A mechanism converting psychosocial stress into mononuclear cell activation

By A. Bierhaus, J. Wolf, M. Andrassy, Nicolas Rohleder, P. Humpert, Dimitri Petrov, R. Ferstl, M. von Eynatten, T. Wendt, G. Rudofsky and 6 more. Proceedings of the National Academy of Sciences of the United States of America, 2003

901 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Biological Psychiatry, Physiology

View Paper: https://www.semanticscholar.org/paper/10042fecc21d0a6579b42d71e8384d1e519803df

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Citations in the corpus

The effects of acute psychological stress on circulating and stimulated inflammatory markers: A systematic review and meta-analysis (2017, background): “In support of this stress response system, rodent and in vitro findings show that sympathoadrenal activation drives stress-related increases in circulating markers of inflammation (Bierhaus et al., 2003; Johnson et al., 2005; Szabo et al., 1997).”
The Sleep-Immune Crosstalk in Health and Disease (2019, background): “, the neuroendocrine hypothalamus-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS), will also induce an inflammatory response (52, 525).”
Adverse childhood experiences, allostasis, allostatic load, and age-related disease. (2012, background): “The increase in inflammation levels could be due both to repeated stimulation of the sympathetic nervous system [15] and to progressive impairment in glucocorticoid signaling”
Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load. (2006, neutral): “parasympathetic activity has the opposite effect [6,7].”
Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. (2007, background): “Interestingly, stressor exposure, a well-known precipitant of depression, has been shown to activate both proinflammatory cytokines and inflammatory signaling pathways (e.g. NF-kB) in humans and laboratory animals (Bierhaus et al., 2003).”
Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression (2009, positive): “In addition, in vitro studies have demonstrated that stimulation of both alpha- and beta-adrenergic receptors can activate inflammatory signaling pathways, including NF-κB(87).”
Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017, methodology): “This increased norepinephrine production in PTSD in response to stressful or threatening stimuli can induce cytokine release (Bierhaus et al, 2003).”
Reciprocal regulation of the neural and innate immune systems (2011, background): “, activate NF-κB in peripheral blood mononuclear cell”
The Effect of Antidepressant Medication Treatment on Serum Levels of Inflammatory Cytokines: A Meta-Analysis (2011, positive): “…inflammatory cytokines may occur because of a dysfunction in the brain’s anti-inflammatory mechanisms, which include the hypothalamic–pituitary–adrenal axis, the efferent vagus (Bierhaus et al, 2003; Pavlov and Tracey, 2005; Shaked et al, 2009), and noradrenergic innervation (Selmeczy et al, 2003).”
Brain on stress: How the social environment gets under the skin (2012, background): “Sympathetic stimulation increases inflammatory cytokine production (30), and this production, in turn, increases glucocorticoid production, which typically has antiinflammatory and immune modulatory actions (31) but can also exacerbate inflammation under some circumstances (32).”
Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior (2012, methodology): “In addition, a- and b-adrenergic agonists have been shown to directly activate NF-kB in vitro (Bierhaus et al, 2003).”
Cytokine Targets in the Brain: Impact on Neurotransmitters and Neurocircuits (2013, background): “, neurogenesis)[7], (2) the capacity of psychosocial stress and trauma to activate inflammatory signaling pathways, in part through stimulation of the sympathetic nervous system,[14] and (3) the inflammatory nature of fatty tissue which contains high levels of activated macrophages responding to exp”
Exposure to a Social Stressor Alters the Structure of the Intestinal Microbiota: Implications for Stressor-Induced Immunomodulation (2010, background): “Recent studies indicate that the sympathetic nervous system (SNS) is involved in stressor-induced immune enhancement (Bierhaus et al., 2003; Cole et al., 2010), and blocking the activation of the SNS through the use of the a- and b-adrenergic receptor antagonists has been reported to block the stres”