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)

There is increasing evidence that depression and related neurotic illnesses are associated with alterations in immune function that may contribute to their pathogenesis. For example, clinical and experimental studies have shown that abnormal HPA-axis activation and monoamine neurotransmission may be related to an increased release of proinflammatory cytokines from stimulated lymphocytes in the periphery and brain. In the present investigation, the effects of tryptophan depletion (TD) on unstimulated plasma interleukin-6 (IL-6) concentrations were investigated in order to determine whether acute changes in serotonin (5-HT) neurotransmission would induce a proinflammatory response in healthy individuals. The effects of TD were compared with the analogous procedure of tyrosine depletion (TPD), which reduces catecholamine metabolism in humans. Thirteen female participants completed three experimental sessions: TD, TPD and a balanced-control condition (B). Mood-ratings and blood sampling were performed at baseline and 5 h after the administration of the mixtures. Analyses revealed that TD and TPD markedly reduced tryptophan and tyrosine/phenylalanine levels, respectively. No changes in plasma IL-6 production or ratings of lowered mood were observed, however, subjects did report feeling more fatigued after TD. These findings indicate that a transient disruption in global monoamine function does not stimulate a proinflammatory response of IL-6 in normal volunteers.
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PMID:Effects of serotonin and catecholamine depletion on interleukin-6 activation and mood in human volunteers. 1240 74

Despite mounting evidence that psychiatric depression heightens risk for cardiac morbidity and mortality, little is known about the mechanisms responsible for this association. The present study examined the relation between depression and the expression of inflammatory risk markers implicated in the pathogenesis of coronary heart disease (CHD). One hundred adults were enrolled (68% women, 48% Caucasian, 48% African-American, mean age 30 +/- 2 years). Fifty subjects met the diagnostic criteria for clinical depression; the remaining 50 were demographically matched controls with no history of psychiatric illness. All subjects were in excellent health, defined as having no acute infectious disease, chronic medical illness, or regular medication regimen aside from oral contraceptives. The depressed subjects exhibited significantly higher levels of the inflammatory markers C-reactive protein (3.5 +/- 0.5 vs 2.5 +/- 5 mg/L, p = 0.04) and interleukin-6 (3.0 +/- 0.3 vs 1.9 +/- 0.2 pg/ml, p = 0.007) compared with control subjects. Mediational analyses aimed at identifying the pathways contributing to this association revealed that neither cigarette smoking nor subclinical infection with cytomegalovirus or Chlamydia pneumoniae had been responsible. However, depressed subjects exhibited greater body mass than control subjects, and analyses were consistent with adiposity accounting for a portion of the relation between clinical depression and increased expression of inflammatory markers. These findings indicate that in otherwise healthy adults, depression is associated with heightened expression of inflammatory markers implicated in the pathogenesis of CHD. Increased body mass appears to be partially, although not completely, responsible for this relation.
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PMID:Clinical depression and inflammatory risk markers for coronary heart disease. 1248 34

A 30-year-old man was admitted to our hospital for left lobar pneumonia with septic shock. Acute left-sided heart failure became evident as sepsis developed. Echocardiography revealed diffuse severe hypokinesis of the left ventricle (LV) and a pulmonary artery catheter showed Forrester subset II hemodynamics. Along with amelioration of sepsis and decrease of the serum concentrations of tumor necrosis factor-alpha and interleukin-6, LV hypokinesis improved. It is suggested that the patient's heart failure may have been due to functional depression of myocardial contractility resulting from a direct effect of the cytokines towards the cardiomyocytes, the so-called "septic myocardial depression".
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PMID:Acute reversible myocardial depression associated with sepsis. 1258 21

Cytokines, signaling molecules of the immune system, have been implicated as a contributing factor for mood disorders such as depression. Several lines of evidence supporting this contention are briefly reviewed and caveats are introduced. Essentially, a relationship between cytokines and depression is based on the findings that: 1) proinflammatory cytokines (interleukin-1, 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, 2) cytokines induce neuroendocrine and central neurotransmitter changes reminiscent of those implicated in depression, and these effects are exacerbated by stressors, 3) severe depressive illness is accompanied by signs of immune activation and by elevations of cytokine production or levels, and 4) immunotherapy, using interleukin-2 or interferon-alpha, promotes depressive symptoms that are attenuated by antidepressant treatment. It is argued that cytokine synthesis and release, elicited upon activation of the inflammatory response system, provoke neuroendocrine and brain neurotransmitter changes that are interpreted by the brain as being stressors, and contribute to the development of depression. Furthermore, such effects are subject to a sensitization effect so that a history of stressful experiences or cytokine activation augment the response to later challenges and hence the evolution of depression
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PMID:Cytokines, stress and depressive illness: brain-immune interactions. 1269 7

Despite mounting evidence that depression increases risk for cardiovascular morbidity and mortality, little is known about the mechanisms responsible for this association. The current study examined the inter-relationships between depression, adiposity, and inflammatory molecules implicated in the pathogenesis of coronary heart disease. One hundred adults were enrolled. Half were clinically depressed; the others were matched controls with no history of psychiatric illness. All subjects were in excellent health, defined as having no acute infectious disease, chronic medical illness, or prescribed medication regimen. Structural equation modeling yielded support for a model in which depressive symptoms promote weight accumulation, which in turn activates an inflammatory response through two distinct pathways: expanded adipose tissue release of interleukin-6 and leptin-induced upregulation of interleukin-6 release by white blood cells (CFI =.99; NNFI =.99; RMSEA =.05). It did not support a sickness behavior model in which the inflammatory molecules arising from expanded adipose tissue promote depressive symptoms.
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PMID:Pathways linking depression, adiposity, and inflammatory markers in healthy young adults. 1283 30

Social position and psychosocial factors are associated with coronary disease, but the underlying pathophysiologic mechanisms remain unclear. In a sample of 283 nonsmokers, we found that social position was inversely associated with interleukin-6 and C-reactive protein and that participants with mild depression had impaired endothelial function.
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PMID:Social and psychosocial influences on inflammatory markers and vascular function in civil servants (the Whitehall II study). 1455 80

Although the prognostic significance of depression and hostility has been established, little is known about how they operate together to influence disease processes. This study explored the independent and interactive relationships between these constructs and the expression of inflammatory markers implicated in the pathogenesis of coronary heart disease. One hundred adults completed measures of cynical hostility and depressive symptoms, and had blood drawn to assess serum levels of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha. Depression was directly related to inflammatory markers, but hostility was not. A significant interaction between hostility and depression emerged. Among participants scoring low in depressive symptoms, hostility was positively associated with interleukin-6 and tumor necrosis factor-alpha concentrations. Hostility's association with these inflammatory markers was much weaker among participants with moderate depressive symptoms, however, and virtually nil among participants with severe depressive symptoms. Neither depression nor hostility was associated with interleukin-1 beta concentrations. These findings highlight the importance of considering both the independent and interactive relationships among psychosocial characteristics involved in disease.
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PMID:Cynical hostility, depressive symptoms, and the expression of inflammatory risk markers for coronary heart disease. 1467 9

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

There is increasing evidence that an ongoing cytokine-induced acute-phase response (sometimes called low-grade inflammation, but part of a widespread activation of the innate immune system) is closely involved in the pathogenesis of type 2 diabetes and associated complications such as dyslipidemia and atherosclerosis. Elevated circulating inflammatory markers such as C-reactive protein and interleukin-6 predict the development of type 2 diabetes, and several drugs with anti-inflammatory properties lower both acute-phase reactants and glycemia (aspirin and thiazolidinediones) and possibly decrease the risk of developing type 2 diabetes (statins). Among the risk factors for type 2 diabetes, which are also known to be associated with activated innate immunity, are age, inactivity, certain dietary components, smoking, psychological stress, and low birth weight. Activated immunity may be the common antecedent of both type 2 diabetes and atherosclerosis, which probably develop in parallel. Other features of type 2 diabetes, such as fatigue, sleep disturbance, and depression, are likely to be at least partly due to hypercytokinemia and activated innate immunity. Further research is needed to confirm and clarify the role of innate immunity in type 2 diabetes, particularly the extent to which inflammation in type 2 diabetes is a primary abnormality or partly secondary to hyperglycemia, obesity, atherosclerosis, or other common features of the disease.
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PMID:Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes. 1498 10

The aim of this study was to investigate the effects of antidepressant treatment on serum cytokines and nutritional status in hemodialysis patients. Twenty-eight hemodialysis patients with a depressed mood were given 20 mg of fluoxetine for 8 weeks. The degree of depressive symptoms, the serum levels of interleukin-1beta, interleukin-2, interleukin-6, tumor necrosis factor-alpha, c-reactive protein, and markers of nutritional status were assessed at baseline and after treatment. The outcome was assessed in terms of response to treatment (>50% reduction in the score of the Hamilton depression rating scale). Antidepressant treatment decreased the serum level of interleukin-beta1 in both response and nonresponse groups, and increased the serum level of interleukin-6 only in the response group. At baseline, the level of interleukin-6 in the response group was lower than in the nonresponse group. Antidepressant treatment also increased fat distribution significantly in the response group which might have slightly improved the nutritional status. This study suggests that antidepressant treatment improve depressive symptoms and may affect immunological functions and nutritional status in chronic hemodialysis patients with depression.
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PMID:The effects of antidepressant treatment on serum cytokines and nutritional status in hemodialysis patients. 1520 4


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