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 activity of human peripheral blood monocytes and pulmonary alveolar macrophages was examined with a rosette assay that detects changes in Fc receptor expression. Compared with peripheral blood monocytes from normal subjects, the peripheral blood monocytes of patients with carcinoma of the lung were found to be activated in this respect. In contrast, compared with pulmonary alveolar macrophages from normal subjects, carcinomas exhibited depressed function in terms of receptor alveolar macrophages from lungs bearing primary expression. Trypsinization of macrophages to remove bound immunoglobulin indicated that this depression of receptor activity was not due to blocking of receptors by immunoglobulin or immune complexes. In an in vitro study the expression of Fc receptors by cultured macrophages was shown to be depressed by a heat-stable, low-molecular-weight material in supernatants of cultured carcinoma tissue from the lung, breast, and urinary bladder.
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PMID:Human macrophage function in cancer: systemic and local changes detected by an assay for Fc receptor expression. 693

Specific receptor-mediated delivery of the contents of small, sonicated liposomes was studied with three murine tumor cell types: an IgG Fc receptor-negative nonphagocytic line (EL4); an Fc receptor-positive phagocytic line (P388D1); and an Fc receptor-positive nonphagocytic line (P388). The liposomes (formed from phosphatidylcholines, cholesterol, and dinitrophenyl-substituted phosphatidylethanolamine) contained carboxyfluorescein as a fluorescent marker and methotrexate as a pharmacologic agent. Binding and internalization of the liposomes were observed by fluorescence microscopy and measured by flow microfluorometry. The hapten-derivatized lipid was used as a binding point on the liposome for the antibody-combining site of the immunoglobulin. In the presence of IgG anti-dinitrophenyl, but not F(ab')2 or IgA anti-dinitrophenyl, liposomes bound to the Fc receptor-bearing cells. The liposomes underwent endocytosis by the P388D1 cells and, to a lesser extent, by the P388 cells. As measured by depression of [3H]deoxyuridine incorporation, methotrexate in IgG-opsonized liposomes had a much greater pharmacologic effect on the P388D1 cells than did the same amount in unopsonized liposomes or in free solution. This observation indicates that an appropriately chosen drug, incorporated in liposomes, can exert its effect on a cytoplasmic target after endocytosis. P388 cells showed a moderate effect of the drug in liposomes. Neither P388 nor P388D1 cells bound or ingested unopsonized liposomes, and the Fc receptor-negative EL4 line neither bound nor ingested opsonized liposomes. The data demonstrate specific interaction of opsonized liposomes with the cells' IgG Fc receptor.
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PMID:Receptor-mediated endocytosis of antibody-opsonized liposomes by tumor cells. 700 54

We have previously found that natural killer (NK) activity is profoundly decreased in BALB/c mice bearing large mammary tumors. Kinetic studies showed that after 14 days of tumor implantation a reduction of 25-40% of NK cytotoxicity can be observed and by 21 days only very low levels of NK reactivity can be detected in the spleens of tumor bearers. Phenotypic analyses of the splenic NK cells of tumor bearing mice revealed that they have similar density, granularity and comparable levels of NK 2.1 antigen on their surfaces as compared to NK cells from normal mice. However, in tumor bearers there was a shift from a high surface asialo GM1-bearing NK population to low-density surface asialo GM1-positive bearing cells. Phenotypically characterized NK cells were quantitated to test the possibility that splenic NK cells from tumor bearers migrated to other organs and were therefore at lower levels in the spleen. No significant differences were observed in the percentages of NK cells from spleens from normal and tumor bearing mice. Using single cell conjugate assays it was found that there was no impairment in the capacity of NK from tumor bearers to bind the NK-sensitive Yac-1 cells, however, this event did not result in lysis of the target cells. To elucidate whether the lytic machinery of the tumor bearers' NK cells was inactivated, their capacity to effect antibody dependent cellular cytotoxicity (ADCC) was evaluated. In contrast to the results observed when NK activity was evaluated, NK cells from tumor bearing mice exerted higher levels of ADCC than their normal counterparts and they had a higher expression of Fc receptors on their surfaces. These results suggest that the depression of NK activity observed in tumor bearing mice occurs at a triggering step that is not necessary for the activation of the NK effectors via the Fc receptor and that no major impairment of the lytic machinery occurs during mammary tumorigenesis.
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PMID:NK cells from mammary tumor bearing mice do not exert natural killer activity but function as antibody dependent cellular cytotoxicity effectors. 847 11

The phagocytosis of erythrocytes may contribute to the increased susceptibility to life-threatening infections in patients with burn injury, sickle cell anemia, and malaria. The phagocytosis of immunoglobulin G-coated erythrocytes (EIgG) is followed by a transient depression of several macrophage functions including phagocytosis, respiratory burst capacity, and killing of bacteria. The present study suggests the possibility that after erythrophagocytosis hemoglobin-derived iron conspires with reactive oxygen products of the macrophage respiratory burst to cause oxidant damage to the phagocyte. Challenge of elicited peritoneal macrophages with EIgG phagocytosis was followed by an increase in lipid peroxidation as assessed by thiobarbituric acid-reactive substances (TBARS). Doses of EIgG associated with increased TBARS also caused a depression of Fc receptor-mediated phagocytosis and phorbol myristate acetate (PMA)-stimulated hydrogen peroxide production. Time course experiments demonstrated that the increase in TBARS coincided with the depression of macrophage function. There was no increase in TBARS following the phagocytosis of IgG-coated erythrocyte ghosts, suggesting that hemoglobin iron is involved in the generation of TBARS. The phagocytosis of erythrocyte ghosts did not depress macrophage function. Since complement receptor-mediated phagocytosis does not stimulate the respiratory burst, the role of the respiratory burst in causing lipid peroxidation was assessed using the phagocytosis of complement-coated erythrocytes. Phagocytic challenge with complement-coated erythrocytes caused neither an increase in TBARS nor a depression of macrophage function. However, there was an increase in TBARS when the respiratory burst was stimulated with PMA following complement receptor-mediated phagocytosis of erythrocytes. These results suggest that hemoglobin iron and phagocyte-generated oxidants collaborate to cause the depression of macrophage function following EIgG phagocytosis.
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PMID:Macrophage dysfunction following the phagocytosis of IgG-coated erythrocytes: production of lipid peroxidation products. 860 13

Phagocytosis of IgG-coated erythrocytes (EIgG) can depress several macrophage functions. Our previous studies have suggested that this macrophage dysfunction may be due to an oxidative stress caused by the interaction of hemoglobin-derived iron with superoxide and/or hydrogen peroxide. Since lysosomotropic agents are capable of altering iron handling by macrophages, the present study evaluated the ability of these agents to prevent the macrophage dysfunction and lipid peroxidation caused by a phagocytic challenge with EIgG. Elicited rat peritoneal macrophages showed a depression of PMA-stimulated hydrogen peroxide production, calcium ionophore-stimulated arachidonate release and Fc receptor-mediated phagocytosis. The lysosomotropic agents; chloroquine, quinacrine, ammonium chloride and methylamine all prevented the depression of hydrogen peroxide production and arachidonate release but did not alter the depression of phagocytic function. These agents also prevented the increase in lipid peroxidation products caused by a phagocytic challenge with EIgG. These results suggest that the ability of lysosomotropic agents to prevent some aspects of macrophage dysfunction after a phagocytic challenge may be due to their ability to block the oxidative stress caused by the challenge.
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PMID:Lysosomotropic agents ameliorate macrophage dysfunction following the phagocytosis of IgG-coated erythrocytes: a role for lipid peroxidation. 942 9

The effect of bovine respiratory syncytial virus (BRSV) and non-cytopathic bovine viral diarrhea virus (ncpBVDV) infection on selected bovine alveolar macrophage (AM) functions was investigated. Alveolar macrophages were harvested from 2- to 6-month-old calves seronegative for BRSV and BVDV and inoculated with approximately 1 median cell culture infective dose of virus per AM. Control, BRSV infected, ncpBVDV-infected and BRSV-ncpBVDV coinfected AM cultures were evaluated for Fc receptor expression, phagosome-lysosome fusion, superoxide anion (O2-) production, and chemotactic activity on Days 1, 3, 5, and 7 post-infection. Both single and combined viral infections significantly depressed AM Fc receptor expression, phagosome-lysosome fusion, and secretion of chemotactic factors with a more significant synergistic depression seen in BRSV-ncpBVDV coinfection. Production of O2- by AM was not decreased by either BRSV or ncpBVDV infection, but was significantly decreased by coinfection with BRSV-ncpBVDV. The present study confirms previous reports of BRSV effects on AM functions and indicate that ncpBVDV affects AM functions in vitro. Coinfection with BRSV-ncpBVDV produced a synergistic depression on AM functions.
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PMID:Synergistic effects of bovine respiratory syncytial virus and non-cytopathic bovine viral diarrhea virus infection on selected bovine alveolar macrophage functions. 991 33

The aim of this study was to verify a non-traditional assessment of respiratory exposure to outdoor air pollutants in industrial areas. The technique involved environmental biological monitoring' using domestic rabbits in the neighborhood of a mercury-producing plant. Rabbits were exposed whole-body to mercury emissions for 6 months in special cages near the plant. Control rabbits were kept using the same schedule outside the polluted area. Potential toxicity was assessed by: (a) measurement of Hg-accumulation in lungs and other body tissues by atomic absorption spectroscopy (AAS); (b) scanning electron microscopy (SEM) of the tracheal surface; and (c) measurement of toxic effects on pulmonary alveolar macrophages (PAM) by a rossette assay (Fc immunoglobulin binding). We found increased Hg concentrations in the lungs, kidneys, liver, heart, brain and bone; changes in the mucosal relief of the trachea, and depression of PAM Fc receptor (FcR) activity to IgG. A 6-month chamber exposure of Wistar rats to the aerosol created from solid particles of the mercury-producing plant revealed the increase of Hg-content in the same body tissues except the brain, and, less intense morphologic changes on the tracheal relief. Biomonitoring using environmental exposure of domestic rabbits might be useful in screening for possible health hazards to the respiratory system from complex outdoor aerosols.
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PMID:A non-traditional approach to risk assessment of respiratory exposure to outdoor air pollutants. 1015 49

The phenotype and function of peripheral blood monocytes change after trauma and during sepsis. The aim of the study was to evaluate monocyte expression of human leucocyte antigen (HLA)-DR and Fc receptor III (FcR III) (CD16) in neonates and small children with high risk of sepsis (hospitalized at the intensive care unit). The reduced proportion of CD14+HLA-DR+ monocytes was observed in all patients at the intensive care unit, while the increase of CD16 expression on monocytes was observed in the course of sepsis. The measurement of CD16 expression on monocytes also proved to be more useful for monitoring patient. The proportion of both CD14dimCD16+ and CD14highCD16+ monocytes increased during sepsis; however, monocytes showed reduced ability to phagocytose Escherichia coli, compromised ability to cooperate with T cells and reduced CD86 expression in parallel to HLA-DR depression. The reduced interleukin (IL)-1 but rather increased IL-10 production was associated with sepsis. The differences between CD14+CD16+ monocytes of healthy donors and patients with sepsis are discussed.
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PMID:CD14+CD16+ monocytes in the course of sepsis in neonates and small children: monitoring and functional studies. 1202 67

Excessive influx of immunoglobulin (IgG) into the brain has been reported to induce central nervous system (CNS) dysfunction. Depressed patients may exhibit immune activation manifested by elevated inflammatory markers and pro-inflammatory cytokines. The brain and especially the limbic system contain high concentrations of high affinity Fc receptors. We reviewed the literature on this phenomena and present data on the behavioral effects of pooled normal IgG on the brain. Many disease states are associated with depression and we examined whether this may be linked to high IgG influx. Female Balb/C mice were injected intra-cerbroventricularly with human immunoglobulin whole molecule, or human IgG F(ab')2 or Fc fragments. Control mice were injected with saline. The four groups were subjected to behavioral (staircase, forced swimming test, and elevated plus maze) and cognitive tests (passive avoidance test). IgG-injected mice exhibited depression-like behavior as reflected by significantly higher immobility time in the forced swimming test (p < 0.05) and hyperactive behavior as reflected by higher number of stairs climbed in the staircase test compared to controls (p < 0.01). Fc-fragments-injected mice showed hyperactive behavior as reflected by both higher number of stairs climbed and rearing events in the staircase test compared to controls. The results indicate that high levels of normal IgG in the cerebrospinal fluid can cause hyperactivity and depression-like behavior. The mechanism involved in these CNS manifestations include possibly Fc receptor binding.
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PMID:Immunoglobulin-mediated neuro-cognitive impairment: new data and a comprehensive review. 2332 32


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