From inflammation to sickness and depression: when the immune system subjugates the brain

By Robert Dantzer, Jason C. O'Connor, G. Freund, Rodney W. Johnson, Keith W. Kelley. Nature Reviews Neuroscience, 2008

6,948 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Biological Psychiatry, Neurology

View Paper: https://www.semanticscholar.org/paper/43dbbd63534cfef01b73e6845158ca9a77363fcc

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Citations in the corpus

Prevalence of low-grade inflammation in depression: a systematic review and meta-analysis of CRP levels (2019, background): “…commonly seen following an acute infection, shares many characteristics with depression, such as fatigue, sleep disturbance and decreased motivation (Dantzer et al., 2008); early-life infection and autoimmune diseases are associated with a higher risk of depression in adulthood (Benros et al.,…”
A mentalization-based approach to the understanding and treatment of functional somatic disorders (2012, background): “Pro-inflammatory cytokines induce feelings of lethargia, increased fatigability, concentration loss, light fever, generalized hyperalgesia and hypersensitivity to physical and mental stressors, as well as a tendency to withdraw from the outside world (Dantzer, O'Connor, Freund, Johnson, & Kelley, 2”
Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “In animals, depressive-like behavior, reflected by decreased sucrose consumption and increased immobility (or behavioral despair) in the forcedswimming test or tail-suspension test, can be induced by acute or chronic treatment with inflammatory challenges (Yirmiya, 1996; Anisman et al., 2005; Dantze”
Multidisciplinary research priorities for the COVID-19 pandemic: a call for action for mental health science (2020, background): “110 Better understanding of how the intense systemic immune response to SARS-CoV-2 infection affects mental health and neurological symptoms, 97,111,112 and of the mechanisms of immune clearance of SARS-CoV-2, is also needed.”
Cumulative meta-analysis of interleukins 6 and 1β, tumour necrosis factor α and C-reactive protein in patients with major depressive disorder (2015, neutral): “Li Z, Qi D, Chen J, Zhang C, Yi Z, Yuan C, Wang Z, Hong W, Yu S, Cui D, Fang Y. Venlafaxine inhibits the upregulation of plasma tumor necrosis factor-alpha (TNF-alpha) in the Chinese patients with major depressive disorder: a prospective longitudinal study.”
Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, neutral): “Immun. brain cells, which in turn produce and secrete pro-inflammatory mediators (Dantzer et al., 2008; Maier and Watkins, 1998).”
Microglia promote learning-dependent synapse formation through BDNF (2013, background): “Because deficits in peripheral myeloid cells could have significant effects on the CNS (Dantzer et al., 2008), caution is warranted in deducing the precise function of microglia in the brain from experiments using knockout mice that affect both peripheral and CNS myeloid cells.”
Minocycline attenuates lipopolysaccharide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia (2008, background): “Because sickness can also be associated with longer lasting changes in motivation [38], we next sought to determine if minocycline abrogated LPS-induced anhedonia [54,55].”
The Adverse Effects of Air Pollution on the Nervous System (2012, background): “In addition, circulating cytokines that are released by inflamed peripheral organs or endothelial cells could stimulate peripheral innate immune cells, activate peripheral neuronal afferents, or enter the brain by diffusion and active transport thereby worsening the condition synergistically [27, 28”
Associations of Depression With C-Reactive Protein, IL-1, and IL-6: A Meta-Analysis (2009, background): “A second body of research, largely articulated by Dantzer and colleagues, supports an inflammation to depression causal pathway (73).”
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).”