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Leukocytes respiratory burst

CC, and one CX3C and XC chemokine receptors have been cloned so far [2]. Receptor binding initiates a cascade of intracellular events mediated by the receptor-associated heterotrimeric G-proteins. These G-protein subunits trigger various effector enzymes that lead to the activation not only of chemotaxis but also to a wide range of fimctions in different leukocytes such as an increase in the respiratory burst, degranulation, phagocytosis, and lipid mediator synthesis. [Pg.352]

Leukocytes are activated on exposure to bacteria and other stimuh NADPH oxidase plays a key role in the process of activation (the respiratory burst). Mutations in this enzyme and associated proteins cause chronic granulomatous disease. [Pg.624]

Suematsu, M., Suzuki, M., Kitahora, T. et al. (1987a). Increased respiratory burst of leukocytes in inflammatory bowel disease - the analysis of free radical generation by using chemiluminescence probe. J. Clin. Lab. Immunol. 24, 125-128. [Pg.172]

De Guise, S. et al., Immune functions in beluga whales (Delphinapterus leucas) Evaluation of phagocytosis and respiratory burst with peripheral blood leukocytes using flow cytometry, Vet. Immunol. Immunopathol., 47, 351, 1995. [Pg.417]

Following a stimulation by the yeast cell wall extract zymosan, phagocytosing human leukocytes show an enhanced oxygen consumption, the cyanide-insensitive respiratory burst , after a lag period of 30-40 s. The production of superoxide anions, measured by the reduction of Fe(ni)-cytochrome c, followed the same... [Pg.4]

Eisner, J., Oppermann, M Czech, W., and Kapp, A. (1994) C3a activates the respiratory burst in human polymorphonuclear neutrophilic leukocytes via pertussis toxin-sensitive G-proteins. Blood 83, 3324-3331. [Pg.156]

K17. Kobayashi, M., Tanaka, T., and Usui, T., Inactivation of lysosomal enzymes by the respiratory burst of polymorphonuclear leukocytes. Possible involvement of myeloperoxidase-H202-halide system. J. Lab. Clin. Med. 100, 896-907 (1982). [Pg.240]

Baggiolini, M., Boulay, F., Badwey, J. A., and Gurnutte, J. T. (1993). Activation of neutrophil leukocytes Ghemoattractant receptors and respiratory burst. FASEB J. 7, 1004-1010. [Pg.382]

The antibacterial activity of polymorphonuclear leukocytes is based on the production of superoxide anions and H2O2 in the respiratory burst. Combinations of an antibacterial agent and an anti-inflammatory drug are commonly used in immunosuppressed patients whose respiratory burst of poljmiorphonuclear leukocytes is impaired. An in vitro study has shown that the combination of a glucocorticoid (dexamethasone, methylpredniso-lone, betamethasone, hydrocortisone) with ofloxacin 10 mg/ml neutralizes the inhibitory effect of the former on the respiratory burst (15). [Pg.2597]

Perlingeiro RC, Queiroz ML. 1995. Measurement of the respiratory burst and chemotaxis in polymorphonuclear leukocytes from mercury-exposed workers. Human Exper Toxicol 14(3) 281-286. [Pg.637]

The scavenging effect of berbamine on active oxygen radicals was studied via a spintrapping technique and a chemiluminescence (CL) method in phorbol myristate acetate (PMA) stimulated polymorphonuclear leukocytes (PMN) and in four-cell superoxide (02+) or hydroxyl radical (OH ) generating systems. The alkaloid (0.1-0.3 mM) effectively reduced active oxygen radicals in PMA-stimulated PMN, but had no obvious effect on oxygen consumption during the respiratory burst of PMN (as measured with spin probe oxymetry). In addition, berbamine (0.3 mM) inhibited the CL response of PMA-stimulated PMN, and quenched 02 in the xanthine/xanthine oxidase and irradiation riboflavin systems, as well as OH in the Fenton... [Pg.120]

Peroxide is the ammunition of your killer cells. Your body s elite corps of bacterial assassins, called polymorphonuclear leukocytes (PMN s), engulf bacteria then kill them with the "respiratory burst." The cell combines oxygen and water, making H202. That s the respiratory burst. The H202 then zaps the bacteria. [Pg.18]

O2) during respiratory bursts of phagocytic leukocytes (Babior, 1982) and could aggravate inflammatory processes and reperfusion injury (McCord, 1987). Thus, biosynthesis of CAT, peroxidases and SOD have to be rigorously controlled to ensure protection. [Pg.444]

Dasatinib, the Abl-antagonist tyrosine kinase inhibitor, suppressed adhesion-mediated respiratory burst and superoxide release of neutrophil leukocytes antagonized the leukocytes immune complex-induced activation, and their migration toward fibrinogen-coated substrate, but it did not block LPS- or TNF signaling, stimulation by zymosan, and phagocytosis. Dasatinib blocked Syk activation (spleen tyrosine kinase, agonist of Fey receptors) [2215] (Table XXVI). [Pg.489]

The subsequent signaling events downstream of chemokine-mediated G-protein activation are complicated. It has already been mentioned that signaling events from chemokine receptors are commonly inhibited by pertussis toxin, leading to the assumption that chemokine receptors are Ga linked. One of the most rapid occurrences following chemokine receptor activation is a rise in the intracellular calcium concentration dCa +]i), and this has commonly been used as a measurement for the functional response of receptor activation. Increases in [Ca " "] are mediated via the jSy subunit of the G-protein that activates phospholipase CjS, leading to 1) hydrolysis of phosphatidylinositol to IP3 and 2) DAG formation, which respectively induce the release of Ca + from intracellular stores and subsequent activation of PKC. PKC activation is necessary for certain leukocyte responses, such as neutrophil respiratory burst (Li et al., 2000), and it also plays a role in receptor phosphorylation, leading to desensitization and internalization, which will be discussed later. [Pg.83]


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See also in sourсe #XX -- [ Pg.4 , Pg.72 , Pg.221 , Pg.222 , Pg.269 , Pg.270 ]




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