title: 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.
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.
authors.affiliation: Center of Internal Medicine and Dermatology CC12, Charité, University of Medicine, Berlin, Germany.
authors.forename: Ricarda Alcira
authors.initials: RA
authors.lastname: Joachim
authors.forename: Bori
authors.initials: B
authors.lastname: Handjiski
authors.forename: Sandra Maria
authors.initials: SM
authors.lastname: Blois
authors.forename: Evelin
authors.initials: E
authors.lastname: Hagen
authors.forename: Ralf
authors.initials: R
authors.lastname: Paus
authors.forename: Petra Clara
authors.initials: PC
authors.lastname: Arck
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology / Q000473:pathology; D017209:Apoptosis; D039521:CD11c Antigen / Q000378:metabolism; D002449:Cell Aggregation; D002452:Cell Count; D002454:Cell Differentiation; D002465:Cell Movement; D020405:Dermis / Q000473:pathology; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D005260:Female; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D015603:Keratinocytes / Q000473:pathology; D007801:Langerhans Cells / Q000276:immunology / Q000473:pathology*; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018448:Models, Immunological; D020078:Neurogenic Inflammation / Q000473:pathology*; D010641:Phenotype; D011485:Protein Binding; D012867:Skin / Q000276:immunology / Q000473:pathology*; D013312:Stress, Physiological / Q000473:pathology
chemical_list: D039521:CD11c Antigen; D016169:Lymphocyte Function-Associated Antigen-1; D018799:Intercellular Adhesion Molecule-1