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.
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.
Joachim
Ricarda Alcira
RA
Center of Internal Medicine and Dermatology CC12, Charité, University of Medicine, Berlin, Germany.
Handjiski
Bori
B
Blois
Sandra Maria
SM
Hagen
Evelin
E
Paus
Ralf
R
Arck
Petra Clara
PC
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
D039521:CD11c Antigen; D016169:Lymphocyte Function-Associated Antigen-1; D018799:Intercellular Adhesion Molecule-1