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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Journal ArticleDOI
Mice lacking interleukin-18 gene display behavioral changes in animal models of psychiatric disorders: Possible involvement of immunological mechanisms.
S.F. Lisboa,A.C. Issy,Caroline Biojone,Karina Montezuma,Victor Fattori,Elaine Del-Bel,Francisco Silveira Guimarães,Fernando Q. Cunha,Waldiceu A. Verri,Samia R. L. Joca,Samia R. L. Joca +10 more
TL;DR: Deletion of the IL-18 gene resembled features similar to symptoms observed in schizophrenia (positive and cognitive symptoms, aggressive behavior), in addition to increased susceptibility to stress, and could provide new insights into how changes in brain immunological homeostasis induce behavioral changes related to psychiatric disorders, such as schizophrenia.
Journal ArticleDOI
Comorbid risks of psychological disorders and gastroesophageal reflux disorder using the national health insurance service-National Sample Cohort: A STROBE-compliant article.
TL;DR: The results of this study in GERD patients compared with non-GERD patients in Korea suggested that psychological disorders and GERD may be inter-related.
Book ChapterDOI
Probiotics in Neurology and Psychiatry
Paul Forsythe,John Bienestock +1 more
TL;DR: Patients with major depression who are otherwise healthy have activated inflammatory pathways, as indicated by increased proinflammatory cytokines, increased acute-phase proteins, and greater expression of chemokines and adhesion molecules.
Journal ArticleDOI
Novel association between TGFA, TGFB1, IRF1, PTGS2 and IKBKB single-nucleotide polymorphisms and occurrence, severity and treatment response of major depressive disorder.
Katarzyna Bialek,Piotr Czarny,Cezary Watala,Paulina Wigner,Monika Talarowska,Piotr Gałecki,Janusz Szemraj,Tomasz Sliwinski +7 more
TL;DR: Interestingly, A/C of rs2070729 IRF1 and T/T of rs5029748 IKBKB may modulate the effectiveness of selective serotonin reuptake inhibitors therapy.
Journal ArticleDOI
Translating the evidence for gene association with depression into mouse models of depression-relevant behaviour: current limitations and future potential.
TL;DR: This review of the translational evidence makes specific recommendations in terms of how future research in human and mouse should be designed in order to deliver evidence for depression aetio-pathology and thereby to inform the development of novel and improved antidepressant treatments.
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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.