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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.

American Journal Of Pathology
Publication Date
  • Animals
  • Immunology: Antigen-Presenting Cells
  • Metabolism: Antigens
  • Cd11C
  • Apoptosis
  • Cell Aggregation
  • Cell Count
  • Cell Differentiation
  • Cell Movement
  • Pathology: Dermis
  • Metabolism: Endothelial Cells
  • Female
  • Metabolism: Intercellular Adhesion Molecule-1
  • Pathology: Keratinocytes
  • Immunology: Langerhans Cells
  • Metabolism: Lymphocyte Function-Associated Antigen-1
  • Mice
  • Mice
  • Inbred C57Bl
  • Models
  • Immunological
  • Pathology: Neurogenic Inflammation
  • Phenotype
  • Protein Binding
  • Immunology: Skin
  • Pathology: Stress
  • Physiological


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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