Fartasch M, Diepgen T L
Department of Dermatology, University of Erlangen, Germany.
Acta Derm Venereol Suppl (Stockh). 1992;176:26-31.
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.
非湿疹性特应性干性皮肤（DS）表现出经表皮水分流失增强，这表明水渗透屏障（WPB）功能受损。WPB由位于角质层（SC）角质形成细胞之间的细胞间脂质片层形成。脂质通过膜包被颗粒（MCG）的胞吐作用提供。通过区分MCG的两种动态状态，对特应性DS和对照健康皮肤进行超微结构形态计量学比较，发现这些细胞器的挤出机制延迟且不完全。此外，通过应用特殊的初次固定（丙烯醛蒸汽）和四氧化钌后固定，对DS和健康皮肤中表皮脂质的结构和空间组织进行了可视化和分析。目前的研究结果表明，DS中MCG的某些病理性挤出机制可能至少部分地导致了最近检测到的表皮脂质生化改变和WPB缺陷。
