Topical Ceramide Corrected Epidermal Cell Hyperproliferation and Stratum Corneum Dysmaturation in Atopic eczema

Abstract

Until now, the common strategy for atopic eczema (AE) therapy is how to treat or suppress the already established eczema, or how to control the general immune responses against antigens. It has been accepted that AE shows a delayed-type hypersensitivity to exogenous antigens especially in adulthood [1]. The characteristic distribution of skin lesions, of the exposed and flexure regions, are also suggestive of dose dependency of exogenous antigen distribution over the skin. On the other hand, dry and rough surface of AE patients’ skin [2] strongly suggests decreased skin surface water content [3] and lipid [4], which was supported by the increased transepidermal water loss (TEWL) in AE patients. The increased TEWL dose does not mean simply increased transport of water, but also easier penetration of larger materials such as antigens, which is compatible to deteriorated skin barrier function. Recently, we showed the importance of epidermal ceramides in cutaneous barrier function in the essential fatty acid deficiency rat model [5]. Among the variety of ceramides, pseudo-o-acylceramide with linoleic acid (OAC) only showed significant effects in the recovery of TEWL in the rat experimental model. As we expected, topical OAC treatment on AE skin successfully suppressed TEWL close to normal level. Since the vehicle (OAC cream minus OAC) alone and white petrolatum had no significant effects in restoring of TEWL, we could confirm the effect of OAC in AE-related dry skin.