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)

Various effects of glucocorticosteroids on the avian immune system were examined in chickens treated intramuscularly with 0.1 to 2.5 mg dexamethasone or prednisolone. Kinetic changes in body weight gain, percentages of lymphocyte subpopulations, and T-cell functions were examined following treatment with dexamethasone or prednisolone every other day. Chickens treated with dexamethasone or prednisolone showed a decrease in body-weight gain compared with age-matched, untreated chickens. In general, the total number of splenic lymphocytes of chickens treated with the two drugs was significantly lower than in controls in a dose-dependent manner. Flow cytometric analysis of splenic lymphocyte subpopulations revealed that the percentages of lymphocytes expressing CD8, gamma delta T-cell receptor, Ia, or IgM antigens and natural killer cells were lower in dexamethasone-treated chickens than in the controls, whereas the percentages of T lymphocytes bearing CD3, CD4, or alpha beta TCR antigens were higher. Furthermore, splenic T cells obtained from dexamethasone-treated chickens showed a significant depression in concanavalin A-induced lymphoproliferation and interleukin 2 and gamma-interferon production. The results characterize a variety of immunosuppressive effects of glucocorticoids on the avian immune system.
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PMID:Effects of corticosteroids on lymphocyte subpopulations and lymphokine secretion in chickens. 141 90

Hemorrhagic shock causes a severe suppression of cellular immunity and an increased susceptibility to sepsis that may be due to increased release of prostaglandin E2 by macrophages. Since chloroquine inhibits the secretion of prostaglandin E2 by macrophages in vitro, the effects of chloroquine administration in vivo following hemorrhagic shock on macrophage prostaglandin E2 secretion and on depressed cellular immunity were examined. Inbred C3H/HeN male mice, aged 6 to 8 weeks, were bled to a mean blood pressure of 35 mm Hg, which was maintained for 60 minutes, and adequately, resuscitated. Mice then received intramuscular injections of either saline (vehicle) or chloroquine (10 mg/kg of body weight). Prostaglandin E2 in macrophage supernatants (radioimmunoassay) concanavalin A-dependent splenocyte proliferation, and interleukin 2 in splenocyte supernatants (CTLL 20 interleukin 2-dependent proliferation) were determined 2 or 24 hours later. Hemorrhage caused a significant decrease of splenocyte proliferation (47%) and interleukin 2 release (49%) at 24 hours, while prostaglandin E2 secretion from macrophages was elevated at 2 hours. Chloroquine treatment attenuated depression of splenocyte functions and reduced prostaglandin E2 release. Furthermore, chloroquine treatment decreased the mortality of septic mice after hemorrhage to levels comparable with those of sham-operated mice. Thus, chloroquine may be a useful adjunct in the clinical setting for the treatment of shock-induced immunodepression and increased susceptibility to sepsis following hemorrhage.
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PMID:Chloroquine attenuates hemorrhagic shock-induced immunosuppression and decreases susceptibility to sepsis. 173 52

The effect of salazosulfapyridine (SASP) on the antibody response of murine spleen cells in vitro was studied. SASP inhibited the response to sheep red blood cells (SRBC), a T-cell-dependent (TD) antigen, dose-dependently and was most effective at a dose of 2 x 10(-4) M without cell toxicity. No remarkable inhibition was seen with the main metabolites of SASP, 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP). SASP failed to inhibit antibody production to T-cell-independent antigens such as dinitrophenyl-Ficoll or trinitrophenyl (TNP)-lipopolysaccharides, although the response to TNP-keyhole limpet hemocyanin, another TD antigen like SRBC, was inhibited. Further, this drug did not show any depression of the anti-SRBC plaque-forming cell (PFC) response in spleen cells treated with anti-Thy1.2 antibody plus complement. The inhibition of anti-SRBC PFC response by SASP was accompanied by a reduction of interleukin 2 (IL-2) secretion. Our results suggest that SASP may act on T cell populations and may inhibit the T-cell-dependent antibody response partly through a depression of IL-2 production. The active compound appears to be SASP itself, rather than its metabolites.
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PMID:The effect of salazosulfapyridine on the in vitro antibody production in murine spleen cells. 196 49

Dysfunctional monocytes (M phi), exerting their inhibitory functions via prostaglandin E2 (PGE2), have been implicated in the depression of immune responses following major surgical, accidental, and burn trauma. A randomized prospective study of the PG-synthetase inhibitor indomethacin (Indo) was performed in 43 patients undergoing major surgical procedures, to evaluate its efficacy in correcting postoperative abnormalities of the cell-mediated immune system (CMI) and preventing infectious morbidity and mortality. Patients, following gastrectomy (GX) or reconstruction of the abdominal aorta (AG), in the treated group (PIndo), received 100 mg IV of Indo 6 hours postoperatively and 3 x 50 mg IV Indo over 24 hours on postoperative days (D) 1,2,3,4. The rate of infectious complications was recorded. Parameters of CMI evaluated preoperatively (D0) and on D1,D3,D5,D7 were: Delayed type hypersensitivity (DTH) response to recall antigens, mitogen-induced lymphocyte proliferation (LP), interleukin 2 (IL-2) synthesis, and phenotyping of mononuclear blood leukocytes (PBMC's) with the monoclonal antibodies for CD3+, CD4+, IL-2 receptor (IL-2R)+ and LeuM3+ receptor sites. In contrast to the group of untreated patients (Pc), PIndo did not show a depression of their preoperative DTH responses, and they also showed a lower rate of early opportunistic infections. The in vitro test of CMI revealed that there was a higher LP capacity in PBMC's of PIndo (p less than 0.05); the postoperative profile of IL-2 synthesis was not statistically different between the groups. Indomethacin administration resulted in a considerable alleviation of postoperative monocytosis (p less than 0.05) and in a protective effect on lymphocyte receptor expression of CD3+, CD4+, and IL-2R+ cells. From these data it is concluded that in vivo cyclooxygenase inhibition may be useful to prevent impairment of CMI, a crucial predisposing factor of the high susceptibility to postoperative infection.
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PMID:Immunoprotective effects of cyclooxygenase inhibition in patients with major surgical trauma. 210 39

Of 467 cat serums tested for antibody to feline immunodeficiency virus (FIV) 120 (26%) were positive. The average age of positive cats was 7.5 years (range 1 to 16 years), and 67% were male. Of 110 serums collected in 1980, 27 (24.5%) were positive. A wide variety of clinical signs including oral cavity disease, anorexia, weight loss, lethargy, depression, fever, respiratory and urinary tract disease, conjunctivitis, abscesses, anaemia and lymphadenopathy were observed in the cats with serum antibody. There was often a history of chronic disease or recurrence of particular or various clinical signs in these cats. FIV was isolated from 4 of 8 FIV antibody positive cats by cocultivation of patient lymphocytes with donor lymphocytes in the presence of interleukin 2.
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PMID:Feline immunodeficiency virus: prevalence, disease associations and isolation. 216 64

The activation of T lymphocytes by an antigenic challenge requires that the CD3 T cell receptor alpha/beta (TcR) is bound to an appropriate ligand, i.e. major histocompatibility complex antigen, on an antigen-presenting cell. In addition, numerous studies suggest that the accessory molecules CD4 and CD8 participate in the recognition process, and may have inhibitory as well as augmenting effects depending on the ways in which they participate. In the present study we attempt to define the conditions by which CD8 exerts enhancing and inhibitory effects on resting CD8+ T cell activation, and which parameters of activation are regulated through participation of CD8/CD4. We find that experimental procedures leading to TcR-CD8 aggregation induce T cell activation whereas experimental procedures preventing TcR-CD8 aggregation inhibit T cell activation. CD8/CD4-induced variations in the extent of T cell activation are apparent as variations in interleukin 2 (IL 2)-dependent growth and in the number of blastoid cells bearing IL 2 receptors. Inhibition of CD8+ T cell activation is successful only if the majority, if not all CD8 molecules are occupied by soluble antibody. This latter finding argues against the suggestion of other groups that CD8 may be a receptor for negative signaling. Rather, the results support the alternative notion that a basal level of TcR-CD8 aggregation, existing in the resting state or induced by TcR-ligand interaction, is an essential prerequisite for CD8+ T cell activation. Enhancement or depression of this basal level of aggregation causes facilitation or inhibition, respectively, of activation. This may be a mechanism for the regulation of IL 2-dependent clonal expansion of T cells in immune responses.
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PMID:Immunoregulation through CD8 (Ly-2): state of aggregation with the alpha/beta/CD3 T cell receptor controls interleukin 2-dependent T cell growth. 249 22

Normal development of pregnancy requires maternal immune system tolerance towards the fetoplacental allograft. Natural Killer (NK) cells can display spontaneous lytic activity against tumoral, and poorly differentiated cells, without a prior sensitization. Moreover this cytotoxic activity is not restricted by the Major Histocompatibility Complex (MHC). We investigated the existence of modifications in the NK activity mediated by peripheral blood mononuclear cells (PBMC) from pregnant women. A significant depression was found in this activity from the first trimester to the puerperium that cannot be ascribed to a defective number of NK cells among pregnant's PBMC. However this impaired NK activity can be reconstituted in vitro by incubation of PBMC with interleukin 2 (IL 2). Pregnancy is also associated with an absence of effectors and/or precursors which mediate other cytotoxic non MHC-restricted activities after long term incubation with IL 2, the so called Lymphokine Activated Killer (LAK) cells.
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PMID:[Immunobiology of materno-fetal relations]. 270 69

The administration of interleukin 2 (IL-2) and lymphokine-activated killer (LAK) cells can mediate the regression of cancer. Treatment with IL-2 is associated with significant cardiorespiratory effects, as well as a leaky capillary syndrome requiring careful fluid management. A mild reversible depression of cardiac function is also associated with IL-2 treatment. All patients treated with recombinant IL-2 alone, with transfer of LAK cells, or with cyclophosphamide between December 1984 and September 1987 (total of 423 treatment courses in 317 total patients) were evaluated as to the development of significant cardiorespiratory toxicity. Of the 423 treatment courses, only 1.8% were associated with severe peripheral edema and only 2.8% and 3.1% respectively, were associated with significant ascites or pleural effusions. Thirty-nine of 423 patients (9.2%) had severe respiratory distress and 27 patients required intubation (6.4%). Cardiovascular effects included tachycardia and hypotension requiring vasopressor administration in 65% and intravenous (IV) fluid administration. Weight gain greater than or equal to 10% of body weight was noted in 32% of the 423 patients. Arrhythmias were primarily supraventricular (9.7%) and responded well to conventional medical treatments. Angina or ischemic changes were noted in 2.6% of patients and myocardial infarction in 1.2%. IL-2 caused peripheral vasodilation, with a significant decrease in peripheral vascular resistance (2,254 +/- 398 v 1,303 +/- 351 dyne.s.cm-5, P less than .0001), and an increase in heart rate (66.2 +/- 10 v 104.3 +/- 9.6 beats/min, P less than .0001). There was also evidence of mild cardiac dysfunction, with a significant decrease in the left ventricular stroke work (LVSW) index (P less than .0001) and ejection fraction (LVEF) (from 58% +/- 10% to 52% +/- 9%, P less than .03). A repeat LVEF performed after 1 to 3 months, had returned to baseline values (60% +/- 10%). A mean 64% increase in the rate of disappearance of radioactive iodine (125I) albumin (P less than .05) consistent with the development of a leaky capillary syndrome was noted. Patients with underlying cardiorespiratory diseases may be at greater risk during IL-2 administration and should not be selected to undergo this treatment.
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PMID:Cardiorespiratory effects of immunotherapy with interleukin-2. 278 38

Type beta transforming growth factor (TGF-beta) is a unique polypeptide that has been isolated from a number of different tissues and can induce the phenotypic transformation of non-neoplastic fibroblasts as measured by the stimulation of their growth in soft agar. Recently, TGF-beta has been demonstrated to exert profound inhibitory effects on T and B lymphocyte proliferation. In this study, the effects of TGF-beta on natural killer (NK) cell function were investigated. After 20 hr of culture in the presence of TGF-beta, the NK activity of peripheral blood lymphocytes (PBL) was significantly reduced compared with PBL cultured in medium alone. Similarly, TGF-beta produced a significant depression in the cytolytic activity of highly enriched large granular lymphocytes (LGL). This effect of TGF-beta appeared to be mediated directly on the effector cells, because cultivation of the K562 target cells in TGF-beta did not affect target cell susceptibility to lysis. Binding studies with 125I-TGF-beta indicated that LGL possess approximately 1400 high-affinity (Kd = 1PM) receptors/cell, which represents a considerably higher affinity receptor for TGF-beta than that found on fibroblasts. Culturing of PBL and LGL in TGF-beta resulted in a marked blunting of the boosting of NK cytolysis by interferon-alpha but not by interleukin 2, which suggested that TGF-beta may down-regulate interferon-alpha receptors on NK cells. These results, indicate that in addition to inhibitory effects on T and B cells, TGF-beta also inhibits NK cell function. Although the in vivo role of TGF-beta is presently undefined, it may be an important immunoregulatory protein that has a negative influence on lymphocyte activation.
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PMID:Effects of transforming growth factor beta on the functions of natural killer cells: depressed cytolytic activity and blunting of interferon responsiveness. 287 Nov 7

Effect of exogenous interleukin 2 (IL 2) on the postoperative depression of cell-mediated immune response in vitro was studied in 8 patients with benign lesion and 11 patients with various carcinoma, undergoing major surgical procedures. When peripheral blood mononuclear cells (PBM) were obtained from patients 3 days after surgery, the proliferative response of PBM in mixed lymphocyte culture (MLC) was significantly decreased, as compared to that before operation. The depressed proliferative response was significantly increased and improved to the preoperative level, when exogenous IL 2 was added at a concentration of 50 per cent in culture. The defective generation of cytotoxic cells in MLC 3 days after operation was also significantly augmented and improved to the preoperative range by addition of 25 per cent IL 2 in culture. IL 2 produced minimal increase in these responses when PBM were obtained preoperatively. There was no significant difference between each value in these responses obtained from patients with benign lesion and carcinoma. These results show that PBM from patients who had undergone major surgery were responsive to exogenous IL 2. The postoperative depression of cell-mediated immune response may be reversible with exogenous IL 2.
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PMID:In vitro effect of interleukin 2 on depression of cell-mediated immune response after surgery. 293 68


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