Surfactant-Induced Depletion of Ceramides and Other Intercellular Lipids: Implication for the Mechanism Leading to Dehydration of the Stratum corneum

Abstract

In order to clarify the mechanisms underlying the surfactant-induced dehydration of the stratum corneum (SC), we first examined the constitutive water-holding function of the SC by removing intercellular lipids as well as hygroscopic materials from intact human SC. The dehydration of the SC can be easily induced by depletion of intercellular lipids, but was not affected by an additional water treatment, which releases a large amount of hygroscopic materials including amino acids. Consistent with this, the application of isolated intercellular lipids or their subfractions to the lipid-depleted and dehydrated SC rescues the decreased water content as well as marked scaling, although glycerine did not have such an effect. Parallel differential scanning calorimetry analysis revealed that lipid depletion causes the SC to reduce the nonfreezable bound water content and that application of isolated intercellular lipids recovered the bound water content up to the control level. On the other hand, the additional release of hygroscopic materials from lipid-depleted SC did not affect the bound water content. Based upon the above constitutive water-holding mechanism in the SC, we assessed the physicochemical mechanisms involved in surfactant-induced dehydration of the SC, leading to tight sensation and skin roughness. Similar to treatment with acetone/ether, treatment with surfactant releases a significant amount of intercellular lipids, the intensity of which varies among various surfactants but correlates well with the intensity of the induced dehydration of the SC leading to the tight skin sensation and skin roughness. Recovery or inhibition experiments revealed that the dehydration of the SC induced by surfactant treatment is significantly attenuated by the application of isolated intercellular lipids or by the addition of monoglyceride (MG) during the washing process, which results in a significant reduction in skin roughness. The latter study showed that whereas the release of sebum components and amino acids during surfactant treatment is not affected by the addition of MG, the removal of ceramides is significantly attenuated by the addition of MG, which suggests an essential role for ceramide depletion in the induction of the surfactant-induced dehydration of the SC. In conclusion, the above findings collectively suggest that the ceramide content in the SC is strongly associated with the regulation of SC hydration and that its deficiency due to surfactant treatment is essentially responsible for the surfactant-induced dehydration of the SC. This hypothesis is further strengthened by the fact that synthetic pseudoceramides are remarkably effective in preventing or abolishing the dehydration of the SC which is an intrinsic factor for inducing the tight sensation and roughness of the skin and which provides a pathological basis for atopic dry skin.