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J Invest Dermatol. 2014 Dec;134(12):2890-2897. doi: 10.1038/jid.2014.265. Epub 2014 Jul 3.

Paradoxical benefits of psychological stress in inflammatory dermatoses models are glucocorticoid mediated.

Author information

1
Dermatology Service, Department of Veterans Affairs Medical Center, University of California, San Francisco, San Francisco, California, USA; Department of Dermatology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
2
Dermatology Service, Department of Veterans Affairs Medical Center, University of California, San Francisco, San Francisco, California, USA.
3
Dermatology Service, Department of Veterans Affairs Medical Center, University of California, San Francisco, San Francisco, California, USA; Department of Dermatology, Hospital General Universitario de Ciudad Real, Ciudad Real, Spain.
4
Dermatology Service, Department of Veterans Affairs Medical Center, University of California, San Francisco, San Francisco, California, USA; Department of Dermatology, University of California, San Francisco, San Francisco, California, USA.
5
Department of Dermatology, Hospital del Mar-IMIM, Universitat Autonoma de Barcelona, Barcelona, Spain.
6
ISDIN, Research and Development, Barcelona, Spain.
7
Medical Service, Department of Veterans Affairs Medical Center, San Francisco, California, USA; Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
8
Dermatology Service, Department of Veterans Affairs Medical Center, University of California, San Francisco, San Francisco, California, USA; Department of Dermatology, University of California, San Francisco, San Francisco, California, USA. Electronic address: eliasp@derm.ucsf.edu.

Abstract

Acute psychological stress (PS) mobilizes metabolic responses that are of immediate benefit to the host, but the current medical paradigm holds that PS exacerbates systemic and cutaneous inflammatory disorders. Although the adverse consequences of PS are usually attributed to neuroimmune mechanisms, PS also stimulates an increase in endogenous glucocorticoids (GCs) that compromises permeability barrier homeostasis, stratum corneum cohesion, wound healing, and epidermal innate immunity in normal skin. Yet, if such PS-induced increases in GC were uniformly harmful, natural selection should have eliminated this component of the stress response. Hence, we hypothesized here instead that stress-induced elevations in endogenous GC could benefit, rather than aggravate, cutaneous function and reduce inflammation in three immunologically diverse mouse models of inflammatory diseases. Indeed, superimposed exogenous (motion-restricted) stress reduced, rather than aggravated inflammation and improved epidermal function in all three models, even normalizing serum IgE levels in the atopic dermatitis model. Elevations in endogenous GC accounted for these apparent benefits, because coadministration of mifepristone prevented stress-induced disease amelioration. Thus, exogenous stress can benefit rather than aggravate cutaneous inflammatory dermatoses through the anti-inflammatory activity of increased endogenous GC.

PMID:
24991965
PMCID:
PMC4227540
DOI:
10.1038/jid.2014.265
[Indexed for MEDLINE]
Free PMC Article

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