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)

The primary purpose of this exploratory study was to compare percentages of natural killer (NK) cells and activated NK and T cells, and both cytotoxic and in vitro cytokine production activity in women with and without symptomatic irritable bowel syndrome (IBS). A secondary purpose was to examine the relationships of psychological distress and low sense of coherence with immune function indicators and stress hormones. NK cell percentage and activity have been shown to vary in response to many psychological and physiological stressors. The authors compared 2 groups of women: symptomatic IBS (n = 12) and control (n = 12). Between-subject variability for all immune measures was large. The percentage of activated NK and Tcells was significantly lower in the IBS group compared to control (Mann-Whitney U = 30, P = 0.05). Relationships were significant between activated NK and T cell percentage and depression, anxiety, and overall distress (r = -0.54, -0.49, and -0.47, respectively, P < 0.03) and between interferon-gamma production and anxiety (r = -0.45, P < 0.03). There was a trend toward a positive relationship between sense of coherence and NK cytotoxicity (r = 0.39, P = 0.11). Thesefindings are important because they suggest that nursing interventions targeting ongoing physical and psychological distress might also be helpful in improving immune function.
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PMID:Natural killer cell function and psychological distress in women with and without irritable bowel syndrome. 1236 80

The cytokine interferon-gamma stimulates human monocytes/macrophages to release large amounts of neopterin. Increased neopterin concentrations in body fluids of patients are observed during diseases with activated cellular (=TH1-type) immune response such as allograft rejection, virus infections, autoimmune disorders, or malignant tumors but also in neurodegenerative diseases or during pregnancy. In various cells interferon-gamma induces indoleamine 2,3-dioxygenase (IDO) which degrades tryptophan via the kynurenine pathway. Therefore like increased neopterin formation, enhanced tryptophan degradation is observed in diseases concomitant with cellular immune activation. Disturbed metabolism of tryptophan affects biosynthesis of neurotransmitter 5-hydroxytryptamine (serotonin), and it appears to be associated with an increased susceptibility for depression. In fact, enhanced neopterin concentrations together with increased degradation of tryptophan and low serum levels of tryptophan correlate with neuropsychiatric abnormalities like cognitive decline and depressive symptoms especially in long-lasting and chronic diseases. Activation of IDO could represent an important link between the immunological network and the pathogenesis of depression.
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PMID:Neopterin production, tryptophan degradation, and mental depression--what is the link? 1240 73

There is some evidence that major depression is accompanied by activation of the inflammatory-response system (IRS). It has been hypothesized that increased production of proinflammatory cytokines may play a role in the etiology of major depression. If increased production of proinflammatory cytokines is at all involved in the etiology of depression, one would expect antidepressive treatments to have negative immunoregulatory effects. This paper reviews the effects of antidepressants, such as tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), heterocyclic antidepressants (HCAs), serotonin-noradrenaline reuptake inhibitors (SNRIs), lithium, l-5-hydroxytroptophan (L-5-HTP), reversible inhibitors of MAO-A (RIMA) on the production of proinflammatory cytokines, e.g. interferon-gamma (IFNgamma), and negative immunoregulatory cytokines and agents, e.g. interleukin-10 (IL-10). In depressed patients, prolonged treatment with antidepressants and mood stabilizers normalizes signs of activation of the IRS, such as increased serum IL-6 and acute phase protein concentrations. In vitro, it has been shown that various types of antidepressive drugs, including TCAs (imipramine; clomipramine); SSRIs (citalopram, fluoxetine, sertraline); lithium; SNRIs (venlafaxine); HCAs (trazodone); RIMAs (moclobemide) and L-5-HTP significantly suppress the ratio of IFNgamma/IL-10 production by peripheral blood immunocytes. These antidepressant drugs appear to have a common effect on the IRS, i.e. in vitro they increase the production of IL-10 by peripheral blood leukocytes. Thus, the results suggest that antidepressants have negative immunoregulatory effects. It may be speculated that antidepressants exert some of their antidepressant effects through their negative immunoregulatory capacities. Copyright 2001 John Wiley & Sons, Ltd.
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PMID:The immunoregulatory effects of antidepressants. 1240 4

This Special Section of the International Journal of Neuropsychopharmacology presents papers which review the current status of the relationship between the inflammatory response system (IRS) and major 'endogenous' and 'organic' (due to a medical condition) depression. Studies published over the last 11 years and reviewed in this Special Section begin to test the necessary conditions which are needed to accept the hypothesis that an activation of the IRS is involved in the pathophysiology and aetiology of 'endogenous' and 'organic' depression. This hypothesis suggests that some types of 'endogenous' and 'organic' depression may be related to IRS activation, such as an increased production of pro-inflammatory cytokines, such as interleukin-1beta (IL-1beta), IL-6, tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN)-gamma. These cytokines are stress-sensitive, may cause depression, they have specific effects on brain systems involved in the pathogenesis of major depression, such as the serotonergic system and the hypothalamic-pituitary-adrenal (HPA) axis, and their production may be suppressed by antidepressants. Future research should examine whether anti-inflammatory drugs are effective in the treatment of depression and whether naturally occurring variants of the 'IRS' genes confer susceptibility to the development of the depressive phenotype through altered function of the respective gene products.
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PMID:Introduction to the special section. 1246 32

There is now evidence that major depression is associated with an up-regulation of the inflammatory response system (IRS). One of the major factors in this IRS activation is the hyperproduction of pro-inflammatory cytokines. Recently, a number of studies examined whether there is a causative role of these inflammatory mediators in the aetiology of major depression. Studies with animal models and cytokine immune therapy in humans suggest that pro-inflammatory cytokines induce depressive symptomatology. Moreover, these depressive symptoms can be effectively reversed by antidepressant treatment. Thus, it may be suggested that antidepressants suppress pro-inflammatory cytokine production and/or action, resulting in improvement of depressive symptoms. The influence of antidepressants on cytokine production has been examined in culture systems in vitro, and in animal models of depression - in which cytokine production is induced by endotoxin administration. Results suggest that antidepressants of several classes decrease the production of pro-inflammatory cytokines such as interferon-gamma and tumour necrosis factor-alpha, and increase that of interleukin-10, an anti-inflammatory cytokine. Further, the effect of antidepressive treatment on cytokine secretion and on plasma levels of cytokines in depressed patients has been studied. Unfortunately, different approaches to examine cytokine production and different techniques to measure cytokines in plasma are used in these studies. Despite this, current data indicate a normalization of cytokine plasma levels and cytokine production after antidepressant treatment. It is clear, however, that more research is warranted and we strongly argue the need for higher standardization in the methodology used to examine the cytokine network in depressed patients.
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PMID:Effects of antidepressants on the production of cytokines. 1246 38

The most important sequelae of splenectomy is immunity depression. This study, conducted in three phases, was aimed at confirming this clinical condition. Data from our phase 1 study clearly show that patients undergoing splenectomy for trauma are in a critical condition because of a latent immunodeficiency shown by skin tests (ST) and in vitro evaluation of the aspecific immune activity. Because the in vitro study of the unspecific immunity that we used seems to be more expensive and complicated than ST, the aim of the phase 2 study was to compare the efficacy and the limits of the two assays (ST versus in vitro study) in detecting the immunodeficiency status of the splenectomized patient. The aim of the phase 3 study was to ascertain whether postsplenectomy immunodeficiency could be a consequence of an altered equilibrium between the lymphocyte subpopulations T helper (Th)1/Th2, evaluated by serum dosage of interferon-gamma and interleukin-4.
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PMID:Postsplenectomy immunodepression and its implications: an underestimated problem. 1257 9

We have previously shown that the glucocorticoid dexamethasone prevents the cardiodepressant actions of interferon-gamma plus lipopolysaccharide in cardiac tissue in vitro. We now demonstrate that an N-terminal fragment of annexin-1 (Ac2-26, 1 microM), a putative mediator of glucocorticoid actions, completely protects against interferon-gamma+lipopolysaccharide-induced depression of the inotropic response to isoprenaline in rat isolated papillary muscles. However, Ac2-26 does not preserve resting contractile function. Fifteen hours incubation with interferon-gamma+lipopolysaccharide also markedly induced mRNA expression (by real time polymerase chain reaction, PCR) of both the nitric oxide synthase 2 (NOS2) isoform of nitric oxide synthase (by 6.7 +/- 1.7-fold, P < 0.01) and cyclo-oxygenase-2 (by 3.4 +/- 0.6-fold, P < 0.05) in cardiomyocytes. Pretreatment with Ac2-26 (1 microM) prevented the induction of cyclo-oxygenase-2 mRNA, but not NOS2 mRNA, whereas dexamethasone (1 microM) suppressed the expression of both NOS2 mRNA and cyclo-oxygenase-2 mRNA. Co-incubation of dexamethasone with an anti-annexin-1 antibody did not attenuate the suppression of NOS2 mRNA. Thus, Ac2-26 reproduces some, but not all, of the cardioprotective effects of glucocorticoids in vitro in the absence of neutrophils. These protective actions are independent of changes in NOS2 expression.
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PMID:Cardioprotective actions of an N-terminal fragment of annexin-1 in rat myocardium in vitro. 1258 12

In the present study, we examined the effect of prostaglandin (PG) E2 on interleukin (IL) -12 production in monocytes stimulated with a combination of lipopolysaccharide (LPS) from Actinobacillus actinomycetemcomitans and interferon-gamma (A. actinomycetemcomitans-LPS/IFN-gamma). Indomethacin, a cyclooxygenase inhibitor, enhanced IL-12 production, but inhibited PGE2 generation in A. actinomycetemcomitans-LPS/IFN-gamma-stimulated monocytes. Exogenous PGE2 inhibited IL-12 release in the cells. EP2, EP3 and EP4 receptor mRNA expression was detected in monocytes by reverse transcription-polymerase chain reaction. 11-deoxy-PGE1 (an EP2/EP4 agonist) inhibited IL-12 production in A. actinomycetemcomitans-LPS/IFN-gamma-challenged monocytes, whereas butaprost (an EP2 agonist) or ONO-AP-324 (an EP3 agonist) had no effect on IL-12 production. Dibutyryl cAMP, a cAMP analogue, and forskolin, an adenylate cyclase activator, mimicked depression of IL-12 production by PGE2. From these results, we suggest that PGE2 inhibits IL-12 production via EP4 receptors by cAMP-dependent pathways in A. actinomycetemcomitans-LPS/IFN-gamma-challenged monocytes.
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PMID:Prostaglandin E2 downregulates interleukin-12 production through EP4 receptors in human monocytes stimulated with lipopolysaccharide from Actinobacillus actinomycetemcomitans and interferon-gamma. 1275 65

Three variants of murine serotonin transporter (5-HTT) mRNA, which consist of a different exon-one (exon 1a, exon 1b or exon 1c) and the same exon-two to exon-five, were identified. The promoter region for each exon 1 (p1a, p1b and p1c, respectively), ligated to pGL-3 enhancer vector, had activities significantly higher than the empty vector in all cell lines tested except p1c in PC-12, whereas the activity of p1c was significantly lower than the others. Effects of the treatment of dibutyryl-cyclic AMP, human interferon-alpha or mouse interferon-gamma have different profiles among COS-7, PC-12, C6 glioma and immortalized rat serotonergic raphe neurons, RN46A. These three promoter regions may play a role in the transcription of the 5-HTT and could offer a model of the regulation of 5-HTT production in humans and further the pathogenesis of depression.
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PMID:Novel variants of murine serotonin transporter mRNA and the promoter activity of its upstream site. 1275 93

The major purpose of this study was to quantify hypergravity-induced changes in erythrocyte and thrombocyte characteristics, spontaneous and mitogen-induced lymphoblastogenesis, and capacity of splenocytes to secrete immunoregulatory cytokines. C57BL/6 mice were subjected to chronic 1, 2, and 3 G; subsets were euthanized after 1, 4, 7, 10, and 21 days of centrifugation. Erythrocyte counts, hematocrit, and hemoglobin were significantly reduced by day 21 in both centrifuged groups. Hemoglobin concentration and volume per red blood cell were generally low, but an early, transient spike above normal was noted in thrombocyte counts in the 3-G group. Fluctuations above and below normal in blood and spleen cell spontaneous blastogenesis were dependent on the length of centrifugation time and not on the level of gravity. Depression in splenocyte responses to phytohemagglutinin and lipopolysaccharide due to gravity were noted when the data were expressed as stimulation indexes. Cytokine production by spleen cells was primarily affected during the first week of centrifugation: IL-2, IL-4, and tumor necrosis factor-alpha increased, whereas interferon-gamma decreased. These findings, although not identical to those reported for spaceflight, indicate that altered gravity can influence both hematological and functional variables that may translate into serious health consequences during extended missions.
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PMID:Hypergravity-induced immunomodulation in a rodent model: hematological and lymphocyte function analyses. 1497 9


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