Cytokines and major depression.

By O. Schiepers, M. Wichers, Michael Maes. Progress in Neuro-psychopharmacology and Biological Psychiatry, 2005

1,270 citations recorded by the source corpus.

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.

Subfields: Behavioral Neuroscience, Biological Psychiatry, Social Psychology

View Paper: https://www.semanticscholar.org/paper/2d14a2e89a21cce7343167205990a9192fe94f58

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Citations in the corpus

Vagus Nerve as Modulator of the Brain–Gut Axis in Psychiatric and Inflammatory Disorders (2018, background): “This might be explained by the fact that cytokine overexpression leads to a reduction of serotonin levels (109).”
Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics (2007, background): “tion may contribute to therapy based on both the (a) depressive effects that cytokines can produce, as well as (b) on much evidence that classical anti-depressants have anti-inflammatory effects [59, 63].”
Etiology of the protein-energy wasting syndrome in chronic kidney disease: a consensus statement from the International Society of Renal Nutrition and Metabolism (ISRNM). (2013, background): “173 ,176 In dialysis patients, symptoms of depression are associated with increased IL-6 levels, 177,178 and 8 weeks of ﬂuoxetine treatment resulted in decreased serum IL-1 b levels.”
A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro)degenerative processes in that illness. (2011, methodology): “Thus, we called this theory the monocyte-T-lymphocyte hypothesis of depression, the cytokine hypothesis of depression, and the inflammatory hypothesis of depression (Maes, 1993, 1995, 1999, 2002; Schiepers et al., 2005).”
One year pre-post intervention follow-up of psychological, immune, endocrine and blood pressure outcomes of mindfulness-based stress reduction (MBSR) in breast and prostate cancer outpatients. (2007, background): “…the putative role of pro-inflammatory cytokines in the etiology of depression, possibly through altering HPA axis reactivity, down regulating serotonin precursors, and impairing processes of neurogenesis (Raison et al., 2006; Hayley et al., 2005; Hayley and Anisman, 2005; Schiepers et al., 2005).”
Major depression after breast cancer: a review of epidemiology and treatment. (2008, background): “Proinflammatory cytokines released in response to the tissue damage that occurs during cancer treatment may contribute to the high rates of depression and related symptoms in cancer patients [176,177,185–188].”
From Stress to Inflammation and Major Depressive Disorder: A Social Signal Transduction Theory of Depression (2014, methodology): “Adapted from Schiepers, Wichers, and Maes (2005), Dantzer, O’Connor, Freund, Johnson, and Kelley (2008), and DellaGioia and Hannestad (2010).”
The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression (2009, methodology): “This hypothesis was termed the monocyte-T-lymphocyte or cytokine hypothesis of depression (Maes 1993, 1995, 1999; Maes et al. 1995b; Schiepers et al. 2005).”
An fMRI Study of Cytokine-Induced Depressed Mood and Social Pain: The Role of Sex Differences (2009, background): “Mounting evidence has demonstrated a relationship between immune system activity and depression (Capuron and Miller, 2004; Raison et al., 2006; Schiepers et al., 2005).”