Chronic social stress ameliorates psoriasiform dermatitis through upregulation of the Hypothalamic-Pituitary-Adrenal axis Journal Article


Authors: Vegas, O.; Poligone, B.; Blackcloud, P.; Gilmore, E. S.; VanBuskirk, J.; Ritchlin, C. T.; Pentland, A. P.; Walter, S. A.; Nousari, Y.; Tausk, F.
Article Title: Chronic social stress ameliorates psoriasiform dermatitis through upregulation of the Hypothalamic-Pituitary-Adrenal axis
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. © 2017
Journal Title: Brain, Behavior, and Immunity
Volume: 68
ISSN: 0889-1591
Publisher: Elsevier, Inc.  
Date Published: 2018-02-01
Start Page: 238
End Page: 247
Language: English
DOI: 10.1016/j.bbi.2017.10.022
PROVIDER: scopus
PMCID: PMC5767548
PUBMED: 29080684
DOI/URL:
Notes: Article -- Export Date: 3 December 2018 -- Source: Scopus
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