Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although depression and immune changes in elderly subjects constitute a considerable health risk, mechanisms underlying the association between depression and immune function are unclear. The question of whether personality and social support can explain the variation in immune function during depression was addressed in 21 elderly depressive and 23 control subjects. The following variables were studied: neuroticism, extraversion, received social support, depression-related immune parameters [i.e. numbers of lymphocytes, lymphocyte subsets CD3+, CD8+, natural killer-like T cells (NKT), CD4/CD8 ratio, and interleukin-6 (Il-6)]. We found that neuroticism reduced the association between depression and Il-6 (from 62 to 22.4%) and between depression and CD3+ (from 27.6 to 21.6%), and was also directly related to Il-6 (i.e. adjusted for age and depression). Social support reduced the association between depression and NKT cells from 25 to 18%, while it was also directly related to NKT cells. Extraversion, adjusted for age and depression, was negatively related to CD4/CD8 ratio. Subjects with high extraversion and high social support had more NKT cells. We concluded that changes in immune function during depression can partly be explained by neuroticism and received social support, whereas immune function is also directly related to these psychosocial variables. Neuroticism may exert its contribution to the risk for depression partly via Il-6 production.
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PMID:Potential psychosocial mechanisms linking depression to immune function in elderly subjects. 1529 23

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

This study prospectively examined the relationship between religious attendance, interleukin-6 (IL-6) levels, and mortality rates in a community-based sample of 557 older adults. Attending religious services more than once weekly was a significant predictor of lower subsequent 12-year mortality and elevated IL-6 levels (> 3.19 pg/mL), with a mortality ratio of.32 (95% confidence interval [CI] = 0.15,0.72; p <.01) and an odds ratio for elevated IL-6 of.34 (95% CI = 0.16, 0.73, p <.01), compared with never attending religious services. Structural equation modeling indicated religious attendance was significantly related to lower mortality rates and IL-6 levels, and IL-6 levels mediated the prospective relationship between religious attendance and mortality. Results were independent of covariates including age, sex, health behaviors, chronic illness, social support, and depression. Findings are consistent with a role for IL-6 in processes mediating the relationship between religious attendance and mortality.
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PMID:Religious participation, interleukin-6, and mortality in older adults. 1536 66

This clinical study compared the expression of circulating proinflammatory (tumor necrosis factor-alpha [TNF-alpha] and interleukin-6) and anti-inflammatory (interleukin-10) cytokines and soluble apoptosis mediators (Fas/Fas ligand) between patients with stable chronic heart failure and depressive symptoms (as estimated by the Zung Self-Rating Depression Scale) (n = 15) and those without these symptoms (n = 20). Patients with depressive symptoms exhibited significantly higher levels of TNF-alpha and soluble Fas ligand, as well as significantly lower levels of interleukin-10, than patients without emotional distress. A disregulated cytokine network and activated apoptosis signaling molecules may be actively implicated in the pathophysiology of chronic emotional distress and depressive symptoms in patients with heart failure.
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PMID:Comparison of circulating proinflammatory cytokines and soluble apoptosis mediators in patients with chronic heart failure with versus without symptoms of depression. 1554 Dec 60

Despite mounting evidence that depressive symptoms increase the risk of morbidity and mortality in patients who have coronary artery disease, little is known about the biologic mechanisms that underlie this association. This study examined whether depressive symptoms are associated with markers of infection and inflammation that have been implicated in the pathogenesis of coronary artery disease. Sixty-five patients who were recovering from an acute coronary syndrome were enrolled (63% men; mean age 61 years, 90% white). Depressive symptoms were assessed through self-report and observer ratings; the inflammatory molecules C-reactive protein, interleukin-6, and tumor necrosis factor-alpha were measured in serum, as were antibody titers to 3 latent viruses associated with atherosclerosis. Patients who had more severe depressive symptoms exhibited higher levels of C-reactive protein (r = 0.27, p = 0.03) and higher rates of seropositivity to the latent viruses (r = 0.41, p = 0.001). These effects were large in magnitude: patients in the highest tertile of the depression distribution had C-reactive protein levels >50% higher than did patients in the middle and lowest tertiles; they also were 2 times as likely to show evidence of infection with all 3 latent viruses. Disparities in the extent, severity, or management of cardiac disease were not responsible for these associations. These findings provide evidence that depressive symptoms are associated with increases in C-reactive protein and pathogen burden in patients who have coronary artery disease. In doing so, they highlight a mechanism through which depressive symptoms might foster morbidity and mortality among patients who have cardiac disease.
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PMID:Relation of depressive symptoms to C-reactive protein and pathogen burden (cytomegalovirus, herpes simplex virus, Epstein-Barr virus) in patients with earlier acute coronary syndromes. 1567 May 37

Viral hepatitis is a common and important problem in immunocompromised cancer patients. The present study was conducted to investigate changes in some cellular and humoral immunological parameters as a consequence of HCV infection in non Hodgkin's lymphoma patients (NHL). The study included 40 NHL patients: 20 anti-HCV antibody positive (Gr. I ), and 20 anti-HCV antibody negative (Gr.II ). In addition, forty non-cancer controls (NCCs) were included: 20 of them were anti-HCV antibody positive (Gr. III) and 20 anti-HCV antibody negative (Gr. IV). The studied immunological parameters included serum levels of interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-6 (IL-6), and soluble tumor necrosis factor receptors (s-TNFr) measured by ELISA, as well as assessment of T and B lymphocyte subsets by PAP immunostaining method. Mean IL-1 level (pg/ml) was significantly higher in Gr. 1 (14 +/- 6) and Gr. III (20 +/- 12) as compared to those in Gr. II (7 +/- 5) and Gr. IV (9 +/- 6). Mean IL-2 level (pg/ml) was also significantly higher in Gr. I (132 +/- 101) and Gr. III (135 +/- 59) compared to those in Gr. II (36 +/- 29) and Gr. IV (31 +/- 48). On the other hand, level of IL-6 showed no significant difference between groups. The mean level of sTNF-r, (ng/ml) was only significantly higher in Gr. I (2.9 +/- 1.7) when compared to that in Gr. IV (1.9 +/- 2.2). In group IV, the average percentage of CD3 (70 +/- 4%) and CD4 (44 +/- 5%) were significantly higher than in those of Gr. I (CD3 = 51 +/- 11%, CD4 = 30 +/- 12%), Gr. II (CD3 = 52 +/- 7%, CD4 = 30 +/- 8%), and Gr. III (CD3 = 52 +/- 9%, CD4 = 26 +/- 8%). From all the above immunological and virological features two main tips could be inferred: (1) HCV leads a mild course of infection in NCCs evidenced by normal ALT level in all but 20% of subjects, normal IL-6, sTNF-r, lower counts of CD4+ T cells and hence a mild hepatocellular injury, and (2) In the immunocompromised NHL patients the virus leads potentially more aggressive course as evidenced by higher viremia, as well as significant elevation in sTNF-r, and CD8+ depression.
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PMID:Hepatitis C Virus and related changes in immunological parameters in non Hodgkin's lymphoma patients. 1572 87

The prevalence of depression among patients diagnosed with cancer is higher than among the general medical population and is associated with faster tumor progression and shortened survival time. Cancer-related depression often occurs in association with anorexia and cachexia, although until recently the relationship between these conditions has not been well understood. Cachexia is associated with poorer quality of life and survival outcomes and is theeventual cause of death in approximately 30% of all patients with cancer. Recent evidence has linked elevated levels of inflammatory cytokines with both depression and cachexia, and experiments have shown that introducing cytokines induces depression and cachectic symptoms in both humans and rodents, suggesting that there may be a common etiology at the molecular level. Therapeutic agents targeting specific cytokine molecules, such as interleukin-6 or tumor necrosis factor-alpha, are currently being evaluated for their potential to simultaneously treat both depression and cachexia pharmacologically. This review summarizes the available data suggesting a dual role for cytokines in the development of cancer-related depression and cachexia and describes how biologic therapies targeting specific cytokines may improve outcomes beyond depression and cachexia, such as survival and quality of life.
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PMID:Are inflammatory cytokines the common link between cancer-associated cachexia and depression? 1572 46

Cytokines whose primary function is that of acting as signaling molecules of the immune system, have been implicated in the provocation or exacerbation of mood disorders such as depression. This position has been supported by several lines of evidence; (1) proinflammatory cytokines (interleukin-1beta, interleukin-6, tumor necrosis factor-alpha) and bacterial endotoxins elicit sickness behaviors (e.g., fatigue, soporific effects) and symptoms of anxiety/depression that may be attenuated by chronic antidepressant treatment. Interleukin-2 (IL-2) induces less profound sickness, but elicits anhedonia, a key symptom of depression; (2) neuroendocrine and central neurotransmitter changes, reminiscent of those implicated in depression, may be elicited by some of these cytokines, and these effects are exacerbated by stressors; (3) severe depressive illness is accompanied by elevations of cytokine production or levels, although these effects are not necessarily attenuated with antidepressant medication; and (4) immunotherapy, using IL-2 or IFN-alpha, promote depressive symptoms that are attenuated by antidepressant treatment. It is proposed that chronic cytokine elevations engender neuroendocrine and brain neurotransmitter changes that are interpreted by the brain as being stressors, and contribute to the development of depression. Further, the effects of the cytokine treatments may act synergistically with stressors, and cytokines may provoke a sensitization effect so that the effects of later stressor experiences are exacerbated.
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PMID:Cytokines as a precipitant of depressive illness: animal and human studies. 1577 47

This preliminary investigation compares peripheral blood cell counts including red blood cells (RBCs), white blood cells (WBCs), neutrophils, peripheral blood lymphocytes (PBLs), CD4(+), CD8(+) and CD16(+) lymphocytes, CD4(+)/CD8(+) ratio, hematocrit, humoral parameters including serum interferon-gamma and interleukin-6, salivary secretory immunoglobulin A (IgA). Psychological measures including the State-Trait Anxiety Inventory (STAI) questionnaire and the Self-rating Depression Scale (SDS) between recipients (n = 11) of carrier oil massage and aromatherapy massage, which includes sweet almond oil, lavender oil, cypress oil and sweet marjoram oil. Though both STAI and SDS showed a significant reduction (P < 0.01) after treatment with aromatherapy and carrier massage, no difference between the aromatherapy and control massage was observed for STAI and SDS. Aromatherapy, in contrast to control massage, did not significantly reduce RBC count or hematocrit. However, aromatherapy massage showed a significant (P > 0.05) increase in PBLs, possibly due to an increase in CD8(+) and CD16(+) lymphocytes, which had significantly increased post-treatment (P < 0.01). Consequently, the CD4(+)/CD8(+) ratio decreased significantly (P < 0.01). The paucity of such differences after carrier oil massage suggests that aromatherapy massage could be beneficial in disease states that require augmentation of CD8(+) lymphocytes. While this study identifies the immunological benefits of aromatherapy massage, there is a need to validate the findings prospectively in a larger cohort of patients.
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PMID:Immunological and Psychological Benefits of Aromatherapy Massage. 1593 58

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


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