1,720,996 research outputs found
Mechanism of the potentiating effect of cytochalasin B on the respiratory burst induced by Concanavalin A in leucocytes.
No full textGlycosylation improves the priming effect exerted by recombinant human granulocyte colony-stimulating factor (lenograstim) on human neutrophil superoxide production.
No full textThe role of glycosylation in modulating the activity of recombinant human granulocyte colony-stimulating factor (rHuG-CSF) on polymorphonuclear leukocytes (PMNs) was investigated. We addressed this study by comparing the effects of lenograstim (glycosylated rHuG-CSF) and its deglycosylated counterpart on superoxide production by PMNs on fibronectin. When the triggering activity of the cytokine was evaluated, no O2- release was elicited from neutrophils treated with either preparation of rHuG-CSF. Instead, a clear potentiation of both fMLP- and TNF-induced respiratory burst was produced by preincubating the cells with rHuG-CSF. Such effect was found to be significantly increased when glycosylated versus deglycosylated preparation was used, leading to the conclusion that the sugar moiety of the molecule could be of importance in improving the priming activity exerted by rHuG-CSF on PMN metabolic response
A dual effect of L-1-tosylamide-2-phenylethyl chloromethyl ketone on the respiratory metabolism of guinea pig phagocytes
No full textpubblicato su:
Title(s):
Bulletin européen de physiopathologie respiratoire.
Other Title(s):
Clinical respiratory physiology, 1980-1987
Clinical respiratory physiology
Continues:
Bulletin de physio-pathologie respiratoire
Merged To :
European journal of respiratory diseases
European respiratory journa
8. Brochetta C., Perrotta M.G., Jeromin A., Romano M., Soranzo MR., Borelli V., Roder J. And Zabucchi G. Identification and Subcellular Localization of Neurtonal Calcium Sensor-1 (NCS-1) in Human Neutrophils and HL-60 cells.
No full textHuman eosinophil peroxidase enhances tumor necrosis factor and hydrogen peroxide release by human monocyte-derived macrophages
No full textBiochemical studies on the leukocytes in Chediak-Higashi syndrome.
No full textBlood leukocytes from a patient with Chediak-Higashi syndrome (CHS) were compared with normal cells for their capacity of extruding (exocytosis) the lysosomal enzyme myeloperoxidase during phagocytosis or after a treatment with the ionophore A23187 and Ca2+. A decreased rate and extent of exocytosis in phagocytizing CHS cells was observed also with the Ca2+ ionophore. This suggests that a defect in Ca2+ mobilization is not responsible for the impaired secretion of granule content. Isolated granules of CHS cells and of leukocytes were treated with the detergent Triton X-100. Since the solubilization of myeloperoxidase from the CHS granules was much lower than from the normal ones, we suggest that the former organelles have a more resistant membrane
The respiratory burst of phagocytic cells: facts and problems
No full text1. The so called "soluble" oxidase(s) are not involved in the respiratory burst of guinea pig and human granulocytes and of guinea pig peritoneal resident and elicited macrophages. 2. The activation of the oxidation of NADPH by a membrane bound NAD(P)H oxidase is the main mechanism responsible for the activation of the respiration of phagocytes. 3. The oxidase is inactive in resting cells and the activated form works on the plasma membrane. 4. More than one mechanism is operative in the oxidation of NAD(P)H by cell free particles in vitro. These mechanisms vary in relation to the conditions of assay (pH and concentration of substrate). 5. Under optimal conditions in vitro the enzymatic oxidation of NADPH practically involves the univalent pathway of oxygen reduction with stoichiometry of two nanomoles of O2 formed for one nanomole of NADPH oxidized. 6. Also in intact cells all O2 is first univalently reduced to O2 and then discharged outside the cell or in the phagocytic vacuoles. 7. The main reactions involved in the O2 balance in intact cells are the univalent reduction of O2, the dismutation of O2 to H2O2 and the degradation of the peroxide through catalatic and peroxidatic mechanisms. 8. The total oxygen univalently reduced by the activated oxidase is 2-4 folds the net oxygen consumed by the cells, depending on the mechanism of H2O2 degradation. 9. All the rate of extrarespiration is accounted for by the rate of oxidation of physiological concentration of NADPH by the membrane-bound enzyme. This adequacy can be observed only under appropriate experimental conditions, because the high activity of the oxidase is not a permanent state
Increase in ferric and ferrous iron in the mouse lung after asbestos exposure
No full textThe growing amounts of Fe2+ in the lung of asbestos exposed mice could support a continuated generation of oxidative stress resulting in clinical manifestations, which culminate in inflammarory, fibrotic and hyperplastic lesions
Eosinophilic granuloma of the bone in Hand-Shuller-Christian disease: extensive in vivo eosinophil degranulation and subsequent binding of released eosinophil peroxidase (EPO) to other inflammatory cells
No full textThe eosinophils from bone granuloma, bone marrow, and peripheral blood of a patient with Hand-Schüller-Christian disease (HSCD) were studied by electron microscopy and cytochemistry. Impressive eosinophil degranulation was observed. Extracellular release of eosinophil peroxidase (EPO) and EPO binding to surrounding cells were seen in the granuloma and bone marrow. Cells with peroxidase-positive plasma membrane were also observed in peripheral blood. The pattern of eosinophil degranulation showed quite different features from those described so far. In the granuloma, the process begins with intracytoplasmic release of the granule matrix content, as revealed by both extensive extragranular accumulation of EPO and progressive decrease of the matrix electron density. Core dissolution follows thereafter, leading to complete disappearance of the granules. At the end of the process, the cells show rupture of the plasma membrane and release of their content into the surrounding environment. This pattern of secretion was also observed in blood and marrow eosinophils of the patient. In view of the previously reported findings that EPO binding to inflammatory cells influences their functions, EPO release and binding to surrounding cells in HSCD may play a role in the evolution of the inflammatory lesion in the disease
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