Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is now some evidence that major depression is accompanied by an immune response with an increased production of pro-inflammatory cytokines. The aim of the present study was to examine serum level of cytokines: interleukin-6 (IL-6), which is considered pro-inflammatory one and anti-inflammatory cytokines: interleukin 10 (IL-10), and interleukin-1 receptor antagonist (IL-1Ra) in acute clinical state of depression and after 6-week antidepressant treatment. Serum IL-6, IL-10, IL-1Ra levels were higher in the subjects with major depression than in normal controls although these results were not statistically significant. The mean score according to the Hamilton Depression Rating Scale (HDRS) in the patients significantly decreased during the 6 weeks of the study, demonstrating an overall improvement. Successful antidepressant treatment had no significant effect on serum level of this cytokines.
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PMID:Plasma levels of interleukin-6, interleukin-10, and interleukin-1 receptor antagonist in depression: comparison between the acute state and after remission. 1105 82

There is now evidence that major depression is accompanied by activation of the inflammatory response system (IRS) as indicated by an increased production of pro-inflammatory cytokines. There is circumstantial evidence implicating pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNFalpha) in the pathogenesis of multiple sclerosis (MS). The aims of the present study were to examine (i) the serum concentrations of interleukin-6 (IL-6), IL-8, TNFalpha, IL-2 receptor (IL-2R) and CC16 (uteroglobulin), an endogenous anti-cytokine, in depressed and MS patients compared to normal controls, and (ii) the effects of treatment with antidepressants on the above IRS variables in depressed patients. Serum TNFalpha was significantly higher in depressed and MS patients than in normal controls. Serum IL-8 was significantly higher in depressed patients than in patients with MS. Serum CC16 was significantly higher in patients with MS than in normal controls and depressed patients. Nonresponders to treatment with antidepressants had significantly higher serum IL-2R and lower serum CC16 concentrations than responders to treatment. The results show that (i) depression is accompanied by activation of the IRS and that this activation is more pronounced in depression than in MS, and (ii) IRS activation in depressed patients is related to a nonresponse to treatment with antidepressants.
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PMID:Increased serum tumor necrosis factor alpha concentrations in major depression and multiple sclerosis. 1141 79

There is some evidence that major depression is accompanied by activation of the inflammatory response system (IRS). There is also evidence that proinflammatory cytokines and induction of IRS activation are associated with sickness behavior in experimental animals. However, no research has examined the IRS in somatization disorder. The aim of this study was to examine possible immunological differences between major depression, somatization and healthy controls. We measured the following IRS variables in patients with major depression (n=36), somatization syndrome (SSI-8; n=37), major depression and somatization (n=40) and healthy controls (n=37): interleukin-6 (IL-6); interleukin-1-receptor-antagonist (IL-1RA); plasma soluble interleukin-6 receptor (IL-6R); soluble suppressor/cytotoxic antigen (CD8); leukemia inhibitory factor (LIF-R); and Clara cell protein (CC16), an endogenous anticytokine. Serum CD8 concentrations were significantly increased in patients with major depression compared with concentrations in patients with somatization syndrome, whereas concentrations in normal controls were intermediate between those of the two groups of patients. Serum CC16 was significantly lower in major depression than in healthy controls. The highest CC16 scores were found in patients with somatization syndrome. Somatizing patients have significantly lower serum IL-6 values than normal controls and depressed patients. The present results indicate (1) an activation of the IRS in depression with signs of T-cell activation (increased CD8), monocytic activation (IL-1RA) and a lowered anti-inflammatory capacity of the serum (lower CC16) and (2) an immune alteration in somatizing syndrome, such as monocytic activation (increased IL-1RA) and indicators of lowered T-lymphocytic activity (lowered CD8 and IL-6). These results suggest different immune alterations in somatization syndrome and depression.
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PMID:Immunological differences between patients with major depression and somatization syndrome. 1181 36

Dysfunction of the hyopthalamo-pituitary adrenal (HPA) system is frequently found in major depression. In addition, signs of non-specific inflammatory system activation have been reported. However, very little is known about interactions between the HPA and immune systems in depressive patients. To assess HPA system function, we performed a combined dexamethasone suppression and corticotropin-releasing hormone stimulation (DEX/CRH) test in 14 depressive patients. Moreover, baseline nocturnal plasma levels of the inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor (TNF)-alpha were measured. In addition, the system was challenged with an intraveneous pulsatile injection of hydrocortisone (1 mg/kg body weight in total) and again cytokine levels were measured across one night. Baseline TNF-alpha levels were negatively correlated with the amount of ACTH released upon CRH stimulation during the DEX/CRH test. Acute hydrocortisone administration suppressed TNF-alpha and IL-6 levels independently of baseline HPA system activity. We conclude that chronic HPA system overactivity in depressed patients might compromise the production of inflammatory cytokines under baseline conditions. However, the responsivity of the cytokine production to acutely administered glucocorticoids does not seem to correlate with the state of the HPA system.
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PMID:Hypothalamo-pituitary-adrenal function in patients with depressive disorders is correlated with baseline cytokine levels, but not with cytokine responses to hydrocortisone. 1456 77

Major depression is a risk factor, associated with a twofold increase in the incidence of ischemic heart disease (IHD). One of every 6 patients suffers from major depression following acute myocardial infarction (AMI). This connection is of major concern, considering that major depression is an independent risk factor for cardiac morbidity and mortality after AMI, increasing overall mortality fourfold. Activation of the immune system has a significant role in the pathogenesis of IHD and depression. Vast physiological responses, mediated mostly by activation of the immune system, accompany post MI depression and may account for increased prevalence of arrhythmias and high mortality. This includes activation of the hypothalamic-pituitary-adrenocortical axis, endothelial dysfunction, platelets activation and alterations of phospholipid composition in cell membranes. On the other hand, activation of the immune system after AMI includes elevated levels of interleukin-1 and interleukin-6. which induce "sickness behavior", characterized by symptoms similar to those observed in major depression. The key question raised by this data, whether inflammation is the common ground for both AMI and depression, or if it is accompanying one and sets the ground for the other, remains unanswered at this time. The significance of major depression as an independent risk factor for post MI mortality and morbidity raises the practical question, whether treatment of depression can reduce mortality after AMI. Several recent studies that evaluated this presumption, failed to prove it. In this review we present an overview of the cross interaction between depression, AMI and inflammation and its diagnostic and therapeutic implications.
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PMID:[Depression, myocardial infarction and the immune system--the chicken before the egg problem]. 1474 93

The role of cytokines in depression was first considered when the cytokine interferon resulted in "sickness behaviour", the symptoms of which are similar to those of major depression. The latter is associated with an increase in pro-inflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-alpha). These cytokines are potent modulators of corticotropin-releasing hormone (CRH) which produces heightened hypothalamic-pituitary-adrenal axis (HPA) activity characterized by increases in ACTH and cortisol, both of which are reported elevated in major depression. Antidepressant treatment has immunomodulatory effects with increases in the production of IL-10, which is an anti-inflammatory cytokine. This review based on a Medline search from 1980-2003, focuses on the evidence available of cytokine changes in acute stress, chronic stress and major depression. It examines the effects of antidepressant treatment on immune parameters in both animal models and clinical trials. We suggest that future antidepressants may target the immune system by either blocking the actions of pro-inflammatory cytokines or increasing the production of anti-inflammatory cytokines.
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PMID:Cytokines: abnormalities in major depression and implications for pharmacological treatment. 1530 43

Major depressive disorder is associated with increases in infectious disease risk as well as the incidence of inflammatory disorders. Declines of natural killer (NK) cell activity are reliably found in depression, whereas other studies report evidence of inflammation in depressed patients. The potential association between NK activity and circulating markers of immune activation has not been previously examined in the context of major depression. In this study, we measured levels of NK activity, circulating levels of interleukin-6 (IL-6), soluble interleukin-2 receptor, and acute phase proteins in 25 male patients with current major depressive disorder and 25 age, gender, and body weight comparable controls. As compared to controls, patients with major depressive disorder showed lower NK activity (p = .05) and higher circulating levels of IL-6 (p < .05). Levels of NK activity were not correlated with IL-6 or with other markers of immune activation. The independent effect of depression on inflammatory markers and natural killer immune responses has implications for understanding individual differences in the adverse health effects of major depressive disorder.
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PMID:Dissociation of inflammatory markers and natural killer cell activity in major depressive disorder. 1602 28

Icariin is one of the major active flavonoids constituents of Epimedium brevicornum MAXIM (Berberidaceae). Icariin and E. brevicornum have a wide range of pharmacological activities. Abnormality in the hypothalamic-pituitary-adrenal (HPA) axis is considered to be a key neurobilogical factor in major depression, and cytokines have a close relationship with the activation of the HPA axis. In the present study, the aim was to determine whether icariin possesses an antidepressant-like activity, and to explore the effects of icariin on the HPA axis and cytokine levels in chronic mild stress (CMS) model of depression in Sprague-Dawley rats. Icariin significantly increased the sucrose intake of CMS-treated rats from week 3. It not only attenuated the CMS-induced increases in serum corticotropin-releasing factor (CRF) and cortisol levels, but also reversed the abnormal levels of serum interleukin-6 (IL-6) and tumor-necrosis-factor alpha (TNF-alpha) to the normal in the stressed rats. These results suggested that icariin possessed an antidepressant-like property that was at least in part mediated by neuroendocrine and immune systems.
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PMID:Effects of icariin on hypothalamic-pituitary-adrenal axis action and cytokine levels in stressed Sprague-Dawley rats. 1714 71

An association or a casual link has been proposed between the neuroendocrinological and neuroimmunological changes attributed to either depression or cancer. This study investigated whether breast cancer patients with and without major depression exhibit plasma interleukin-6 abnormalities and dexamethasone suppression test results. Four groups, each consisting of 30 women (1--healthy women, 2--patients with major depression, 3--breast cancer patients without major depression, 4--breast cancer patients with major depression), were compared to each other. Psychiatric evaluations were made by structured clinical interview for DSM-IV. Severity of depression was measured with the Hamilton Depression Rating Scale. Plasma levels of interleukin-6 were measured. A dexamethasone suppression test was applied. Breast cancer patients with major depression had markedly higher plasma levels of interleukin-6 than the other group. All breast cancer patients with depression had abnormal dexamethasone suppression test results. These findings suggest a hypothalamo-pituitary-adrenal axis activation and plasma levels of interleukin-6 and plasma interleukin-6 elevation and plasma levels if interleukin-6 and plasma levels of post cortisol concentrations. Evidence for a casual link or association of major depression with immune and endocrinological activation needs to be investigated further.
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PMID:Interleukin-6 levels and HPA axis activation in breast cancer patients with major depressive disorder. 1758 77

Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.
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PMID:Consensus paper of the WFSBP Task Force on Biological Markers: biological markers in depression. 1962 59


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