Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neutrophils demonstrate increased complement receptor activity, measured by rosetting of C3b-coated erythrocytes, after asthma that was provoked experimentally. However, it is not clear whether the increased rosetting is due simply to increase in receptor numbers or whether other factors, such as cell adhesiveness, are involved. We have therefore enumerated granulocyte complement receptors, after asthma provoked experimentally, with monoclonal antibodies against the receptors and flow cytometry. There was a maximal 28.2 +/- 7.5% and 33.4 +/- 9.5% (mean +/- SEM; n = 15) increase in granulocyte CR1 and CR3, respectively, at 3 hours after asthma induced by antigen. There was a maximal 32.0 +/- 7.3% (mean +/- SEM; n = 7) increase in granulocyte CR1, but no change in granulocyte CR3, at 1 hour after exercise-induced asthma. No significant changes in granulocyte CR1 or CR3 were observed up to 6 hours after methacholine challenge, or after exercise in subjects who did not develop exercise-induced asthma. There was a maximal 33 +/- 9% (mean +/- SEM; n = 8) increase in granulocyte CR1 at 30 minutes, but no increase in granulocyte CR3, after histamine challenge of subjects with asthma. Incubation of whole blood with histamine in vitro did not lead to any enhancement in expression of granulocyte CR1. This suggests that antigen- and exercise-induced release of histamine may augment granulocyte CR1 expression through an indirect mechanism. These data indicate that there is increase in the numerical expression of CR1 on granulocytes, after asthma provoked experimentally, which is accompanied by increases in granulocyte CR3 after bronchoprovocation with antigen, but not histamine or exercise.
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PMID:Expression of complement receptors type 1 (CR1) and type 3 (CR3) on circulating granulocytes in experimentally provoked asthma. 292 84

Sixteen patients with acne vulgaris were studied. All patients had severe inflammatory lesions, nodulocystic and conglobata. Of them, 12 was male and 4 female, their age was between 16 and 24 years old. In all the cases laboratory test to evaluate chemotactic, nitroblue-tetrazolium and lysosomal activity of granulocyte were performed. The protocol included in vitro incubations with and without autologous serum for considered their action on the phagocytic cell. The results shows an inhibitory action of the autologous serum in chemotactic (d-mean, 34.25%; SEM, 2.39, p less than 0.01), nitroblue-tetrazolium test (d-mean, 21.06%; SEM, 2.85, p less than 0.05), and lysosomal activity (d-mean, 21.43%; SEM, 2.80, p less than 0.05). The authors suggest that granulocyte alterations that occur in inflammatory forms of acne vulgaris is a secondary phenomenon may be caused by seric IgE or vasoactive substances released during immune responses.
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PMID:[Inhibition of the function of the neutrophil granulocyte caused by autologous serum from patients with acne vulgaris]. 297 40

Normodense human peripheral blood eosinophils were isolated under sterile conditions from the 22/23 and 23/24% interfaces and the cell pellet of metrizamide gradients. After culture for 7 d in RPMI media in the presence of 50 pM biosynthetic (recombinant) human granulocyte/macrophage colony-stimulating factor (rH GM-CSF), 43 +/- 7% (mean +/- SEM, n = 8) of the cells were viable; in the absence of rH GM-CSF, no eosinophils survived. The rH GM-CSF-mediated viability was concentration dependent; increased survival began at a concentration of 1 pM, a 50% maximal response was attained at approximately 3 pM, and a maximal effect was reached at concentrations of greater than or equal to 10 pM rH GM-CSF. In the presence of rH GM-CSF and mouse 3T3 fibroblasts, 67 +/- 6% (mean +/- SEM, n = 8) of the eosinophils survived for 7 d. In a comparative analysis, there was no difference in eosinophil viability after 7 and 14 d (n = 3) in the presence of 50 pM GM-CSF and fibroblasts. Culture with fibroblasts alone did not support eosinophil survival. The addition of fibroblast-conditioned media to rH GM-CSF did not further improve eosinophil viability, indicating a primary role for GM-CSF in supporting these eosinophil cell suspensions ex vivo and a supplementary role for 3T3 fibroblasts. Eosinophils cultured for 7 d localized on density gradient sedimentation at the medium/18, 18/20, and 20/21 interfaces of metrizamide gradients, indicating a change to the hypodense phenotype from their original normodense condition. In addition, the cultured eosinophils generated approximately 2.5-fold more LTC4 than freshly isolated cells when stimulated with the calcium ionophore A23187 and manifested sevenfold greater antibody-dependent killing of S. mansoni larvae than the freshly isolated, normodense cells from the same donor. Thus we demonstrate the rH GM-CSF dependent conversion in vitro of normodense human eosinophils to hypodense cells possessing the augmented biochemical and biological properties characteristic of the hypodense eosinophils associated with a variety of hypereosinophilic syndromes. In addition, these studies provide a culture model of at least 14 d suitable for the further characterization of hypodense eosinophils.
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PMID:Regulation of human eosinophil viability, density, and function by granulocyte/macrophage colony-stimulating factor in the presence of 3T3 fibroblasts. 311 Mar 47

The human eosinophil contains lysosomal enzymes that can contribute directly to tissue injury and inflammation. Characterization of lysosomal-enzyme release from the eosinophil has been largely limited to isolates from patients with hypereosinophilia. Because eosinophils from such individuals may not demonstrate normal functional responses, we established a method to obtain purified, normal human eosinophils with a Percoll gradient. With this method, it is possible to isolate eosinophils (95.5 +/- 3.9%) and neutrophils (greater than 99%) in high purity from normal subjects. With these granulocyte isolates, we evaluated and compared release of the lysosomal enzyme, beta-glucuronidase (BG), after cell activation with opsonized zymosan particles. Neutrophils released 33.0 +/- 1.2% (mean +/- SEM; n = 5) of total BG (30 minutes of incubation with zymosan), whereas eosinophil secretion was 24.2 +/- 1.7% (n = 5). The fungal metabolite, cytochalasin B (CB), which inhibits microfilament activity, enhanced BG secretion from neutrophils (33.0 +/- 1.2% to 42.8 +/- 2.8% with CB; p less than 0.01). In contrast, CB had no effect on eosinophil BG release. Interestingly, BG content in eosinophils is 101.2 +/- 3.9 micrograms phenolphthalein per 10(6) cells per 18 hours, which compares to a neutrophil level of 51.0 +/- 3.2 (p less than 0.001). Thus, although eosinophils and neutrophils release a similar percentage of total cellular BG on stimulation with zymosan particles, the absolute amount of enzyme per cell is greater in the eosinophil than in the neutrophil. Study of eosinophil function promises to elicit a more complete insight into its contribution to tissue injury.
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PMID:Release of lysosomal enzyme beta-glucuronidase from isolated human eosinophils. 317 Sep 99

Six anesthetized dogs treated with indomethacin, prostacyclin (PGI2), and heparin were compared with 7 anesthetized controls (ischemia without treatment) to determine whether cyclooxygenase inhibition would lead to enhanced granulocyte accumulation because of preferential formation of lipoxygenase products. Cortical somatosensory evoked response, [14C]iodoantipyrine autoradiographic blood flow, and 111In-labelled granulocyte accumulation were compared 4 hours after a 60-minute exposure to multifocal brain ischemia. Treatment with indomethacin, PGI2, and heparin eliminated neuron-disabling brain blood flows without altering early postischemic granulocyte accumulation. Granulocyte accumulation after 4 hours of reperfusion was not significantly different in control and treated dogs. The final amplitude of the cortical somatosensory evoked response in the treated group averaged 38.0 +/- 13.6% (mean +/- SEM) of the corresponding baseline value compared with 21.0 +/- 4.6% in the control group, but this difference was not significant.
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PMID:Indomethacin, prostacyclin, and heparin improve postischemic cerebral blood flow without affecting early postischemic granulocyte accumulation. 329 33

In addition to immunologic derangement, hematological abnormalities have been reported in the majority of patients with acquired immunodeficiency syndrome (AIDS). In this study 15 patients with AIDS or AIDS-related complex (ARC) were evaluated for the in vitro growth of hemopoietic progenitor cells. In all patients a significant reduction of growth (mean +/- SEM) of colony-forming unit-granulocyte, erythrocyte, macrophage, (megakaryocyte) (CFU-GEM) (1.2 +/- 0.3), burst-forming unit-erythroid (BFU-E) (17 +/- 10), CFU-megakaryocyte (CFU-Mk) (1.7 +/- 0.6), and CFU-granulocyte-macrophage (CFU-GM) (35 +/- 10) was observed in comparison with normal controls. Depletion of T cells from the bone marrow before culture led to a significant increase in colony growth, which indicated an imbalance of the normally modulating T cell subsets. This increase was reversed by readdition of autologous T cells causing a decrease in colony growth to a degree, dependent on the T4 to T8 ratio. A decreased number of hemopoietic progenitor cells and/or a defective modulation of progenitor cell growth, normally carried out by T lymphocyte subsets, might be the cause of the hematological abnormalities in AIDS patients.
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PMID:Defective in vitro growth of the hemopoietic progenitor cells in the acquired immunodeficiency syndrome. 349 75

Colony-forming units-granulocyte/monocyte (CFU-GM) harvested from normal donors as a byproduct of plateletapheresis can be cryopreserved successfully with 10 percent dimethyl sulfoxide with the use of standard protocols that have been developed for freezing bone marrow. Short-term storage of CFU-GM in polypropylene vials in the liquid phase of liquid nitrogen yielded a recovery rate of 88 +/- 5 percent (mean +/- SEM). Significant loss of committed progenitor cells was not detected until 1 year after freezing (65 +/- 5%). A comparison of CFU-GM recovery with the polyolefin bag technique (107 +/- 13%) was not statistically different from that obtained with polypropylene vials (78 +/- 7%). Although the freezing bags are more expensive and prone to fracture than the vials, they are easier to handle, store, and thaw in the laboratory, and reinfusion to the patient is more convenient. Cryopreservation of CFU-GM harvested from peripheral blood appears feasible in either of two freezing systems.
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PMID:Cryopreservation of hematopoietic progenitor cells collected by hemapheresis. 381 Aug 18

Whether migration of granulocytes across pulmonary vascular endothelium in the absence of structural evidence of endothelial injury causes increased production of thromboxane or prostacyclin is not known. Using bovine pulmonary artery intimal explants mounted in Boyden chambers and homologous separated granulocytes, concentrations of thromboxane B2 and 6-keto-PGF1 alpha in the upper-well fluid were measured by radioimmunoassay over a three-hour period under the following conditions: (1) granulocyte chemotaxis (zymosan-activated plasma in the lower well, granulocytes in the upper well); (2) unstimulated granulocyte migration (serum or plasma in the lower well, granulocytes in the upper well); (3) granulocyte activation without migration (zymosan-activated plasma and granulocytes in the upper well); (4) granulocyte chemotaxis in the absence of endothelium (identical to condition 1 above except that endothelium was scraped from the explant surface); and (5) explants incubated in the absence of granulocytes. Minimal increases in thromboxane B2 concentrations in upper-well fluid occurred under all conditions. In contrast, granulocyte chemotaxis was accompanied by large increases in concentrations of 6-keto-PGF1 alpha evident by two hours of incubation and increasing markedly by three hours, to 524.3 +/- 69.0 ng/mL (m +/- SEM). Unstimulated migration of granulocytes toward serum or plasma and granulocyte activation without migration were accompanied, at three hours, by more modest increases in 6-keto-PGF1 alpha (296.5 +/- 46.4; 128.0 +/- 38.6, and 236.7 +/- 47.0 ng/mL, respectively) and, in the absence of granulocytes or in the absence of endothelium, only minimal increases in this prostacyclin metabolite occurred (137.2 +/- 16.9 and 53.9 +/- 12.6 ng/mL, respectively). The large rises in prostacyclin metabolite occurred at a time when the majority of granulocytes had migrated through the endothelial layer rather than during their adherence or transendothelial passage. We conclude that chemotaxis of granulocytes through pulmonary vascular endothelium causes endothelial production of large amounts of prostacyclin, but this occurs late in the chemotactic process, after granulocytes have transversed the endothelium.
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PMID:Endothelial prostacyclin production is a late event in granulocyte migration into bovine pulmonary artery intimal explants. 390 71

Stimulated by a patient with dyspnea, thrombocytopenia, and leukopenia after sodium morrhuate sclerotherapy, we studied the effect of this agent on the plasma coagulation and complement systems, the formed elements of the blood, and cultured human endothelial cells. The addition of sodium morrhuate to citrated plasma did not cause clotting or shorten the prothrombin time or partial thromboplastin time. Incubation of a 1:100 dilution of the clinical sodium morrhuate preparation in heparinized plasma led to a modest rise in [C3a]. The addition of the drug (dilutions 1:50 to 1:300) to granulocytes caused prompt aggregation (and, at the higher concentrations, granulocyte cytotoxicity [trypan blue exclusion; lactate dehydrogenase release]), but the same dilutions failed to aggregate platelets. However, 0.05% morrhuate added to washed red blood cells caused a prompt 84.0% (+/- 0.8% SEM) hemolysis, rendering the supernatant buffer a potent platelet aggregant. Not only was this sclerosing agent toxic to granulocytes and red cells, but a 1:1000 dilution of the drug also caused the destruction of 35.5% (+/- 6.6%) of cultured endothelial cells as measured by chromium 51 release. Three other agents in current use (ethanolamine oleate, sodium tetradecyl sulfate, and polidocanol) were studied and found to cause effects qualitatively similar to those of sodium morrhuate. We conclude that these drugs cause phlebosclerosis not primarily through induction of plasma coagulation, but by directly damaging endothelium and red cells, triggering platelets, and aggregating granulocytes at the venous wall endothelium. These effects likely derive from the surfactant properties of sodium morrhuate as well as its high arachidonate content.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sodium morrhuate stimulates granulocytes and damages erythrocytes and endothelial cells: probable mechanism of an adverse reaction during sclerotherapy. 405 66

Studies were carried out in dogs to detect alloimmunization to granulocytes by indirect immunofluorescence (GIIF) and to determine the significance of cross-matching in selecting donors for immunized recipients. All recipients were rendered neutropenic (less than 500 per microliter) by chemotherapy. Three groups of transfusions were evaluated. Group I consisted of 14 transfusions administered to sensitized dogs that were GIIF-negative with donor cells; Group II, 12 transfusions to the same dogs with GIIF-positive donor cells; Group III, 16 transfusions to nonimmunized control dogs. At 1 hour following transfusion, circulating granulocytes demonstrated increments of 956 +/- 137 per microliter (mean +/- SEM) in Group I dogs compared to 236 +/- 57 per microliter for Group II (p less than 0.001). Group III transfusions yielded increments of 888 +/- 116 per microliter, not significantly different from Group I. GIIF correlated better with transfusion results than granulocyte cytotoxicity or lymphocyte cytotoxicity tests or leukoagglutination cross-matching. Nineteen sera with alloantibodies to granulocytes were produced by random or intrafamilial immunizations with granulocytes. Partial characterization of specificities showed that granulocyte specificities were independent of DLA, and consistent with a genetic system of dominant alleles. It was concluded that a) alloimmunization to granulocytes is detected by the GIIF, b) positive tests predict transfusion effects, and c) a genetic system independent of DLA could be recognized on dog granulocytes.
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PMID:Detection and significance of granulocyte alloimmunization in leukocyte transfusion therapy on neutropenic dogs. 633 27


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