ABSTRACT
Epidermal barrier function to water loss is maintained by lipid membrane domains located in the interstices of the stratum corneum. Exposure of the epidermis to a dry environment or UV irradiation stimulates barrier lipid synthesis and accumulation of the organic osmolyte taurine in the outermost granular keratinocyte layer. In this work we studied a possible relationship between these two different epidermal responses to environmental challenges. As a model system we selected anionic surfactant-induced barrier perturbation. Incubation of reconstructed epidermis with taurine inhibited cytotoxic and proinflammatory effects induced by sodium dodecyl sulfate including (i) a decrease in interleukin-1 alpha and prostaglandin E2 release, (ii) stabilization of keratinocyte membrane integrity, and (iii) improvement of keratinocyte viability. Repeated exposure of human skin to sodium dodecyl sulfate induced an increase in transepidermal water loss, inflammation, and hyperplasia. Topical application of taurine significantly decreased transepidermal water loss after repeated exposure to sodium dodecyl sulfate. Moreover, taurine significantly stimulated the synthesis of all three classes of barrier lipids (ceramides, cholesterol, and fatty acids) in reconstructed epidermis. In conclusion, our data suggest a role for taurine in preventing surfactant-induced dry and scaly skin by modulating the proinflammatory response and stimulating epidermal lipid synthesis.
