The barrier function in atopic dry skin. Disturbance of membrane-coating granule exocytosis and formation of epidermal lipids?

Non-eczematous atopic dry skin (DS) shows an enhanced transepidermal water loss denoting an impaired water permeability barrier (WPB) function. The WPB is formed by intercellular lipid lamellae located between the horny cells of stratum corneum (SC). The lipids are provided via the exocytosis of membrane-coating granules (MCG). By differentiating two dynamic states of MCG, the ultrastructural morphometric comparison of atopic DS and healthy skin of controls revealed a retarded and incomplete extruding mechanism of these organelles. Additionally the structure and spacial organization of the epidermal lipids in DS and healthy skin were visualized and analysed by applying a special primary fixation (acrolein vapour) and post-fixation with ruthenium tetroxide. The present findings suggest that some pathologic extruding mechanism of MCG in DS may be responsible, at least partly, for the recently detected biochemical alterations of epidermal lipids and for the deficient WPB.