Published online before print October 2, 2008

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(American Journal of Pathology. 2008;173:1379-1388.)
© 2008 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2008.080105

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

Ricarda Alcira Joachim^*, Bori Handjiski^*, Sandra Maria Blois^*, Evelin Hagen^*, Ralf Paus and Petra Clara Arck^*

From the Center of Internal Medicine and Dermatology CC12,^* Charité, University of Medicine, Berlin, Germany; the Department of Dermatology, University Hospital Schleswig-Holstein, University of Luebeck, Luebeck, Germany; and the Royal Free Hospital, University College London, London, England

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 in 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.

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