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

Department

Research

Document Type

Article

Publication Title

Brain, Behavior, And Immunity

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.

First Page

238

Last Page

247

DOI

10.1016/j.bbi.2017.10.022

Volume

68

Publication Date

2-1-2018

Medical Subject Headings

Adrenal Cortex Hormones (metabolism); Animals; Calcitonin Gene-Related Peptide; Corticosterone (pharmacology); Dermatitis; Disease Models, Animal; Ganglia, Spinal (metabolism); Hypothalamo-Hypophyseal System (metabolism); Male; Mice; Mice, Transgenic; Nerve Growth Factor; Neuropeptides; Pituitary-Adrenal System (metabolism); Psoriasis (metabolism, physiopathology); RNA, Messenger; Receptors, Glucocorticoid (metabolism); Stress, Psychological (genetics, metabolism); Substance P; Transcriptional Activation; Up-Regulation

PubMed ID

29080684

Link to Full Text

Share

COinS