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

Center for Internal Medicine and Dermatology, Charité-University Medicine, Berlin, Germany.
Annals of the New York Academy of Sciences (Impact Factor: 4.38). 07/2012; 1262(1):118-26. DOI: 10.1111/j.1749-6632.2012.06647.x
Source: PubMed


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.

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    • "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). For the study of the SNS role in the regulation of immune functions, interventions affecting the sympathetic neurotransmission are used. "
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