Epidermal pathogenesis of inflammatory dermatoses.
Epidermal pathogenesis of inflammatory dermatoses.
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DOI：
10.1016/s1046-199x(99)90054-4
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发表时间：
1999-09-01
期刊：
影响因子：
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通讯作者：
Feingold, K R
中科院分区：
文献类型：
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作者：
Elias, P M;Wood, L C;Feingold, K R
一般认为，无论是过敏性还是刺激性皮炎，主要是一种免疫/炎症性疾病。在这篇文章中，我们回顾了最近的信息，支持表皮的贡献，这些疾病，以及其他几种皮肤病。我们首先回顾新概念的表皮屏障，最近的证据表明，角质层是一个生物传感器，调节表皮脂质和DNA代谢反应的各种外源性的侮辱。各种信号传导机制，包括表皮细胞因子和生长因子水平的变化，是介导这些代谢反应的潜在候选者。我们的研究结果表明，这些信号分子可能产生不响应渗透性屏障的要求，但作为一个可避免的后果，伴随着所有类型的急性屏障废除的表皮损伤。虽然细胞因子/生长因子作为导致屏障恢复的代谢事件的调节剂的作用仍然未知，但它们在引发导致皮肤病理学的细胞因子级联反应中的作用似乎更确定。我们的结论是，信号分子，角质层损伤后释放，启动细胞因子级联反应，诱导炎症，这是负责特定皮肤病的临床特征。因此，“由外到内”的信号传导可能有助于以异常屏障功能为特征的各种皮肤病的发病机制。
It is generally assumed that dermatitis, whether of allergic or irritant origin, is primarily an immunological/inflammatory disorder. In this article, we review recent information that supports an epidermal contribution to these disorders, as well as several other dermatoses. We first review new concepts of the epidermal barrier, with recent evidence that the stratum corneum is a biosensor that regulates the epidermal lipid and DNA-metabolic responses to a variety of exogenous insults. Various signaling mechanisms, including changes in levels of epidermal cytokines and growth factors, are potential candidates to mediate these metabolic responses. Our results show that these signaling molecules may be generated not in response to permeability barrier requirements, but as an avoidable consequence of the epidermal injury that accompanies all types of acute barrier abrogation. Although the role of cytokines/growth factors as regulators of metabolic events leading to barrier recovery is still unknown, their role in initiating a cytokine cascade leading to cutaneous pathology seems more certain. We conclude that signaling molecules, released following injury to the stratum corneum, initiate a cytokine cascade that induces inflammation, which is responsible for the clinical features of specific dermatoses. Thus, 'outside-to-inside' signaling may contribute to the pathogenesis of a variety of dermatoses characterized by abnormal barrier function.