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Brain Behav Immun. 2018 Feb;68:238-247. doi: 10.1016/j.bbi.2017.10.022. Epub 2017 Nov 7.

Chronic social stress Ameliorates psoriasiform dermatitis through upregulation of the Hypothalamic-Pituitary-Adrenal axis.

Author information

1
Facultad de Psicología, Universidad del País Vasco UPV/EHU, San Sebastián, Spain. Electronic address: o.vegas@ehu.es.
2
Rochester General Hospital Research Institute, Center for Cancer & Blood Disorder, Rochester, NY, United States.
3
Sloan Kettering Memorial Hospital, Department of Medicine, New York, NY, United States. Electronic address: pblackcloud@mednet.ucla.edu.
4
Universal Dermatology, PLLC, Fairport, NY, United States.
5
University of Rochester, Department of Dermatology, Rochester, NY, United States. Electronic address: JoAnne_VanBuskirk@URMC.Rochester.edu.
6
University of Rochester, Division of Allergy, Immunology and Rheumatology, Rochester, NY, United States. Electronic address: Christopher_Ritchlin@URMC.Rochester.edu.
7
University of Rochester, Department of Dermatology, Rochester, NY, United States. Electronic address: Alice_Pentland@URMC.Rochester.edu.
8
Boston Medical Center, Department of Dermatology, Boston, MA, United States. Electronic address: scott.walter@bmc.org.
9
Integral Rheumatology and Immunology Specialists, Plantation, FL, United States.
10
University of Rochester, Department of Dermatology, Rochester, NY, United States. Electronic address: Francisco_Tausk@URMC.Rochester.edu.

Abstract

Acute stress is a physiological response of an organism to adverse conditions, contributing to survival; however, persistence through time may lead to disease. Indeed, exacerbation of inflammatory conditions such as psoriasis has been reported to follow stressors in susceptible patients. Because chronic stress cannot ethically be elicited in patients under controlled laboratory conditions, we studied genetically modified mice that naturally develop psoriasiform dermatitis, and subjected them to an ethological chronic social contact stress paradigm. Although we found elevated pro-inflammatory neuropeptide production of substance P (SP), calcitonin-gene-related peptide (CGRP) and nerve-growth factor (NGF) mRNA in the dorsal root ganglia (DRG) as well as pro-inflammatory cytokines in response to the social stressor, stress paradoxically prevented the development of the skin lesions. This effect of stress could be reversed by the treatment with glucocorticoid (GC) receptor blockers, suggesting that it was mediated through the upregulation of corticosterone secretion. Extrapolating to humans, the worsening of disease in susceptible patients with psoriasis could be attributed to a defect in the Hypothalamic-Pituitary-Adrenal (HPA) axis with an impaired production of GC during situations of adversity, thus rendering them unable to counteract the pro-inflammatory effects of chronic stressors.

KEYWORDS:

Chronic stress; Hypothalamus-pituitary-adrenal axis; Mouse disease models.; Neuropeptides; Psoriasis

PMID:
29080684
PMCID:
PMC5767548
DOI:
10.1016/j.bbi.2017.10.022
[Indexed for MEDLINE]
Free PMC Article

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