Abnormal epidermal barrier in the pathogenesis of contact dermatitis
Abnormal epidermal barrier in the pathogenesis of contact dermatitis
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DOI：
10.1016/j.clindermatol.2011.08.019
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发表时间：
2012-05-01
影响因子：
2.7
通讯作者：
Brasch, Jochen
中科院分区：
文献类型：
--
作者：
Proksch, Ehrhardt;Brasch, Jochen
表皮通透性屏障在接触性皮炎中的重要作用是显而易见的。完整的皮肤屏障可防止有害物质渗透到皮肤中。刺激物和过敏原停留在皮肤表面，只与角质层接触，不会伤害皮肤。然而，在破坏皮肤屏障后，刺激物可能渗透到活的表皮层中，损伤角质形成细胞膜，并释放细胞因子，这导致炎症和刺激性接触性皮炎。皮肤屏障经常因长期暴露于水加洗涤剂、溶剂或其他刺激物而被破坏。刺激性接触性皮炎中屏障的破坏也允许过敏原的渗透。过敏原可能与朗格汉斯和T细胞接触，诱导免疫反应，并引起炎症，导致过敏性接触性皮炎。接触性皮炎的治疗应恢复皮肤屏障，以防止疾病复发。局部皮质类固醇，最常用于治疗接触性皮炎，减少免疫反应和炎症，但不会导致完全的屏障修复。用钙调磷酸酶抑制剂和温和的脂质基润肤剂治疗后，皮肤屏障修复更完全;因此，这些制剂应首选用于接触性皮炎的长期治疗。(C)2012 Elsevier Inc. All rights reserved.
A crucial role of the epidermal permeability barrier is obvious in contact dermatitis. An intact skin barrier prevents the penetration of harmful substances into the skin. Irritants and allergens that stay on the skin surface and come into contact with the stratum corneum only do not harm the skin. After disruption of the skin barrier, however, irritants may penetrate into the living epidermal layers, injure the keratinocyte membrane, and release cytokines, which leads to inflammation and to irritant contact dermatitis. The skin barrier is often disrupted by chronic exposure to water plus detergents, solvents, or other irritants. A disrupted barrier in irritant contact dermatitis also allows for the penetration of allergens. Allergens may come into contact with Langerhans and T cells, induce immunological reactions, and cause inflammation, which results in allergic contact dermatitis. Treatments in contact dermatitis should restore the skin barrier to prevent relapse of the disease. Topical corticosteroids, most often used in treating contact dermatitis, reduce immunological reactions and inflammation but do not lead to a complete barrier repair. Skin barrier repair is more complete after treatment with calcineurin inhibitors and bland lipid-based emollient; therefore, these preparations should be preferred for long-term treatment of contact dermatitis. (C) 2012 Elsevier Inc. All rights reserved.