Journal ArticleDOI
Pro-inflammatory cytokines and treatment response to escitaloprsam in major depressive disorder
TLDR
In this article, the levels of soluble interleukin-2 receptor (sIL-2R), IL-8, and tumor necrosis factor alpha (TNF-alpha) were measured at baseline and at 4th and 12th week of the treatment and compared to cytokine concentrations in healthy volunteers.Abstract:
Alterations in the immune system may have importance for the pathophysiology of depression. Several studies have linked increased production of pro-inflammatory cytokines to depression and depressive symptoms. There is growing evidence that antidepressive treatment may influence the production of pro-and anti-inflammatory cytokines. In the present study we aimed to find associations between the levels of soluble interleukin-2 receptor (sIL-2R), interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-alpha) and the response to antidepressant treatment in patients with major depression. Our study group consisted of 100 patients (35 males and 65 females) who were treated with escitalopram 10-20 mg/day for 12 weeks. Responders and non-responders were identified according to Montgomery-Asberg's Depression Rating Scale (MADRS) scores. The levels of cytokines were measured at baseline and at 4th and 12th week of the treatment and compared to cytokine concentrations in healthy volunteers (n=45; 19 males and 26 females). Our data indicated that a higher level of TNF-alpha might predict a non-response to treatment with escitalopram and that changes in concentrations of sIL-2R during the treatment were different in responders and non-responders.read more
Citations
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Journal ArticleDOI
A Meta-Analysis of Cytokines in Major Depression
Yekta Dowlati,Nathan Herrmann,Nathan Herrmann,Walter Swardfager,Walter Swardfager,Helena Liu,Lauren Sham,Elyse K. Reim,Krista L. Lanctôt,Krista L. Lanctôt +9 more
TL;DR: A meta-analysis of studies measuring cytokine concentration in patients with major depression reports significantly higher concentrations of the proinflammatory cytokines TNF-alpha and IL-6 in depressed subjects compared with control subjects, strengthening evidence that depression is accompanied by activation of the IRS.
Journal ArticleDOI
A meta-analysis of blood cytokine network alterations in psychiatric patients: comparisons between schizophrenia, bipolar disorder and depression.
TL;DR: Overall, there were similarities in the pattern of cytokine alterations in schizophrenia, bipolar disorder and MDD during acute and chronic phases of illness, raising the possibility of common underlying pathways for immune dysfunction.
Journal ArticleDOI
So depression is an inflammatory disease, but where does the inflammation come from?
Michael Berk,Lana J. Williams,Lana J. Williams,Felice N. Jacka,Felice N. Jacka,Adrienne O'Neil,Adrienne O'Neil,Julie A. Pasco,Julie A. Pasco,Steven Moylan,Nicholas B. Allen,Amanda L Stuart,Amie C. Hayley,Michelle L. Byrne,Michael Maes,Michael Maes +15 more
TL;DR: The identification of known sources of inflammation provides support for inflammation as a mediating pathway to both risk and neuroprogression in depression.
Journal ArticleDOI
The effect of antidepressant medication treatment on serum levels of inflammatory cytokines: a meta-analysis
TL;DR: Overall, while pharmacological antidepressant treatment reduced depressive symptoms, it did not reduce serum levels of TNFα, but antidepressant treatment did reduce levels of IL-1β and possibly those ofIL-6, which are consistent with the possibility that inflammatory cytokines contribute to depressive symptoms and that antidepressants block the effects ofinflammatory cytokines on the brain.
Journal ArticleDOI
Interleukin (IL)-6, tumour necrosis factor alpha (TNF-α) and soluble interleukin-2 receptors (sIL-2R) are elevated in patients with major depressive disorder: a meta-analysis and meta-regression.
TL;DR: Age, samples source and ethnic origins may play a potential role in heterogeneity, and European but not non-European subjects have higher levels difference of sIL-2R, TNF-α and IL-1β between MDD patients and controls.
References
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Journal ArticleDOI
Cytokines and major depression.
TL;DR: 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.
Journal ArticleDOI
Cytokine Production and Treatment Response in Major Depressive Disorder
TL;DR: The data indicate that unstimulated secretion of TNF-α is related to the psychopathological improvement; whereas, IL-6 levels might dichotomize the patients into subsequent responders and nonresponders already at admission.
Journal ArticleDOI
Increased serum il-6 and il-1 receptor antagonist concentrations in major depression and treatment resistant depression
TL;DR: Major depression and TRD are accompanied by an activation of the monocytic arm of cell-mediated immunity, and the latter may be related to the immune an acute phase response in major depression; and the above disorders may persist despite successful antidepressive treatment.
Journal ArticleDOI
Increased plasma concentrations of interleukin-6, soluble interleukin-6, soluble interleukin-2 and transferrin receptor in major depression
Michael Maes,Herbert Y. Meltzer,Eugene Bosmans,Raf Bergmans,Eric Vandoolaeghe,Rakesh Ranjan,Roger Desnyder +6 more
TL;DR: It is suggested that a coordinated and upregulated production of IL-6, sil-6R, sIL-2R and TfR may constitute a trait marker of major depression; and an up regulated production ofIL-6 may represent a contributing factor to the various immune disorders encountered in major depression and maybe to the pathophysiology or pathogenesis of that illness.
Journal ArticleDOI
Cytokines and psychopathology: Lessons from interferon-α
Lucile Capuron,Andrew H. Miller +1 more
TL;DR: Findings from interferon-α may provide important clues regarding the pathophysiology and treatment of cytokine-induced behavioral changes in medically ill patients, while also potentially modeling the development of neuropsychiatric symptoms in patients without medical disorders.