammatory skin disease characterized by eczematous lesions, xerosis, and pruritus. It is associated with a defective permeability barrier and increased susceptibility to Staphylococcus aureus colonization. It has been demonstrated that the abrogated epidermal barrier is related to a decreased mass of ceramides and long-chain fatty acids in the stratum corneum (SC). The inherent pH of healthy SC is below 5, and a low pH is required for proper assembly of the barrier lipids. In AD, the pH is elevated.

A defective permeability barrier of the SC is the primary defect in AD. This defect reflects a reduction of ceramide and fatty acid mass in the SC due to reduced glucocerebrosidase and acid sphingomyelinase activity and a shift in fatty acid synthesis from long-chain to short-chain fatty acids and the incorporation of these shorter fatty acids into ceramides. Topically applied ceramides can restore epidermal function to a damaged barrier. Ceramide-containing moisturizers have produced partial restoration of the barrier function in AD by influencing lipid organization. Other topical and systemic therapies are also discussed.

Correcting the barrier defect by topically supplied ceramides and long-chain fatty acids in sufficient amounts could contribute to restoration of the microbiome and decreasing irritation and pruritus.