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)

Dimethylnitrosamine (DMN) exposure altered the cell-mediated immune response of B6C3F1 adult female mice as assessed by several immunological assays. Following 14 daily exposures (i.p.) to 1.5, 3.0, or 5.0 mg DMN/kg, mice exhibited a depression in their lymphoproliferative response to the T-cell mitogens concanavalin A and phytohemagglutinin, and in their mixed lymphocyte response to mitomycin-treated DBA-2 spleen cells. The delayed hypersensitivity response (DHR) to keyhole limpet hemocyanin (KLH), as measured by vascular permeability changes, was decreased by over 50% at the 5.0-mg/kg dose. When the DHR to KLH was measured by an influx of endogenously 125I-iododeoxyuridine (IUdR)-labelled monocytes, there was a 300% increase in the response of the 5.0-mg-DMN/kg group. Adoptive transfer studies using exogenously radiolabelled (51Cr) bone marrow cells from either vehicle- or DMN-treated (5 mg/kg) donors indicated a greater than 60% reduction in the DHR to KLH in DMN-treated mice (5.0 mg/kg level) regardless of the donor treatment. Animals exposed to DMN exhibited a decreased susceptibility to Listeria monocytogenes. The dichotomy in the results of the KLH DHR measured by monocyte influx and the increased resistance to the bacterial challenge were interpreted to reflect an effect on bone marrow. The numbers of granulocyte/monocyte stem cells were increased in a dose-related fashion in bone marrow from DMN-treated mice. The results indicate that DMN-treatment impairs cell-mediated immunity while increasing the number of bone marrow cells differentiating to form granulocytes or monocytes with an apparent enhancement in functional activity.
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PMID:Effects of N-nitrosodimethylamine on cell-mediated immunity. 315 99

Pregnant C3H/Anfcum mice were injected ip with 150 micrograms benzo(a)pyrene (BP)/g body weight at the second trimester (12 days). Quantitative and differential changes were assayed in the peripheral blood leukocytes and erythrocytes at various times before and after mating and treatment. Within 5 days after injection, a 2- to 4-fold reduction in leukocytes was observed when compared to controls [corn oil (vehicle for BP)-injected pregnant females] which persisted into the 10th postpartum day. The erythrocytes were also significantly reduced but not to the same degree (1.2- to 1.5-fold). Depression in white blood cells is attributed to lymphocyte depletion since the granulocytes were virtually unchanged and the lymphocyte to granulocyte ratio, ordinarily greater than 2 was 1 or less than one. No change in monocytes was observed and none of the cell populations, including the erythrocytes, appeared to be abnormal (e.g., no increase in reticulocytes). A moderate reduction (1.5-fold) in erythrocytes and leukocytes also occurred in the controls (vs virgin females). Pregnancy also led to transient decreases in medium sized lymphocytes and 3- to 4-fold increase in small lymphocytes shortly after mating to about 3 days before parturition. These results show that, although pregnancy depresses the leukocyte profile, exposure to BP exacerbates this change, and preferentially affects the lymphocytes. These blood profile changes may have important health consequences in the mother and her progeny.
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PMID:Changes in peripheral blood cells in mice after injection with benzo(a)pyrene during pregnancy. 317 Nov 6

Persistent neutropenia (0-0.6 X 10(9) neutrophils/l) was documented during a 10-month period in a 4-year-old spayed female domestic shorthair cat that was presented for anorexia and depression. Salient abnormalities detected on physical examination were fever (40.3 degrees C), dehydration, and gingivitis. The cat was neutropenic (0.5 X 10(9) neutrophils/l) and enzyme-linked immunosorbent assay (ELISA) test for feline leukemia virus was negative. A bone marrow aspirate showed decreased numbers of mature granulocytic cells. In vitro bone marrow cultures for colony-forming units-granulocyte/macrophage (CFU-GM) were performed comparing bone marrow from the patient with that of a normal cat. The patient had fewer CFU-GM than the control. The number of CFU-GM increased when bone marrow mononuclear cells were cultured in the presence of 10(-5) and 10(-6) mol/l of hydrocortisone, but the cat did not respond to oral prednisolone therapy. The pathogenesis of the neutropenia in this cat remains obscure, but resembles the chronic idiopathic neutropenia syndrome of man.
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PMID:Chronic idiopathic neutropenia in a cat. 322 55

Phagocytosis provides one of the body's first-line defences against invading bacteria. The present study evaluated granulocyte microbicidal-related oxidative mechanisms by measurement of chemiluminescence responses in the phagocytosis of zymosan, S. aureus, E. coli and N-formyl-methionyl-leucylphenylalanine (FMLP) in 12 patients undergoing coronary bypass surgery under high-dose fentanyl anaesthesia. With preoperative values as a baseline, a significant depression of in vitro responses to zymosan was seen on days 1, 3-4 after operation and to S. aureus and E. coli on days 3-4 after operation, with recovery by days 6-7. Responses to FMLP were unaffected.
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PMID:Effects of coronary bypass surgery under high-dose fentanyl anaesthesia on granulocyte chemiluminescence. 348 77

The mechanism(s) of stress-induced hypoferremia and hypozincemia remains unclear. We studied the role of granulocytes and lactoferrin (LF) in endotoxin and murine interleukin 1 (IL-1)-induced depression of serum Fe and Zn concentrations in both rabbits and rats. Both endotoxin and IL-1 administration induced significant hypoferremia (P less than 0.01) and hypozincemia (P less than 0.01) after 6 h in both species. Granulocyte depletion before IL-1 infusion significantly (P less than 0.01) diminished the hypoferremia but not the hypozincemia. Moreover, infusion of 5 or 15 mg of human LF into rabbits caused significant hypoferremia (P less than 0.005) without hypozincemia. Significant hypozincemia (P less than 0.01) could only be demonstrated after a 75-mg infusion. In contrast, infusions of human transferrin at equivalent doses (5, 15, and 75 mg) induced neither hypoferremia nor hypozincemia. Therefore endotoxin and IL-1-induced hypoferremia and, to a much lesser degree, hypozincemia are granulocyte dependent. Granulocyte released LF is a specific carrier molecule for transport and removal of Fe from the circulation during the acute phase response. The data suggest a mechanistic dissociation of IL-1-induced hypoferremia and hypozincemia with LF-independent mechanisms for Zn.
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PMID:Interleukin 1-induced depression of iron and zinc: role of granulocytes and lactoferrin. 349 23

The acute and long-term effects of a single dose of partial-body irradiation on the granulocyte/macrophage progenitor cell compartment were studied in dogs. A myeloablative dose of 11.7 Gy (dose rate 6.5 cGy/min) was given to the upper body which contains approximately 70% of the total bone marrow mass. The lower part of the body (pelvis, lower extremities and tail) was shielded by a lead box. In the non-irradiated bone marrow, the concentration of the GM-CFC/10(5) mononuclear cells was slightly decreased within the first 7 days and showed some fluctuations around the normal value for several weeks thereafter. In the irradiated bone marrow, virtually no GM-CFC could be detected on day 1 after exposure. Beginning on day 7, a continuous increase took place up to day 21 when the GM-CFC concentration reached between 25% (sternum) and 43% (humerus) of the initial value. No further increase took place up to day 80. Between day 120 and 380 a secondary increase was observed which reached near-normal bone marrow GM-CFC concentrations. The blood GM-CFC concentration first showed a strong depression followed by a transient increase between day 10 and 30. This coincided with GM-CFC normalization in the protected bone marrow as well as with the initial phase of regeneration in the irradiated sites. A prolonged secondary long-lasting depression between day 33 and 120 amounted to 20 to 50% of normal values. This depression was closely related to the stagnation in the GM-CFC recovery in the irradiated bone marrow sites. The GM-CFC concentration in the blood was found to be supranormal at day 380 when the bone marrow GM-CFC had recovered. The colony stimulating activity in the serum showed an increase within the first 20 days after exposure, that is, within the same interval the bone marrow GM-CFC concentration experienced the strongest alterations, and was inversely related to the changes in the blood granulocyte values.
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PMID:Acute and long-term alterations in the granulocyte/macrophage progenitor cell (GM-CFC) compartment of dogs after partial-body irradiation: irradiation of the upper body with a single myeloablative dose. 372 36

Bone marrow is the commonest site of metastasis in neuroblastoma. This results in minimal to total bone marrow suppression. To establish the mechanism of neuroblastoma suppression of granulopoiesis, the effects of murine C-1300 neuroblastoma cells on granulopoietic activity of normal syngeneic mice was examined. Using a double layer agar system, intact tumor cells, media conditioned by the culture of neuroblastoma cells (NCM) and homogenate of these cells were found to have significant suppressive effects on granulocyte macrophage colony formation (CFU-GM). The rate of production of the NCM was gradual, reaching a plateau by day 4 of the culture. No cell-cell contact was necessary to elicit the CFU-GM depression i.e. regardless of the location of the intact tumor cells or their homogenate in the same or separate layer of the culture, there was a significant linear suppression of CFU-GM (p less than .0005). This suppression proved to be dose dependent. NCM also caused a similar decline in colony formation (p less than 0.005) indicating the suppression is due to diffusible factor(s). The CFU-GM suppressive factor(s) are not dialyzable and cannot withstand 56 degrees C for 15 min. The granulopoietic suppression seen in neuroblastoma may be, at least in part, due to the suppressive effects of these factor(s).
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PMID:Suppressive effects of neuroblastoma cells and conditioned media on in vitro granulopoiesis. 374 44

A semi-solid culture system was used to study the effects of trypanosome infection in two species of mice on the propagation of progenitor cells from the bone marrow and spleen. The deer mouse (Peromyscus maniculatus) survived infection with Trypanosoma (T.) equiperdum for more than 15 days. During the first 10 days there was inhibition of development of granulocyte-monocyte colonies from progenitor cells in the bone marrow. B-lymphocyte progenitors in the spleen showed increased activity, producing colonies 140-300% above normal control groups during the same period. - Conversely, all Balb/c mice infected with the trypanosomes died within 10 days with fulminating parasitemia and massive spleen enlargement. There was a general activation of progenitor cells; B-lymphocytes from the spleen and bone marrow and granulocyte-monocyte colonies from bone marrow, although this was not sustained more than 4 days after infection. - In chronically infected deer mice the pattern of response of the bone marrow and spleen progenitor cells was significantly different over successive weekly intervals. Periodicity of response in these organs was displayed by recurring waves of activation and depression of the progenitor cells. - Thus, there were significant differences in response patterns of deer mice and Balb/c mice to T. equiperdum infection which could be established by the behavior of host lymphohaematopoietic progenitor cells in culture. We therefore suggest that such in vitro cultures may be useful in assessment of the immune response to trypanosomiasis by the host and also for the study of the pathology of both chronic and acute trypanosomiasis.
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PMID:Chronic and acute trypanosomiasis in mice: a study by in vitro cloning of lymphohaematopoietic progenitors. 387 80

Acute and chronic alcohol intoxication may lead to various types of corpuscular hemolytic anemias, irrespective of other coexisting organ damage such as liver cirrhosis. It also suppresses hemopoiesis in the bone marrow, leading to hyporegenerative anemia and to a pathogenetically unclear red cell macrocytosis, which in turn represents a sensitive and valuable index for occult alcoholism. Alcohol also suppresses platelet production. Acute intoxication may, furthermore, lead to reversible thrombocytopenia due to platelet sequestration. Platelet function is affected by alcohol both in vitro and in vivo, the defect being similar to that provoked by aspirin. The impaired host defense in chronic alcoholism is not yet adequately explained. It appears to be based on depression of bone marrow granulocyte reserve, granulocyte mobilization and granulocyte function, and also on impressive functional abnormalities of the lympho-plasmocellular system. The clinical relevance of alcohol-mediated hematological changes has not yet been sufficiently defined. It is certainly underestimated.
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PMID:[Alcohol and the blood]. 391 82

Anti-My-26, a mouse monoclonal IgG1 antibody, was raised against human granulocytes and has been shown to inhibit luminol-enhanced, glucose-independent chemiluminescence (CL) of human granulocytes (or monocytes) responding to the soluble secretagogues A23187 or ionomycin (calcium ionophores) and phorbol myristate acetate (PMA). Anti-My-26 inhibition of CL was reversible and was dependent on both secretatogue and monoclonal antibody concentration. This inhibition appeared to be directed at the component of granulocyte CL that is independent of NAD(P)H-oxidase-catalyzed formation of superoxide anion, because neither opsonized zymosan-stimulated CL nor the PMA-induced decrease in NAD (P)H-associated autofluorescence was affected by anti-My-26. In addition, ionomycin, over a wide concentration range, failed to generate any decrease in granulocyte autofluorescence. The A23187-induced CL inhibited by anti-My-26 was correlated with its depression of oxygen consumption. Furthermore, anti-My-26 was not cytotoxic and did not itself induce oxidative metabolism when used as a stimulant. Binding of anti-My-26 to phagocytic cells was not decreased by pre-exposure of cells to either A23187 or PMA. Evidence is presented to suggest that the binding of anti-My-26 to the granulocyte surface inhibits the oxidative response to calcium ionophore and PMA by blocking a common pathway(s) stimulated by these different secretagogues.
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PMID:Anti-My-26: a monoclonal antibody inhibiting human phagocyte chemiluminescence. 391 9


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