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)

Recent studies suggest beneficial effects of castration before soft tissue trauma and hemorrhagic shock on splenocyte immune functions. Nonetheless, it remains unknown whether this effect of testosterone depletion is limited to splenocytes or is a generalized effect on immune function. The present study was therefore carried out to determine whether androgen depletion before trauma-hemorrhage also has salutary effects on splenic and peritoneal macrophage as well as on Kupffer cell function, as indicated by interleukin (IL)-1 and IL-6 release. Male C3H/HeN mice were castrated or sham-castrated 2 wk before the experiment and were killed at 24 h after trauma-hemorrhage and resuscitation. Significant depression of macrophage IL-1 and IL-6 release was only observed in sham-castrated mice, as opposed to normal levels of cytokine release from castrated animals after trauma-hemorrhage. In addition, only sham-castrated animals showed significantly increased levels of IL-6 release from Kupffer cells, which is believed to contribute to the systemic inflammatory response to trauma-hemorrhage. These observations suggest that the beneficial effects of androgen depletion before trauma-hemorrhage are not limited to splenocyte immune functions but are more global in nature. These results in surgically castrated animals suggest that androgen-blocking agents should be studied for their potential to reverse the immunodepression associated with trauma-hemorrhage.
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PMID:Male sex steroids are responsible for depressing macrophage immune function after trauma-hemorrhage. 935 78

There is now some evidence that major depression is accompanied by an immune response with an increased production of pro-inflammatory cytokines, such as interleukin 1(IL-1), IL-6 and interferon gamma (IFN-gamma). The aims of the present study were to examine serum IL-6, IL-1 receptor antagonist (IL-1Ra), IL-6R, Clara cell protein (CC16) and the soluble CD8 (sCD8) molecule in chronic, treatment resistant depression (TRD) both before and after subchronic treatment with antidepressants. Serum IL-6 and IL-1Ra were significantly higher in subjects with major depression and TRD than in normal controls. Subchronic treatment with antidepressants had no significant effects on serum IL-6, IL-1Ra, CC16 or sCD8, but reduced serum sIL-6R levels significantly. There were significant and positive correlations between serum IL-6, on the one hand, and sIL-6R, IL-1Ra, sCD8, number of peripheral blood leukocytes, neutrophils, CD2(+)T and CD19(+)B cells (all positive) and serum zinc (negative), on the other. These results suggest that: (1) major depression and TRD are accompanied by an activation of the monocytic arm of cell-mediated immunity; (2) the latter may be related to the immune an acute phase response in major depression; and (3) the above disorders may persist despite successful antidepressive treatment.
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PMID:Increased serum IL-6 and IL-1 receptor antagonist concentrations in major depression and treatment resistant depression. 936 46

Extensive evidence exists associating depression with changes in the immune system. The present study evaluates the levels of complement components C3 and C4, C-reactive proteins, and IL-6 in patients who met DSM-III-R diagnostic criteria for major depressive disorder, as well as controls. Whereas no significant differences between the mean levels of C3 could be detected between depressed patients and controls, the levels of C4, IL-6 (where detected), and C-reactive protein were significantly raised in the group with a depressive disorder. Our study suggests an interaction between psychological state and immune systems operative in host defenses.
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PMID:Acute phase proteins in major depression. 939 69

The immediate responses to aerosolized staphylococcal enterotoxin B (SEB) in respiratory toxic shock were studied in the circulation of rhesus monkeys with low antibody levels following immunization with SEB toxoid-containing microspheres. Both the surviving and dying monkeys had toxic shock syndrome 4-48 h after SEB challenge and all showed three distinctive patterns of immediate responses. The first pattern, characterized by the responses of all T cells, HLA-DRlo cells, monocytes, IL-2R+ cells, IFN-gamma, and augmented lymphocyte mitotic responses to lipopolysaccharide (LPS) and SEB in culture, was a rapid increase at 20 min followed by a quick decrease at 90 min to approximately the original levels. The second pattern, which included responses of HLA-DRhi cells, NK cells, adrenocorticotropic hormone (ACTH) and cortisol, was characterized by a moderate decrease at 20 min and a further decrease at 90 min. The third pattern, the inverse of the second pattern, including responses of polymorphonuclear leukocytes (PMN), concanavalin A (Con A) mitogenesis, IL-6 and IL-2, was a moderate increase at 20 min and a further increase at 90 min. Between the surviving and dying monkeys, the responses of T cells, HLA-DRhi cells, PMN and cortisol did not differ significantly, suggesting that they are the basic causes that initiated toxic shock. However, significant differences were seen in the responses of HLA-DRlo cells, monocytes, IL-2R+ cells and lymphocyte mitogenesis in culture at 20 min, and of Con A mitogenesis, NK cells, IL-2, IL-6 and ACTH at 90 min. These different responses are apparently the exacerbating causes of death of the monkeys. All together, the immediate responses seem to be caused by the combined effects of SEB superantigenicity, activation of NK cells and non-lymphoid cells, and depression of the neuroimmune defense system.
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PMID:Immediate responses of leukocytes, cytokines and glucocorticoid hormones in the blood circulation of monkeys following challenge with aerosolized staphylococcal enterotoxin B. 946 10

Traditionally, both stress and depression have been associated with impaired immune function and increased susceptibility to infectious and neoplastic disease. However over the last number of years a large body of evidence suggests that major depression is associated with signs of immunological activation. Moreover it has been suggested that cytokine hypersecretion may be involved in the aetiology of depressive disorders. The present article reviews the evidence from both clinical and experimental studies which implicates immunological activation and particularly hypersecretion of cytokines in the onset and maintenance of depressive illness. Both clinical and experimental studies indicate that stress and depression are associated with increased circulating concentrations of cytokines such as IL-1beta, IL-6 and gamma-IFN and positive acute phase proteins, and hyperactivity of the HPA-axis. In addition, it has been reported that immunological activation induces "stress-like" behavioural and neurochemical changes in laboratory animals. Although for many years it has been suggested that stress acts a predisposing factor to depressive illness, the precise mechanisms by which stress-induced depressive symptoms occur are not fully understood. Nevertheless, behavioural changes due to stress have often been explained in terms of changes in neurotransmitter function in the brain. In the present article increased cytokine secretion is implicated as a mechanism whereby stress can induce depression.
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PMID:Depression, stress and immunological activation: the role of cytokines in depressive disorders. 947 19

The fetal liver is the main hematopoietic organ during intrauterine life. Morphometrical studies were performed on liver sections to detect changes occurring with intrauterine growth retardation and preeclampsia. Compared with the controls (n = 10), fetuses from preeclamptic mothers showed a severe reduction of erythroid cells by 60% on average (n = 18). Closer examination revealed that the erythroid cells at early stages of differentiation were more affected (80% reduction) than at later stages (55%). Seven out of 18 fetuses from preeclamptic mothers did not show growth retardation but exhibited severely reduced hepatic erythropoiesis. We suggest that the prime factor for impaired red blood cell production is preeclampsia itself rather than intrauterine growth retardation. Regulation of erythropoiesis in utero might depend on the interaction of many hematopoietic growth factors, and preeclampsia might alter the balance. To test this notion, we quantitated erythropoietin in fetal blood and various cytokines in the amniotic fluid. An elevation of erythropoietin and interleukin (IL)-3 levels was seen in babies born under the conditions of preeclampsia, whereas the concentrations of granulocyte/macrophage-colony-stimulating factor (CSF), granulocyte-CSF, and IL-1 beta were reduced, and the levels of IL-6 and IL-8 remained constant. With preeclampsia, a discrepancy between elevation of erythrocyte numbers in peripheral blood and depression of hematopoiesis at the main production site, the fetal liver, is seen. Concomitantly, there is elevation of some but reduction of other hematopoietic cytokines. We envision that during the course of preeclampsia quantitation of hematopoietic growth factors might allow to predict the deterioration of in utero life conditions.
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PMID:Fetuses from preeclamptic mothers show reduced hepatic erythropoiesis. 950 73

Murine fibroblast NIH3T3 cells engineered to secrete interleukin-6 (NIH3T3-IL-6) were implanted intraperitoneally into mice and observed for their hematopoietic effects with or without 5-fluorouracil (5-FU) administration. In normal mice, the platelet and neutrophil counts in peripheral blood increased significantly after implantation of NIH3T3-IL-6 cells, but the total white blood cell numbers showed no obvious elevation. The granulocyte-macrophage colony-forming unit (CFU-GM) and megakaryocyte colony-forming unit (CFU-MK) numbers formed by stem cells in bone marrow and spleen were also found to be significantly increased after implantation of NIH3T3-IL-6 cells when compared with those in mice after implantation of NIH3T3 cells transduced with neomycin gene (NIH3T3-Neo). To observe the protective effects of NIH3T3-IL-6 cells on hematopoietic depression in chemotherapy-treated mice, the mice were preinjected with 5-FU at a dosage of 150 mg/kg before implantation of NIH3T3-IL-6 cells. The platelet and neutrophil counts showed accelerated recovery after implantation of NIH3T3-IL-6 cells. The numbers of CFU-GM and CFU-MK in bone marrow and spleen were also found to be markedly increased in hematopoietic-depressed mice when compared with those in mice implanted with NIH3T3-Neo cells. These data suggest that fibroblast-mediated IL-6 gene therapy, which can augment hematopoiesis in mice with or without chemotherapy, will be of great help in the recovery from hematopoietic depression after chemotherapy.
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PMID:Augmentation of hematopoiesis by fibroblast-mediated interleukin-6 gene therapy in mice with chemotherapy. 956 24

The effects of glucan-based immunomodulators curdlan sulfate (CRDS) and lentinan on cytokine production stimulated by lipopolysaccharide (LPS) in bacillus Calmette-Guerin (BCG)-primed mice were investigated. Pretreatment with CRDS or lentinan before LPS administration induced a striking inhibition of up to 89% of circulating tumor necrosis factor-alpha (TNF), a moderate reduction of 25% of interleukin (IL)-1beta, no significant differences in IL-6 or IL-10 levels, and a marked depression of chemiluminescence activity. Animals receiving CRDS prior to infection with alpha-hemolysin positive Escherichia coli inhibited measurable TNF production by 63%. The ability of CRDS and lentinan to significantly reduce the TNF production in vivo indicates the potential of glucans in possible therapeutic strategies that are based on down-regulation of TNF.
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PMID:Down-regulation of tumor necrosis factor-alpha, moderate reduction of interleukin-1beta, but not interleukin-6 or interleukin-10, by glucan immunomodulators curdlan sulfate and lentinan. 963 39

Sepsis remains a major cause of mortality in surgical intensive care units. Patients who survive the initial shock phase but die weeks later from multiple organ dysfunction still are a challenge to basic and clinical research. We addressed whether fulminant sepsis results in rapid changes (24 h) in the cellular capacity to produce cytokines in whole blood of septic patients on further stimulation after the initial systemic inflammatory response. Interleukin (IL)-6 plasma concentrations from 279 pg/mL to 5979 pg/mL confirmed the presence of a systemic inflammatory response. Anti-inflammatory IL-10 concentrations up to 275 pg/mL were detected, but there was no biologically active tumor necrosis factor-alpha (TNFalpha) detectable (by bioassay) at the time of investigation. On stimulation with Escherichia coli ex vivo, pro-inflammatory TNFalpha (130 pg/mL), IL-6 (4061 pg/mL), and anti-inflammatory IL-10 (711 pg/mL) production were markedly depressed in all patients compared with controls (2339 pg/mL, 50,319 pg/mL, and 9654 pg/mL, respectively). Septic shock resulted in early depression of the capacity for pro- and anti-inflammatory cytokine production. Monitoring of this effect, including its relationship to outcome, may offer a target variable for therapeutic efforts to maintain or restore adequate immune reactions to improve survival.
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PMID:Depression of tumor necrosis factor-alpha, interleukin-6, and interleukin-10 production: a reaction to the initial systemic hyperactivation in septic shock. 965 91

Two lineages of B cells, designated B1 and B2 cells, have been identified based upon their origins, anatomical distribution, cell surface markers, antibody repertoire and self-replenishing potential. B1 cells are maintained by self-renewal of cells resident in the peritoneal cavity (PerC) and they utilize a limited repertoire of germline V-region genes, mostly directed against ubiquitous bacterial antigens such as phosphoryl choline (PC). B2 cells are replenished from bone marrow precursors and use a larger repertoire of immunoglobulin V-region genes. Whereas most immunoglobulin A (IgA) plasma cells in the intestine derive from B2 lineage precursors in the Peyer's patch, a subpopulation of Per C-derived B1 cells populate the intestinal lamina propria where they mature into IgA plasma cells. In previous in vivo studies we have shown that whereas IgA+ B2 cells are interleukin (IL)-6 dependent, B1 cells are IL-6 independent. In view of the in vitro evidence that IL-5 is also involved in IgA expression, in the studies reported here we have used IL-5-deficient mice to evaluate the role of IL-5 in vivo in IgA expression in the gut. The results demonstrate that although total IgA cell numbers are only marginally depressed in IL-5-deficient mice, there is a marked selective depletion of IgA+ cells of the B1 lineage in the gut and a corresponding depression in the capacity of these mice to mount an intestinal response to a B1 antigen (PC) but not to a B2 antigen (oralbumin; OVA), reflecting intact B2-derived IgA cell function but a defect in the B1 cell contribution to IgA responses in IL-5 deficient mice. Collectively these data demonstrate differential cytokine regulation of subsets of IgA+ cells in the gut in that IgA+ cells of the B2 lineage are IL-6 dependent but IL-5 independent, but B1-derived IgA+ cells are IL-5 dependent and IL-6 independent.
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PMID:Intestinal IgA plasma cells of the B1 lineage are IL-5 dependent. 974 39


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