Cytokines sing the blues: inflammation and the pathogenesis of depression.

By Charles L Raison, L. Capuron, Andrew H. Miller. Trends in immunology, 2006

3,001 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Biological Psychiatry, Social Psychology

View Paper: https://www.semanticscholar.org/paper/cc56465fdc5a4efc142b1f467194a8d952ddfedb

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Citations in the corpus

ELEVATED INFLAMMATION LEVELS IN DEPRESSED ADULTS WITH A HISTORY OF CHILDHOOD MALTREATMENT (2008, positive): “However, not all individuals with depression have elevated levels of inflammation.(5) Those who do could be at highest risk for cardiovascular disease.”
Depressive disorders and immunity: 20 years of progress and discovery. (2007, background): “At least three pathways have been invoked: (1) passage through leaky regions in the blood brain barrier, (2) active transport via cytokine-specific transport molecules and (3) activation of vagal afferent nerves which signal relevant brain nuclei such as the nucleus of the solitary tract (Raison et ”
Control of Brain Development, Function, and Behavior by the Microbiome (2015, positive): “In fact, the role of pro-inflammatory cytokines in modulating human behavior is exemplified by the finding that one-third of patients who have been treated with IL-2 and IFNa (used as immunotherapy against cancer and certain viral infections) develop major depressive disorder (Raison et al., 2006).”
Minocycline attenuates lipopolysaccharide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia (2008, background): “Because IDO mediated TRP degradation impacts both serotonergic and glutamatergic pathways, this may be an important mechanism underlying mood and behavior complications concomitant with inflammation [37-39].”
Inflammation Causes Mood Changes Through Alterations in Subgenual Cingulate Activity and Mesolimbic Connectivity (2009, positive): “Clinical and animal studies implicate systemic inflammation in the pathogenesis of depression (1).”
Psychobiological Responses to Social Self Threat: Functional or Detrimental? (2009, background): “Studies in animals and humans have demonstrated that acute administration of proinflammatory cytokines can induce these behavioral and motivational changes (Dantzer et al, 2008 ; Raison, Capuron, & Miller, 2006 ).”
Effect of Compassion Meditation on Neuroendocrine, Innate Immune and Behavioral Responses to Psychosocial Stress (2008, background): “Major depression has also been repeatedly associated with increased plasma concentrations of IL-6 (Raison et al., 2006).”
Positive Psychological Well-Being and Mortality: A Quantitative Review of Prospective Observational Studies (2008, background): “Reverse causal mechanisms may also be operating because subclinical pathophysiological changes, such as increased levels of endogenous opioids and inflammatory cytokines, may influence affect, especially in populations with preexisting disease (91,92).”
The Bidirectional Relationship of Depression and Inflammation: Double Trouble (2020, background): “Cytokines are one of the most studied components of the immune system in depression (for review, Dantzer et al., 2008; Miller and Raison, 2016; Raison et al., 2006), but little is known about the source and the contribution of cytokines in MDD and their mechanisms of action in the brain.”
From Stress to Inflammation and Major Depressive Disorder: A Social Signal Transduction Theory of Depression (2014, background): “As we describe in more detail below, these transcription factors in turn drive the expression of proinflammatory immune response genes such as tumor necrosis factor- (TNF- ) and interleukin-1 (IL-1) that produce small protein molecules called cytokines, the main effectors of the inflammatory respons”
Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression (2009, positive): “In general, cytokines have been shown to access the brain and interact with virtually every pathophysiologic domain relevant to depression, including neurotransmitter metabolism, neuroendocrine function, and neural plasticity (5,17).”
Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. (2007, background): “NF-kB is a lynchpin in the inflammatory response to challenge, and when chronically activated, is believed to be a major contributor to the association between inflammation and a number of medical disorders including cardiovascular disease, diabetes, cancer and osteoporosis (Raison et al., 2006).”