Le M, Schalkwijk J, Siegenthaler G, van de Kerkhof P C, Veerkamp J H, van der Valk P G
Department of Dermatology, University Hospital Nijmegen, The Netherlands.
Arch Dermatol Res. 1996 Oct;288(11):684-90. doi: 10.1007/BF02505278.
Although the induction of acute irritant dermatitis by detergents has been studied extensively in recent years, our understanding of the cell biological events in the repair phase, and its relevance for the development of chronic irritant dermatitis is limited. Here we studied the reaction pattern of human skin to short-term application of sodium dodecyl sulphate (SDS) in a model that induced a minimal acute inflammatory reaction (absence of polymorphonuclear leucocytes, PMN) and did not have cytopathic effects on the epidermal keratinocytes as determined by histological investigation. All parameters were measured up to 14 days after exposure to SDS. Application of SDS caused disturbances of barrier function as measured by transepidermal water loss and had vascular effects as judged by erythema. Several cell biological markers for epidermal growth and differentiation were examined by immunohistochemistry. A rapid and strong induction of the cornified envelope precursor protein involucrin was seen in the stratum spinosum, with a peak at 24 h. Within 24 h a strong upregulation of epidermal fatty acid binding protein (E-FABP) was noted, with a peak at 7 days after injury. Cellular proliferation in the basal layer was increased fivefold as assessed by nuclear staining for the Ki-67 antigen, showing a peak at 48 h. Surprisingly, no significant induction of cytokeratin 16 and SKALP/elafin expression, two markers associated with epidermal hyper-proliferation and inflammation, was seen. These findings suggest that the cellular changes following exposure to detergent are distinct from those seen in other forms of skin injury. We would speculate that the epidermal response to detergent exposure is primarily directed at restoration of barrier function.
尽管近年来洗涤剂诱发急性刺激性皮炎已得到广泛研究,但我们对修复阶段细胞生物学事件及其与慢性刺激性皮炎发生发展的相关性了解有限。在此,我们在一个诱导最小急性炎症反应(无多形核白细胞,PMN)且组织学检查显示对表皮角质形成细胞无细胞病变作用的模型中,研究了人皮肤对短期应用十二烷基硫酸钠(SDS)的反应模式。在接触SDS后长达14天测量所有参数。应用SDS导致经表皮水分流失所测量的屏障功能紊乱,并通过红斑判断有血管效应。通过免疫组织化学检查了几种表皮生长和分化的细胞生物学标志物。在棘层中观察到角质包膜前体蛋白兜甲蛋白迅速且强烈诱导,在24小时达到峰值。在24小时内注意到表皮脂肪酸结合蛋白(E-FABP)强烈上调,在损伤后7天达到峰值。通过Ki-67抗原的核染色评估,基底层细胞增殖增加了五倍,在48小时达到峰值。令人惊讶的是,未观察到细胞角蛋白16和SKALP/弹性蛋白酶表达的显著诱导,这两种标志物与表皮过度增殖和炎症相关。这些发现表明,接触洗涤剂后的细胞变化与其他形式的皮肤损伤不同。我们推测表皮对洗涤剂暴露的反应主要针对屏障功能的恢复。