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During the last decade it has been shown that the central nervous system can influence the immune system. In healthy individuals, catecholamines can inhibit the production of pro-inflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) via interaction with beta 2-adrenergic receptors. In contrast, we show here that(More)
Posttraumatic stress disorder (PTSD) is typically accompanied by acute and chronic alterations in the stress response. These alterations have mostly been described in individuals under baseline conditions, but several studies have also used a challenge model to further assess the role of the hypothalamic-pituitary-adrenal (HPA) axis in the stress response.(More)
Interleukin-8 (IL-8) is an important cytokine in inflammatory processes by functioning as a chemoattractant and as an activator of oxygen metabolism. In the present study we demonstrate that beta 2-adrenergic agonists potentiate the lipopolysaccharide (LPS) and IL-1 induced production of IL-8 by human monocytes. In addition, beta 2-adrenergic activation(More)
Chronic pain associated with inflammation is a common clinical problem, and the underlying mechanisms have only begun to be unraveled. GRK2 regulates cellular signaling by promoting G-protein-coupled receptor (GPCR) desensitization and direct interaction with downstream kinases including p38. The aim of this study was to determine the contribution of GRK2(More)
OBJECTIVE Burnout is a stress-induced work-related syndrome. It is associated with a higher incidence of infections possibly pointing to a compromised immune system. In the present study, endocrine and ex vivo immune function of severe cases of burnout were investigated. METHODS Endocrine and immune variables were compared in 56 persons with burnout and(More)
Besides its established function in erythropoiesis, erythropoietin (EPO) is currently also appreciated for its neuroprotective effects. The detrimental sequelae of prolonged cerebral hypoxia and ischemia have been shown to attenuate by EPO treatment. After binding to the EPO receptor, EPO is capable of initiating a cascade of events which--via different(More)
Beta2-Adrenergic and chemokine receptor antagonists delay the onset and reduce the severity of joint injury in rheumatoid arthritis. beta2-Adrenergic and chemokine receptors belong to the G-protein-coupled receptor family whose responsiveness is turned off by the G-protein-coupled receptor kinase family (GRK-1 to 6). GRKs phosphorylate receptors in an(More)
Many neurotransmitters involved in pain perception transmit signals via G protein-coupled receptors (GPCRs). GPCR kinase 2 (GRK2) regulates agonist-induced desensitization and signaling of multiple GPCRs and interacts with downstream molecules with consequences for signaling. In general, low GRK2 levels are associated with increased responses to agonist(More)
The exact nature and pathophysiology of fatigue remain largely elusive despite its high prevalence in physically ill patients. Studies on the relationship between the immune system and the central nervous system provide a new perspective on the mechanisms of fatigue. Inflammatory mediators that are released by activated innate immune cells at the periphery(More)
Hypoxic-ischemic injury (HI) to the neonatal brain results in delayed neuronal death with accompanying inflammation for days after the initial insult. The aim of this study was to depict delayed neuronal death after HI using Manganese-enhanced MRI (MEMRI) and to evaluate the specificity of MEMRI in detection of cells related to injury by comparison with(More)