Stress Activates Immune Cells in Skin

Byron's Comments:

It is interesting that stress alone begins the migration of extra immune cells towards your skin, a likely genetic response driven by substance P release in nerve endings, to prepare to deal with actual injury.

Study Title:

Stress-induced neurogenic inflammation in murine skin skews dendritic cells towards maturation and migration: key role of ICAM1/LFA-1 interactions.

Study 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.

From press release:

Current research suggests that stress may activate immune cells in your skin, resulting in inflammatory skin disease.

Skin provides the first level of defense to infection, serving not only as a physical barrier, but also as a site for white blood cells to attack invading bacteria and viruses. The immune cells in skin can over-react, however, resulting in inflammatory skin diseases such as atopic dermatitis and psoriasis.

Stress can trigger an outbreak in patients suffering from inflammatory skin conditions. This cross talk between stress perception, which involves the brain, and the skin is mediated the through the “brain-skin connection”. Yet, little is know about the means by which stress aggravates skin diseases.

Researchers lead by Dr. Petra Arck of Charité, University of Medicine Berlin and McMaster University in Canada, hypothesized that stress could exacerbate skin disease by increasing the number of immune cells in the skin. To test this hypothesis, they exposed mice to sound stress. Dr. Arck’s group found that this stress challenge resulted in higher numbers of mature white blood cells in the skin. Furthermore, blocking the function of two proteins that attract immune cells to the skin, LFA-1 and ICAM-1, prevented the stress-induced increase in white blood cells in the skin.

Taken together, these data suggest that stress activates immune cells, which in turn are central in initiating and perpetuating skin diseases. Fostered by the present observation, the goal of future studies in Dr. Arck’s group is to prevent stress-triggered outbreaks of skin diseases by recognizing individuals at risk and identifying immune cells suitable to be targeted in therapeutic interventions.

 

Study Information:

Joachim RA, Handjiski B, Blois SM, Hagen E, Paus R, Arck PC. Stress-induced neurogenic inflammation in murine skin skews dendritic cells towards maturation and migration: key role of ICAM1/LFA-1 interactions.  Am J Pathol,  2008 October 173:1379-1388.
Center of Internal Medicine and Dermatology CC12, Charité, University of Medicine, Berlin, Germany.



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