Article
Neurotrophins act as neuroendocrine regulators of skin homeostasis in health and disease.
Cutaneous Psychoneuroimmunology, Internal Medicine - Psychosomatics, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Hormone and Metabolic Research (impact factor:
2.19).
03/2007;
39(2):110-24.
DOI:10.1055/s-2007-961812
pp.110-24
Source: PubMed
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Citations (0)
- Cited In (4)
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Article: Stress induced neuroendocrine-immune plasticity: A role for the spleen in peripheral inflammatory disease and inflammaging?
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ABSTRACT: Research over the past decade has revealed close interaction between the nervous and immune systems in regulation of peripheral inflammation linking psychosocial stress with chronic somatic disease and aging. Moreover emerging data suggests that chronic inflammations lead to a pro-inflammatory status underlying premature aging called inflammaging. In this context, the spleen can be seen as a switch board monitoring peripherally derived neuroendocrine-immune mediators in the blood and keeping up a close communication with the central stress response via its mainly sympathetic innervation. The effect aims at balanced and well-timed stress axis activation and immune adaptation in acute peripheral inflammatory events. Constant adjustment to the needs generated by environmental and endogenous challenges is provided by neuroendocrine-immune plasticity. However, maladaptive plasticity induced e.g., by chronic stress-axis activation and excessive non-neuronal derived neuroendocrine mediators may be at the heart of the observed stress sensitivity promote inflammaging under chronic inflammatory conditions. We here review the role of neurotransmitters, neuropeptides and neurotrophins as stress mediators modulating the immune response in the spleen and their potential role in inflammaging.Dermatoendocrinol. 07/2012; 4(3). -
Article: Stress induced neuroendocrine-immune plasticity: A role for the spleen in peripheral inflammatory disease and inflammaging?
[show abstract] [hide abstract]
ABSTRACT: Research over the past decade has revealed close interaction between the nervous and immune systems in regulation of peripheral inflammation linking psychosocial stress with chronic somatic disease and aging. Moreover emerging data suggests that chronic inflammations lead to a pro-inflammatory status underlying premature aging called inflammaging. In this context, the spleen can be seen as a switch board monitoring peripherally derived neuroendocrine-immune mediators in the blood and keeping up a close communication with the central stress response via its mainly sympathetic innervation. The effect aims at balanced and well-timed stress axis activation and immune adaptation in acute peripheral inflammatory events. Constant adjustment to the needs generated by environmental and endogenous challenges is provided by neuroendocrine-immune plasticity. However, maladaptive plasticity induced e.g., by chronic stress-axis activation and excessive non-neuronal derived neuroendocrine mediators may be at the heart of the observed stress sensitivity promote inflammaging under chronic inflammatory conditions. We here review the role of neurotransmitters, neuropeptides and neurotrophins as stress mediators modulating the immune response in the spleen and their potential role in inflammaging.Dermato-endocrinology. 07/2012; 4(3):271-9. -
Article: Stress, atopy and allergy: A re-evaluation from a psychoneuroimmunologic persepective.
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ABSTRACT: Since the early days of psychosomatic thinking, atopic disease was considered exemplary. In the 70s and 80s numerous reports stated increased anxiety, depression or ill stresscoping in atopics in correlation with enhanced disease activity. Employed patient groups however were small and diverse and controls rare. Therefore, the question remained, whether psychopathological findings in atopics were of pathogenetic relevance or an epiphenomenon of chronic inflammatory disease. Recently, the discussion has been revived and refocused by psychoneuroimmunological findings. We now know that atopic disease is characterized by an imbalance of the classical stress-axis response along the hypothalamus-pituitary-adrenal axis (HPA) and the sympathetic axis (SA). This imbalance can be found shoulder-to-shoulder with enhanced expression of newly emerging neuroendocrine stress mediators such as substance P (SP) and nerve growth factor that form up to a third stress axis (neurotrophin neuropeptide axis: NNA). Together they can alter the inflammatory as well as the neuroendocrine stress-response on several levels. In skin, the immediate inflammatory response to stress involves neuropeptide release and mast cell degranulation, in short neurogenic inflammation. Systemically, antigen-presentation and TH2 cytokine bias are promoted under the influence of cortisol and neuropeptides. Imbalanced stress-responsiveness may therefore be at the core of exacerbated allergic disease and deserves re-evaluation of therapeutic options such as neutralization of SP-signaling by antagonists against its receptor NK1, cortisol treatment as supplementation and relaxation techniques to balance the stress-response.Dermato-endocrinology. 01/2011; 3(1):37-40.
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Keywords
affinity proneurotrophin receptor
affinity specific tyrosinekinase receptors
ancient growth factor family
cutaneous diseases
cutaneous innervation
design precise interaction tools
differential neurotrophin expression patterns
future research efforts
intracellular adaptor molecules
Janus-faced p75 receptor
low-affinity pan-neurotrophin receptor
modulate cutaneous immune function
multilayered neurotrophin interaction
neuroendocrine peptide family
neuroendocrine tissue
neurotrophin processing enzymes
neurotrophin responsive pathogenetic pathways
peripheral nerve degeneration
specific cutaneous cell populations
structural skin cells
Eva M Peters |