The effects of psychological stress on humans: Increased production of pro-inflammatory cytokines and a Th1-like response in stress-induced anxiety
ABSTRACT There is some evidence that, in humans and experimental animals, psychological stress may suppress or enhance immune functions, depending on the nature of the stressor and the immune variables under consideration. The possibility that psychological stress may affect the production of pro-inflammatory and immunoregulatory cytokines was investigated in 38 medical students, who had blood samplings a few weeks before and after as well as one day before an academic examination. Psychological stress significantly increased the stimulated production of tumour necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), IL-1 receptor antagonist (IL-1Ra), interferon gamma (IFN-gamma) and IL-10. Students with high stress perception during the stressful condition had a significantly higher production of TNF-alpha, IL-6, IL-1Ra and IFN-gamma than students with a low-stress perception. Students with a high anxiety response had a significantly higher production of IFN-gamma and a lower production of the negative immunoregulatory cytokines, IL-10 and IL-4, than students without anxiety. These findings suggest that, in humans, changes in the production of the pro-inflammatory cytokines, TNF-alpha, IL-6 and IFN-gamma, and negative immunoregulatory cytokines, IL-10 and IL-4, take part in the homeostatic responses to psychological stress and that stress-induced anxiety is related to a T-helper-1-like response.
Cardiovascular Research 01/2002; 56(1):15-21. DOI:10.1016/S0008-6363(02)00537-0 · 5.81 Impact Factor
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ABSTRACT: The development and exacerbation of depression and anxiety are associated with exposure to repeated psychosocial stress. Stress is known to affect the bidirectional communication between the nervous and immune systems leading to elevated levels of stress mediators including glucocorticoids (GCs) and catecholamines and increased trafficking of proinflammatory immune cells. Animal models, like the repeated social defeat (RSD) paradigm, were developed to explore this connection between stress and affective disorders. RSD induces activation of the sympathetic nervous system (SNS) and hypothalamic-pituitary (HPA) axis activation, increases bone marrow production and egress of primed, GC-insensitive monocytes, and stimulates the trafficking of these cells to tissues including the spleen, lung, and brain. Recently, the observation that these monocytes have the ability to traffic to the brain perivascular spaces and parenchyma have provided mechanisms by which these peripheral cells may contribute to the prolonged anxiety-like behavior associated with RSD. The data that have been amassed from the RSD paradigm and others recapitulate many of the behavioral and immunological phenotypes associated with human anxiety disorders and may serve to elucidate potential avenues of treatment for these disorders. Here, we will discuss novel and key data that will present an overview of the neuroendocrine, immunological and behavioral responses to social stressors. Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.Neuroscience 01/2015; 289. DOI:10.1016/j.neuroscience.2015.01.001 · 3.33 Impact Factor
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ABSTRACT: The study examines the association of neighborhood socioeconomic deprivation and metabolic syndrome with inflammation. The analysis included 19, 079 black and white participants from the REasons for Geographic And Racial Differences in Stroke Study who were age > 45 years at baseline. Logistic regression examined whether neighborhood deprivation was associated with increased odds of METS and CRP-MetS. Among black adults, residing in the most deprived neighborhoods was associated with increased odds of obesity (p < .01), lower HDL (p < .001), high blood pressure (p < .01), elevated fasting glucose (p < .001), inflammation (p < .01), and CRP-MetS (p < .001). Among white adults, neighborhood deprivation was associated with higher waist circumference (p < .001), lower HDL (p < .001), higher triglycerides (p < .01), higher glucose (p < .001), higher BMI (p < .0001), higher blood pressure (p = .01), METS (p < .001), inflammation (p < .01) and CRP-MetS (p < .001). These findings highlight the role of neighborhood socioeconomic deprivation on METS and CRP-MetS for black and white adults. Interventions tailored to address the contextual effects of deprived neighborhoods may reduce the observed neighborhood disparities.BMC Public Health 12/2014; 14(1):1319. DOI:10.1186/1471-2458-14-1319 · 2.32 Impact Factor