DISTURBED EXTRUDING MECHANISM OF LAMELLAR BODIES IN DRY NONECZEMATOUS SKIN OF ATOPICS

A characteristic feature of non-eczematous atopic dry skin (DS) appears to be an impaired water permeability barrier (WPB) function. The WPB is constituted by intercellular lipid lamellae, located between the horny cells of the stratum corneum (SC), which are provided by exocytosis of lamellar bodies (LB). The aim of this study was to elucidate whether alterations in the dynamics of LB-extrusion could be responsible for this WPB disturbance. In an ultrastructural morphometric comparison the relative volume of LB in the two uppermost subcorneal layers in DS of atopics (n = 9) and healthy skin of controls (n = 7) was determined. The LBs were differentiated into extracytoplasmic LB. i.e. with the cell membrane already fused, and intracytoplasmic 1,B, i.e. entirely located within the cell. The total volume in the two cell layers of the stratum granulosum did not differ between atopics and controls. However, separate evaluation of the two LB-compartments revealed statistically significant differences between atopics and healthy controls. In the second uppermost cell layer of the stratum granulosum only 13% of the total LB volume of this layer had already fused with the cell membrane in the atopics as opposed to 42% in the controls. On the other hand more 1,B remained undelivered within the cells of the uppermost SG cell layer of the atopics (26% in atopics versus 8% in controls. P < 0.01). These findings suggest that a pathological extruding mechanism of 1,B in DS may be at least partly responsible for the recently detected biochemical alterations of epidermal lipids, and for the deficient WPB.