Cytokine-induced sickness behaviour: mechanisms and implications.

By J. Konsman, P. Parnet, Robert Dantzer. Trends in Neurosciences, 2002

991 citations recorded by the source corpus.

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Citations in the corpus

Microglia and neurodegeneration: The role of systemic inflammation (2013, background): “…circumventricular organs, of the perivascular macrophages as well as transport of cytokines across the BBB and stimulation of vagal afferents arising in the viscera have all been well described after systemic inflammation and are discussed elsewhere (Banks and Erickson, 2010; Konsman et al., 2002).”
Microglia as a source and target of cytokines (2002, background): “…Interactions Induction of sickness behavior with fever and food intake suppression or the adjustment of endocrine activities are effects attributed to cytokines in physiological adaptations to immune system challenges or stressful situations (Hanisch, 2001a; Konsman et al., 2002).”
Cytokine, Sickness Behavior, and Depression (2009, background): “in those brain areas that are devoid of a functional blood-brain barrier to the existence of specific saturable transporters [2].”
Exaggerated neuroinflammation and sickness behavior in aged mice after activation of the peripheral innate immune system (2005, background): “These proinflammatory cytokines are known to induce neurobehavioral deficits during infection (6) and are increased in the aged brain (17, 18, 21).”
Stress and neuroinflammation: a systematic review of the effects of stress on microglia and the implications for mental illness (2016, background): “IL-1β, TNF-α, IL-6 Pro-inflammatory cytokines Released by stimulated neutrophils and monocytes (Konsman et al. 2002)”
Central and Systemic Endotoxin Challenges Exacerbate the Local Inflammatory Response and Increase Neuronal Death during Chronic Neurodegeneration (2005, background): “, 1997) and that these cytokines coordinate a group of adaptive behavioral changes collectively known as sickness behavior (Konsman et al., 2002).”
Inflammatory Cytokines in Depression: Neurobiological Mechanisms and Therapeutic Implications (2013, background): “In the brain, endothelial cells and perivascular macrophages respond to circulating cytokines to induce expression of COX-2 and release of PGE2 (Elmquist et al., 1997, Lacroix and Rivest, 1998, Konsman et al., 2002, Konsman et al., 2004).”
Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “…4) transmission of cytokine signals via afferent nerve fibers, such as the vagus nerve, and 5) entry into the brain parenchyma of peripherally activated monocytes (Watkins et al., 1995;Plotkin et al., 1996;Rivest et al., 2000;Konsman et al., 2002;Quan and Banks, 2007;D’Mello et al., 2009).”
Cytokine-induced sickness behavior. (2003, background): “All these data are in accord with the tenet that peripherally administered cytokines induce synthesis of cytokines in the brain, which then act on specific neural substrates to induce sickness behavior ( Konsman et al., 2002 ).”
The Darwinian concept of stress: benefits of allostasis and costs of allostatic load and the trade-offs in health and disease. (2005, background): “Second, kynurenine metabolites such as 3-hydroxy-kynurenine and quinolinic acid have toxic effects on brain function; The former metabolite can lead to oxidative stress by increasing the production of reactive oxygen species, while quinolinic acid may produce overstimulation of hippocampal N-methyl-”