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

NF-kappaB activation, and elevated concentrations of macrophage migration inhibitory factor (MIF), tumor necrosis factor-alpha (TNF-alpha), interleukin-1(IL-1), IL-6, free radicals, inducible nitric oxide (iNO), and stress hyperglycemia occurs in sepsis and this leads to systemic inflammatory response and myocardial depression seen in sepsis and septic shock. Conversely, insulin suppresses production of MIF, TNF-alpha, IL-1, IL-6, and free radicals, enhances endothelial NO generation, and enhances the production of anti-inflammatory cytokines IL-4, and IL-10, corrects stress hyperglycemia and improves myocardial function. This supports my earlier proposal that insulin (with or without glucose and potassium) therapy to maintain euglycemia suppresses the inflammatory response, improves myocardial function, and thus, is of benefit in acute myocardial infarction, sepsis andseptic shock.
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PMID:Insulin in sepsis and septic shock. 1462 Oct 41

A body of evidence indicates that the therapeutic activity of antidepressants is connected with their modulatory effect on the inflammatory response system and cell-mediated immunity. The present study was carried out to examine the effects of antidepressant agents, such as imipramne, venlafaxine, l-5-hydroxytryptophan, fluoxetine and a combination of l-5-hydroxytryptophan and fluoxetine, on the production of the pleotrophic cytokines TNF-alpha and IL-6. Diluted whole blood from fluoxetine-treated patients with treatment-resistant depression (TRD) (mean age: 50.6+/-3.9 years), age-matched healthy controls (mean age: 51.6+/-1.7 years) and younger healthy volunteers (mean age: 35.4+/-1.7 years) was stimulated with phytohemagglutinin (PHA) and lipopolysaccharide (LPS) for 48 h with or without incubation with the antidepressants at 10(-6) and 10(-5) M. The major findings of this study are: (1). imipramine and venlafaxine (at the higher concentration), 5-HTP (at lower and higher concentrations) and a combination of 5-HTP and fluoxetine (both at the lower concentration) increased the production of IL-6; (2). all drugs used did not affect TNF-alpha production. IL-6 production was significantly higher in depressed patients than in age-matched volunteers, whereas TNF-alpha production was significantly higher in older volunteers than in younger ones. We speculate that the therapeutic activity of these antidepressants is at least partly connected with their effect on the cytokine network and IL-6 production.
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PMID:Stimulatory effect of antidepressants on the production of IL-6. 1499 10

Twenty-five barrier-maintained cats had been experimentally infected for 9.5 months with an FIV strain of low pathogenicity, FIV Zurich 2. Animals were clinically healthy and did not exhibit any haematological changes. FIV proviral DNA was demonstrated in peripheral blood lymphocytes of all cats and in monocytes of most animals, identifying FIV Zurich 2 as a both lympho- and monocytotropic strain. Monocytes were isolated from FIV-infected cats as well as from age-matched uninfected control cats, short-term cultured and examined for cytokine (IL-1beta, IL-6, IL-10, IL-12 p40 and TNF-alpha) transcription by real-time PCR. Constitutive transcription of cytokines in monocytes from FIV-infected cats was restricted to IL-1beta and, in the majority of samples, TNF-alpha. For all cytokines, transcription levels were significantly lower in FIV-infected cats than in control cats. Transcription was often least intense in those samples where FIV infection of the monocyte fraction was not demonstrated. Results show that infection of cats with an FIV strain of low pathogenicity was associated with depression of constitutive cytokine transcription in monocytes even if clinical and haematological changes were not observed.
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PMID:Reduced constitutive cytokine transcription in isolated monocytes of clinically healthy cats, infected with an FIV strain of low pathogenicity. 1501 Feb 30

Drug addiction influences many physiological functions including reactions of the immune system. The higher occurence of infectious and other diseases in drug addicts has been explained by the depression of immunity due to the harmful effects of the drug. To test this assumption, we tested the proliferative responsiveness and cytokine production of PBL from a group of heroin addicts (N = 19), patients maintained on methadone (N = 15) and healthy controls (N=15). The results show that Con A-induced proliferation of PBL from heroin addicts was even enhanced in comparison with PBL from the control group. Similarly, production of IL-2, IL-10 and IFNgamma was higher in the group of heroin addicts than in healthy controls. The enhanced proliferation of PBL or the increased production of cytokines observed in heroin addicts was partially or completely normalized in the group of patients maintained on methadone. A significantly higher production of IL-6 was found in both unstimulated and stimulated PBL from heroin addicts and patients maintained on methadone, when compared with PBL from healthy controls. The results thus showed enhanced proliferative activity and increased production of various cytokines in heroin addicts and partial or complete adjustment of these alterations in patients maintained on methadone.
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PMID:The alterations of immunological reactivity in heroin addicts and their normalization in patients maintained on methadone. 1505 40

The purpose of the present study was to investigate the relation between adipose tissue polyunsaturated fatty acids, an index of long-term or habitual fatty acid dietary intake and depression. The sample consisted of 150 elderly males from the island of Crete. The subjects were survivors of the Greek Seven Countries Study group. The mean age was 84 years. The number of subjects with complete data on all variables studied was 63. Subjects were examined by the Preventive Medicine and Nutrition Clinic of the University of Crete. Depression was assessed through the use of the short form of the Geriatric Depression Scale (GDS-15). Depression correlated negatively with adipose tissue alpha-linolenic acid (C18:3n-3). Depressed subjects had significantly reduced (-10.5%) adipose tissue C18:3n-3 levels than non-depressed subjects. The observed negative relation between adipose tissue C18:3n-3 and depression, in the present study, appears to indicate increasing long-term dietary C18:3n-3 intakes with decreasing depression. This agrees with findings of other studies indicating an inverse relation between depression and consumption of fish and n-3 polyunsaturated fatty acids. This is the first literature report of a relation between adipose tissue C18:3n-3 and depression. Furthermore, this is the first report of a relation between adipose PUFA and depression in an elderly sample. Depression has been reported to be associated with elevated cytokines, such as, IL-1, IL-2, IL-6, INF-gamma and INF-alpha. Fish oil and omega-3 fatty acids, on the other hand, have been reported to inhibit cytokine production. The observed negative relation between adipose C18:3n-3 and depression, therefore, may stem from the inhibiting effect of C18:3n-3 or its long-chain metabolites on cytokine synthesis.
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PMID:Depression and adipose polyunsaturated fatty acids in the survivors of the Seven Countries Study population of Crete. 1512 Jul 12

Scopoletin (1-50 microg/ml) inhibited the release of PGE2, TNF-alpha, IL-1beta and IL-6 and suppressed the expression of COX-2 in a concentration-dependent manner. These results suggest that scopoletin might suppress the production of such pro-inflammatory cytokines and exert inhibitory activity on LPS-induced PGE2 production through the depression of COX-2 expression.
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PMID:Scopoletin suppresses pro-inflammatory cytokines and PGE2 from LPS-stimulated cell line, RAW 264.7 cells. 1515 82

The prostaglandin (PG) E2 receptor subtype EP4 has been found to mediate regulation of inflammatory cytokines in macrophages and neutrophils in vitro by PGE2. Yet the role of EP4 receptors in endotoxin shock in vivo and whether EP4 activation is a beneficial treatment are not clear. We tested the effect of an EP4 agonist on hemodynamic changes and production of inflammatory cytokines in a rat endotoxin-induced shock model. In rats under pentobarbital anesthesia, lipopolysaccharide (LPS) was injected, and an EP4 agonist (ONO-AE1-329) was administered at one of three concentrations (1, 3, or 10 microg/kg bolus i.v. hourly). Mean arterial pressure (MAP) was monitored throughout the experiment, and pressor responses to norepinephrine were determined 6 h after LPS injection. Serum tumor necrosis factor (TNF)-alpha and serum interleukin (IL)-6 were measured 1 h and 6 h after LPS injection. Venous nitrosyl hemoglobin (NO-Hb) concentration was measured by electron spin resonance. Expression of mRNAs encoding TNF-alpha and inducible nitric oxide synthase (iNOS) in the left ventricle and descending aorta was determined with a real-time reverse transcription polymerase chain reaction. As time progressed, LPS significantly depressed MAP and decreased reactivity to norepinephrine. Infusion of higher doses of the EP4 agonist at 3 and 10 microg/kg/h attenuated LPS-induced hypotension and hyporeactivity to norepinephrine. LPS significantly increased serum concentrations of TNF-alpha and IL-6, and higher doses of EP4 agonist significantly attenuated these increases. Left ventricular and aortic expression of mRNAs encoding TNF-alpha and iNOS was increased by LPS; again, EP4 agonist at higher doses attenuated the increases. LPS-induced production of inflammatory mediators and cardiovascular depression were attenuated by EP4 agonist administration in an in vivo endotoxin shock model. Anti-inflammatory effects thus would be involved in protection by EP4 agonist against cardiovascular depression in endotoxin shock.
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PMID:A prostaglandin E2 receptor subtype EP4 agonist attenuates cardiovascular depression in endotoxin shock by inhibiting inflammatory cytokines and nitric oxide production. 1520 6

In the context of a large-scale molecular epidemiology study, the possible immunomodulatory effects of mineral fibres, in workers occupationally exposed to asbestos, rockwool and glass fibres, were examined. In each plant, 61, 98 and 80 exposed workers and 21, 43 or 36 control clerical subjects, respectively, were recruited. In the case of the asbestos-exposed subjects, an additional town-control group of 49 people was included. Evidence of pulmonary fibrosis was found in 42% of the asbestos-exposed workers, while evidence of pleural fibrosis was found in 24%. The asbestos-exposed cohort had significantly decreased forced vital capacity of lungs as well as forced expiratory volume per first second. Our findings indicate that exposure to all three types of fibres examined modulates to different degrees the immune response. Suppression of T-cell immunity and to a lesser extent, B-cell immunity was found in the case of workers from a former asbestos cement plant, while stimulation of T-cell response was observed in rockwool workers, and stimulation of T- and B-cell response was seen in glass fibre workers. Depression of the percentage of lymphocyte subpopulation of CD 16+56 (natural killer cells) in peripheral blood was found in glass fibre workers. Statistical analysis showed increased levels of proinflammatory cytokines (IL-6 asbestos; IL-8 all three fibres), expression of adhesion molecule L-selectin on granulocytes and monocytes (asbestos), levels of soluble adhesion molecules (SAMs) in sera (ICAM-1 all three fibres; E-selectin glass fibres), increased levels of immunoglobulin E (asbestos and rockwool) and elevated expression of activation markers on eosinophils (CD66b asbestos, glass fibres; CD69 asbestos). Significant correlations were observed between lymphocyte proliferation and markers of DNA damage and repair. Increased levels of proinflammatory cytokines, SAMs, immunoglobulin E and elevated expression of activation markers on eosinophils was found in people with symptoms of hypersensitivity and an elevated inflammatory status.
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PMID:Immunomodulatory effects of mineral fibres in occupationally exposed workers. 1528 38

Cytokines are involved in ischemic tolerance, including that triggered by spreading depression (SD), yet their roles in neuroprotection remain incompletely defined. The latter may stem from the pleiotropic nature of these signaling molecules whose complexities for interaction might be better deciphered through simultaneous measurement of multiple targeted proteins. Accordingly, the authors used microsphere-based flow cytometric immunoassays and hippocampal organotypic cultures (HOTCs) to characterize the magnitude, time course, and diversity of cytokine (interleukin [IL] 1alpha, IL-1beta, IL-2, IL-4, IL-6, IL-10, granulocyte-macrophage colony-stimulating factor [GM-CSF], interferon-gamma [IFN-gamma], and tumor necrosis factor-alpha [TNF-alpha]) response to SD. GM-CSF was not detected in HOTCs or media. However, SD triggered a significant, generalized increase in seven cytokines evident in HOTCs 6 hours later, with the remaining cytokine, IL-1beta, becoming significantly different at 1 and 3 days. Additionally, these changes extended to include surrounding media for IL-6 and TNF-alpha by 1 and 3 days. This increase was localized to microglia via immunostaining for IL-1alpha, IL-1beta, and interferon-y. IL-10, although significantly more abundant in HOTCs 6 hours after SD, was significantly less abundant in surrounding media at that time and at 1 day. Finally, the generalized early increase in tissue cytokines later settled to a pattern at 3 days of recovery centering on changes in IL-1alpha, IL-1beta, and TNF-alpha, cytokines capable of modulating ischemic injury.
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PMID:Multiplexed cytokine protein expression profiles from spreading depression in hippocampal organotypic cultures. 1536 13

The myocardium generates inflammatory mediators during ischemia-reperfusion (I/R), and these mediators contribute to cardiac functional depression and apoptosis. The great majority of these data have been derived from male animals and humans. Sex has a profound effect over many inflammatory responses; however, it is unknown whether sex affects the cardiac inflammatory response to acute myocardial I/R. We hypothesized the existence of inherent sex differences in myocardial function, expression of inflammatory cytokines, and activation of the p38 mitogen-activated protein kinase (MAPK) signaling pathway after I/R. Isolated rat hearts from age-matched adult males and females were perfused (Langendorff), and myocardial contractile function was continuously recorded. After I/R, myocardium was assessed for expression of TNF-alpha, IL-1beta, and IL-6 (RT-PCR, ELISA); IL-1alpha and IL-10 mRNA (RT-PCR); and activation of p38 MAPK (Western blot). All indexes of postischemic myocardial function [left ventricular developed pressure, left ventricular end-diastolic pressure, and maximal positive (+dP/dt) and negative (-dP/dt) values of the first derivative of pressure] were significantly improved in females compared with males. Compared with males, females had decreased myocardial TNF-alpha, IL-1beta, and IL-6 (mRNA, protein) and decreased activation of p38 MAPK pathway. These data demonstrate that hearts from age-matched adult females are relatively protected against I/R injury, possibly due to a diminished inflammatory response.
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PMID:Sex differences in the myocardial inflammatory response to ischemia-reperfusion injury. 1536 93


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