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 interactionsCitation formats

  • External authors:
  • Ricarda Alcira Joachim
  • Bori Handjiski
  • Sandra Maria Blois
  • Evelin Hagen
  • Petra Clara Arck

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

In: American journal of pathology, Vol. 173, No. 5, 11.2008, p. 1379-1388.

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Joachim, Ricarda Alcira ; Handjiski, Bori ; Blois, Sandra Maria ; Hagen, Evelin ; Paus, Ralf ; Arck, Petra Clara. / 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. In: American journal of pathology. 2008 ; Vol. 173, No. 5. pp. 1379-1388.

Bibtex

@article{1f63e322ba5840a39a38b0ab507bf407,
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. Copyright {\textcopyright} American Society for Investigative Pathology.",
keywords = "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",
author = "Joachim, {Ricarda Alcira} and Bori Handjiski and Blois, {Sandra Maria} and Evelin Hagen and Ralf Paus and Arck, {Petra Clara}",
year = "2008",
month = nov,
doi = "10.2353/ajpath.2008.080105",
language = "English",
volume = "173",
pages = "1379--1388",
journal = "The American Journal of Pathology",
issn = "0002-9440",
publisher = "Elsevier BV",
number = "5",

}

RIS

TY - JOUR

T1 - 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

AU - Joachim, Ricarda Alcira

AU - Handjiski, Bori

AU - Blois, Sandra Maria

AU - Hagen, Evelin

AU - Paus, Ralf

AU - Arck, Petra Clara

PY - 2008/11

Y1 - 2008/11

N2 - 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. Copyright © American Society for Investigative Pathology.

AB - 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. Copyright © American Society for Investigative Pathology.

KW - Animals

KW - immunology: Antigen-Presenting Cells

KW - metabolism: Antigens, CD11c

KW - Apoptosis

KW - Cell Aggregation

KW - Cell Count

KW - Cell Differentiation

KW - Cell Movement

KW - pathology: Dermis

KW - metabolism: Endothelial Cells

KW - Female

KW - metabolism: Intercellular Adhesion Molecule-1

KW - pathology: Keratinocytes

KW - immunology: Langerhans Cells

KW - metabolism: Lymphocyte Function-Associated Antigen-1

KW - Mice

KW - Mice, Inbred C57BL

KW - Models, Immunological

KW - pathology: Neurogenic Inflammation

KW - Phenotype

KW - Protein Binding

KW - immunology: Skin

KW - pathology: Stress, Physiological

U2 - 10.2353/ajpath.2008.080105

DO - 10.2353/ajpath.2008.080105

M3 - Article

VL - 173

SP - 1379

EP - 1388

JO - The American Journal of Pathology

JF - The American Journal of Pathology

SN - 0002-9440

IS - 5

ER -