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19 results on '"Hagen, Evelin"'

9. 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

Author

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

Subjects
Keratinocytes, integumentary system, Models, Immunological, Antigen-Presenting Cells, Endothelial Cells, Apoptosis, Cell Count, Cell Differentiation, Dermis, Intercellular Adhesion Molecule-1, Lymphocyte Function-Associated Antigen-1, CD11c Antigen, Mice, Inbred C57BL, Mice, Phenotype, Cell Movement, Stress, Physiological, Langerhans Cells, Animals, Female, Neurogenic Inflammation, Regular Articles, Cell Aggregation, Protein Binding, Skin
Abstract

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.

Published
2008

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