Journal ArticleDOI
Cytokines and major depression.
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TLDR
Although the central effects of proinflammatory cytokines appear to be able to account for most of the symptoms occurring in depression, it remains to be established whether cytokines play a causal role in depressive illness or represent epiphenomena without major significance.Abstract:
In the research field of psychoneuroimmunology, accumulating evidence has indicated the existence of reciprocal communication pathways between nervous, endocrine and immune systems. In this respect, there has been increasing interest in the putative involvement of the immune system in psychiatric disorders. In the present review, the role of proinflammatory cytokines, such as interleukin (IL)-1, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma, in the aetiology and pathophysiology of major depression, is discussed. The 'cytokine hypothesis of depression' implies that proinflammatory cytokines, acting as neuromodulators, represent the key factor in the (central) mediation of the behavioural, neuroendocrine and neurochemical features of depressive disorders. This view is supported by various findings. Several medical illnesses, which are characterised by chronic inflammatory responses, e.g. rheumatoid arthritis, have been reported to be accompanied by depression. In addition, administration of proinflammatory cytokines, e.g. in cancer or hepatitis C therapies, has been found to induce depressive symptomatology. Administration of proinflammatory cytokines in animals induces 'sickness behaviour', which is a pattern of behavioural alterations that is very similar to the behavioural symptoms of depression in humans. The central action of cytokines may also account for the hypothalamic-pituitary-adrenal (HPA) axis hyperactivity that is frequently observed in depressive disorders, as proinflammatory cytokines may cause HPA axis hyperactivity by disturbing the negative feedback inhibition of circulating corticosteroids (CSs) on the HPA axis. Concerning the deficiency in serotonergic (5-HT) neurotransmission that is concomitant with major depression, cytokines may reduce 5-HT levels by lowering the availability of its precursor tryptophan (TRP) through activation of the TRP-metabolising enzyme indoleamine-2,3-dioxygenase (IDO). Although the central effects of proinflammatory cytokines appear to be able to account for most of the symptoms occurring in depression, it remains to be established whether cytokines play a causal role in depressive illness or represent epiphenomena without major significance.read more
Citations
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Brain Region-dependent Heterogeneity and Dose-dependent Difference in Transient Microglia Population Increase during Lipopolysaccharide-induced Inflammation.
TL;DR: It is demonstrated that transient increase in microglia density depends on the brain region and dose of LPS during infection-induced inflammation and could provide a new insight on microglial functions in inflammation and pathogenesis of brain diseases.
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The Cancer Chemotherapy Drug Etoposide (VP-16) Induces Proinflammatory Cytokine Production and Sickness Behavior–like Symptoms in a Mouse Model of Cancer Chemotherapy–Related Symptoms
TL;DR: Findings support the idea that the induction of IL-1β, TNF-α, and IL-6 by cancer chemotherapy drugs underlies the fatigue and associated symptoms experienced by people undergoing cancer chemotherapy.
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Evangelos Oikonomou,Dimitris Tousoulis,Gerasimos Siasos,Marina Zaromitidou,Athanasios G. Papavassiliou,Christodoulos Stefanadis +5 more
TL;DR: Hippokration Hospital 114 Vasilissis Sofias Ave. 115 28 Athens, Greece e-mail: drtousoulis@ hotmail.com
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Depression as a risk factor for cancer: from pathophysiological advances to treatment implications.
TL;DR: Research is needed to determine whether optimal depression treatment improves cancer survival and to develop antidepressant strategies that target molecular and cellular mechanisms mediating inflammation and the neurobiological pathways influenced by the proinflammatory cytokines.
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Depression, traumatic stress and interleukin-6
Petr Bob,Jiri Raboch,Michael Maes,Marek Susta,Josef Pavlat,Denisa Jasova,Jan Vevera,Jana Uhrova,Hana Benakova,Tomáš Zima +9 more
TL;DR: The findings of the present study indicate that increased level of IL-6 in depression could be directly related to symptoms of traumatic stress and somatoform dissociation.
References
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Book
Immunobiology: The Immune System in Health and Disease
TL;DR: Introductory immunology textbook for medical students, advanced undergraduates, and graduate students.
Journal ArticleDOI
The inflammatory reflex
TL;DR: The discovery that cholinergic neurons inhibit acute inflammation has qualitatively expanded understanding of how the nervous system modulates immune responses, and the opportunity now exists to apply this insight to the treatment of inflammation through selective and reversible 'hard-wired' neural systems.
Journal ArticleDOI
The catecholamine hypothesis of affective disorders: a review of supporting evidence
TL;DR: The "catecholamine hypothesis of affective disorders" as discussed by the authors suggests that depression is associated with an absolute or relative decrease in catecholamines, particularly norepinephrine, available at central adrenergic receptor sites.
Journal ArticleDOI
A trial of etanercept, a recombinant tumor necrosis factor receptor:Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate.
Michael E. Weinblatt,Joel M. Kremer,Arthur D. Bankhurst,Ken J. Bulpitt,Roy Fleischmann,Robert I. Fox,Christopher G. Jackson,Mary Lange,Daniel Burge +8 more
TL;DR: In patients with persistently active rheumatoid arthritis, the combination of etanercept and methotrexate was safe and well tolerated and provided significantly greater clinical benefit than metotrexate alone.