Stress-Induced Neurogenic Inflammation in Murine Skin Skews Dendritic Cells Towards Maturation and Migration Key Role of Intercellular Adhesion Molecule-1/Leukocyte Function-Associated Antigen Interactions
Stress-Induced Neurogenic Inflammation in Murine Skin Skews Dendritic Cells Towards Maturation and Migration Key Role of Intercellular Adhesion Molecule-1/Leukocyte Function-Associated Antigen Interactions
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DOI：
10.2353/ajpath.2008.080105
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发表时间：
2008-11-01
影响因子：
6
通讯作者：
Arck, Petra Clara
中科院分区：
文献类型：
--
作者：
Joachim, Ricarda Alcira;Handjiski, Bori;Arck, Petra Clara
皮肤持续充当多种外源性应激源的生物传感器，并将所产生的反应与个体的中枢和外周内源性反应系统整合到感知的压力中;它还起到保护免受外部挑战如创伤和感染的作用。我们先前已经在小鼠中表明，应激诱导神经生长因子和P物质依赖性神经源性炎症，其中包括MHC II类+细胞的突出聚集。由于树突状细胞（DCs）在应激反应中的作用还不清楚，我们使用一种成熟的小鼠应激模型研究了DCs在小鼠皮肤神经源性炎症中的作用。我们发现，声音应力增加皮内的数量。Langerin（+）和CD 11 c（+）DC并诱导DC成熟，如通过上调CD 11 c、MHC II类和细胞间粘附分子-1（ICAM-1）的表达所示。阻断ICAM-1/白细胞功能相关抗原-1的相互作用可显著抑制体内应激诱导的真皮DC数量增加、成熟和迁移，并降低应激诱导的角质形成细胞凋亡和ICAM-1的内皮细胞表达。总之，压力暴露会导致皮肤免疫系统的警觉状态。这种适应过程可以确保保护免受压力源（如捕食者的攻击）造成的创伤的可能感染。然而，当今的压力源已经改变，这种适应似乎是多余的，并可能通过诱导免疫性皮肤病来破坏皮肤的稳态。(Am J Pathol 2008，173：1379-1388; DOI：10.2353/ajpath.2008.080105）
The skin continuously serves as a biosensor of multiple exogenous stressors and integrates the resulting responses with an individual's central and peripheral endogenous response systems to perceived stress; it also acts to protect against external challenges such as wounding and infection. We have previously shown in mice that stress induces nerve growth factor- and substance P-dependent neurogenic inflammation, which includes the prominent clustering of MHC class II+ cells. Because the contribution of dendritic cells (DCs) in response to stress is not well understood, we examined the role of DCs in neurogenic inflammation in murine skin using a well-established murine stress model. We show that sound stress increases the number of intradermal. langerin(+) and CD11c(+) DCs and induces DC maturation, as indicated by the up-regulated expression of CD11c, MHC class II, and intercellular adhesion molecule-1 (ICAM-1). Blocking of ICAM-1/leukocyte function-associated antigen-1 interactions significantly abrogated the stress-induced numeric increase, maturation, and migration of dermal DCs hi vivo and also reduced stress-induced keratinocyte apoptosis and endothelial cell expression of ICAM-1. in conclusion, stress exposure causes a state of immune alertness in the skin. Such adaptation processes may ensure protection from possible infections on wounding by stressors, such as attack by predators. However, present-day stressors have changed and such adaptations appear redundant and may overrun skin homeostasis by inducing immune dermatoses. (Am J Pathol 2008, 173:1379-1388; DOI: 10.2353/ajpath.2008.080105)