The neuroimmune connection interferes with tissue regeneration and chronic inflammatory disease in the skin

Abstract

Research over the past decades has revealed close interactions between the nervous and immune systems that regulate peripheral inflammation and link psychosocial stress with chronic somatic disease. Besides activation of the sympathetic and the hypothalamus-pituitary-adrenal axis, stress leads to increased neurotrophin and neuropeptide production in organs at the self-environment interface. The scope of this short review is to discuss key functions of these stress mediators in the skin, an exemplary stress-targeted and stress-sensitive organ. We will focus on the skin's response to acute and chronic stress in tissue regeneration and pathogenesis of allergic inflammation, psoriasis, and skin cancer to illustrate the impact of local stress-induced neuroimmune interaction on chronic inflammation.

Hair and stress: A pilot study of hair and cytokine balance alteration in healthy young women under major exam stress

“…Hair loss may indicate underlying organic disease, however, frequently no organic disturbances can be found, which can be disturbing for hair loss patients and their doctors. It was therefor hypothesized that analagous to the animal models, in humans, stress activates neuroendocrine-immune circuits [7], which terminate hair growth in the absence of other clincally noticable health disturbances [8, 9]. Such circuits in mice involve the dense peptidergic innervation of organs at the self-environment interface (e.g.…”

“…There is a large body of research relating to stress and inflammation in animals and humans, that extensively examines cytokines and other pro-inflammatory effects of stress [1, 2, 8, 16–18]. Only a small number of human studies have addressed the association between stress, immune response and tissue regeneration in healthy, non-wounded humans, under prolonged, real life-stress exposure [16, 19–22].…”

Psychological and biological background of the interaction between psoriasis and stress

“…csatornája a bőrt gazdagon beidegző fájdalomérzékelő C-rostokból és gyulladásos sejtekből lokálisan felszabaduló hormonok, neurotranszmitterek és ezek receptorainak hálózata, az NNR, amelynek a különféle noxák hatására történő aktivációja a HPA-és SAM-tengelyek aktivációjával egy időben zajlik, végtermékei pedig, az előbbiekhez hasonlóan, pro-és antiinfl ammátoros hatás-sal is rendelkeznek [67]. A pikkelysömör patogenezisében fontos szerepe van az NNR aktivációját követően kialakuló, neuropeptidek és neurotrofi nok (VIP/PACAP, SP, NGF, CGRP) felszabadulásával, hízósejt-aktivációval és a következmé-nyesen megnövekvő érpermeabilitással, extravasatióval és infi ltrációval járó folyamatnak, a neurogén gyulladás-nak.…”

Chemical sympathectomy increases neutrophil-to-lymphocyte ratio in tumor-bearing rats but does not influence cancer progression

“…NE is able to regulate the immune cells activity by initiating a change on the level of gene expression for cytokines and antibodies (Nance and Sanders, 2007). The SNS modulates also the anti-tumor immune defense response (Bhowmick et al, 2009;Peters et al, 2012;Wirth et al, 2014) by regulation of the activity of macrophages, cytotoxic T cells, NK cells, granulocytes, and by release of cytokines, mainly interleukin-2, interleukin-12, interferon-γ, tumor necrosis factor alpha (TNF-α), chemokines, and other humoral factors (Finn, 2012;Mantovani and Sica, 2010;Tugues et al, 2014).…”