Neutrophils respiratory burst

In vivo administration of y-interferon to atypical X-CGD patients also led to improvements in monocyte and neutrophil respiratory-burst activity and killing, and in some cases spectroscopically-detectable cytochrome b has been observed (occasionally present at up to 50% of normal levels). This improvement followed two subcutaneous doses (0.1 mg/m2) on consecutive days and lasted for up to a month. Because TNF can act synergisti-cally with y-interferon in increasing the expression of the heavy chain of cytochrome b, perhaps the combined use of y-interferon with TNF or some other cytokine(s) will prove even more beneficial. 

Activation of PKC is supposed to be a necessary prerequisite for neutrophil respiratory burst, because it mediates the phosphorylation of the proteins involved in the assembly of NADPH oxidase, which at last produces superoxide anion (02 ) from external oxygen. The isoprenylflavone cycloheterophyllin (12) isolated from Artocarpus heterophyllus (Moraceae) was known to inhibit that respiratory burst, and its interaction with PKC was therefore studied. 

Twomey, B. Dale, M. (1992) Cyclooxygenase-independent effects of nonsteroidal antiinflammatory drugs on the neutrophil respiratory burst. Biochemical Pharmacology, 43, 413-418. 

Rotstein OD, Nasmith PE, Grinstein S The Bac-teroides Byproduct Succinic Acid Inhibits Neutrophil Respiratory Burst by Reducing Intracellular pH. Infect. Immun. 1987 55(4) 864-70. 

Murphy PG, Ogilvy AJ, Whiteley SM. The effect of propofol on the neutrophil respiratory burst. Eur. J Anesthesiol 1996 13 471-3. 

Heine J, Jaeger K, Osthaus A, Weingaertner N, Munte S, Piepenbrock S, Leuwer M. Anaesthesia with propofol decreases FMLP-induced neutrophil respiratory burst but not phagocytosis compared with isoflurane. Brit J Anaesth 2000 85 424-30. 

Shanbhag a, Yang J, Lilien J and Black J (1992) Decreased neutrophil respiratory burst on exposure to cobalt-chrome alloy and polystyrene in vitro. J Biomed Mater Res 26 185-195. 

Perhaps the first demonstration that the PMN respiratory burst activity is critical to normal host defense came from observations of patients with chronic granulomatous disease (CGD). CGD was first established as a clinical entity in 1957 by Brendes, and due to the severity of its nature defined as a fatal disease of childhood. The first understanding of the nature of CGD came in 1966 and 1967 when Holmes was able to show that the neutrophils of CGD patients has normal ingestion but defective intracellular killing with their clinical isolates. In 1967, Holmes revealed that the fundamental abnormality was a complete absence of the neutrophil respiratory burst. The first report of a failure of CGD neutrophils to CL came in 1973 by Stjernholm and has... 

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. 

A.N. Pearce, E.W. Chia, M.V. Berridge, G.R. Clark, J.L. Harper, L. Larsen, E.W. Maas, M.J. Page, N.B. Perry, V.L. Webb, B.R. Copp, Anti-inflammatory thiazine alkaloids isolated from the New Zealand ascidian Aplidium sp. inhibitors of the neutrophil respiratory burst in a model of gouty arthritis, J. Nat. Prod. 70 (2007) 936-940. 

Richardson, M. P Ayliffe, M. J. Helbert, M. Davies, E. G. A simple flow cytometry assay using dihydtor-hodamine for the measurement of the neutrophil respiratory burst in whole blood comparison with the quantitative nitrobluetetrazoUum test. J. Immunol Methods 1998, 219, 187-193. 

Limitations on the use of dihydrorhodamine 123 for flow cytometric analysis of the neutrophil respiratory burst. J. Immunol. Methods 1996,191,187-196. 

Pearce, A.N., Chia, E.W., Berridge, M.V., Maas, E.W., Page, M.J., Harper, J.L., Webb, V.L., and Copp, B.R. (2008) Orfliidines A-E, tubastrine, 3,4-dimethoxyphenetyl-P-guanidine, and 1,14-sperminedihomovanillamide potential anti-inflammatory alkaloids isolated from the New Zealand ascidian ApUdium orthium that acts as irrhibitors of neutrophil respiratory burst Tetrahedron, 64, 5748-5755. 

Ahuja A, OhN, Chao W, Spragg RG, Smith RM. Inhibition of the human neutrophil respiratory burst by native and synthetic surfactant. Am J Respir Cell Mol Biol 1996 14 496-503. 

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