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Polymorphonuclear leucocytic

The neutrophils (also called polymorphonuclear leucocytes, PMNs), which are the professional phagocytes of the body. They constitute >70% of the total leucocyte population, remaining in the circulatory system for less than 48 hours before migrating into the tissues, in response to a suitable stimulus, where they phagocytose material. They possess receptors forFc and activated C3 which enhance their phagocytic ability (see later in chapter). [Pg.280]

Pasquier, C., Mach, P.S., Raichuatg, D., Sar ti, G., Amor, B. and Delbarre, F. (1984). Mn-containing SOD deficiency in polymorphonuclear leucocytes of adults with rheumatoid arthritis. Inflammation 8, 27-32. [Pg.111]

Biemond, P., van Eijk, H.G., Swaak, A.J.G. and Koster, J.F. (1984). Iron mobilisation from ferritin by superoxide derived from stimulated polymorphonuclear leucocytes. J. Clin. Invest. 73, 1576-1579. [Pg.121]

KeUeher, D., Feighery, C. and Weir, D.G. (1990). Chemiluminescence by polymorphonuclear leucocyte subpopulations in chronic inflammatory bowel disease. Influence of the cell separation procedure. Digestion 45, 158-165. [Pg.166]

Nielsen, H. and Andersen, L.P. (1992a). Chemotactic activity of HeUcobacur pylori sonicate for human polymorphonuclear leucocytes and monocytes. Gut 33, 738-742. [Pg.168]

Wandall, J.H. and Binder, V. (1982a). Leucocyte function in Crohn s disease. Studies on mobilisation using a quantitative skin window technique and on the function of circulating polymorphonuclear leucocytes in vitro. Gut 23, 173-180. [Pg.173]

Polymorphonuclear leucocytes (PMNs) employ a system comprising myeloperoxidase, hydrogen peroxide, and a halide factor to kill microorganisms and tumour cells. This process is sometimes loosely called the respiratory burst , which refers to the sudden rise in oxygen consumption by the phagocytosing neutrophils that is independent of the mitochondrial electron transport chain. [Pg.193]

Holt, M.E., Ryall, M.E.T, and Campbell, A.K. (1984). Albumin inhibits human polymorphonuclear leucocyte luminol-dependent chemiluminescence evidence for oxygen radical scavenging. Br. J. Exp. Path. 65, 231-241. [Pg.258]

Simon, L.M. and Suttorp, N. (1983). Lung cell oxidant injury decrease in polymorphonuclear leucocyte mediated cytotoxicity by N-acetyl cysteine. Am. Rev. Resp. Dis. 127, 286. [Pg.261]

CD44 Known to be z leucocyte adhesion molecule also known as hyaluronic acid cell adhesion molecule (H-CAM), Hermes antigen, extracellular matrix receptor III (ECMIII) present on polymorphonuclear leucocytes CI)45 Known to be z pan leucocyte marker... [Pg.280]

Groeneveld and colleagues [119] have shown that serum nitrate concentrations are higher in symptom-free HIV-1-infected patients than in healthy individuals. NO production was measured in vitro from peripheral blood leucocytes of HIV-1-infected patients after measuring nitrite concentrations from peripheral blood mononuclear cells and polymorphonuclear leucocytes [120, 121]. An increase in nitrite production in AIDS patients, especially in those with opportunistic infections, was also seen. [Pg.21]

The concentrations of nitrite or nitrate in the sera of patients infected with H IV-1 are substantially raised, especially in those with low CD4 cell counts [118]. However, during HIV-1 infection, it is difficult to find out whether the NO production is attributable to virus replication or to opportunistic infections, or both. In vitro there is a substantial rise in nitrite concentrations from blood mononuclear cells and polymorphonuclear leucocytes from patients with AIDS, especially in those with neurological disorders and pulmonary disease caused by intracellular opportunistic pathogens [121]. Interestingly, the serum concentrations of nitrate are positively correlated with plasma and cell-associated viral loads, which suggests that HIV-1 may induce NO synthesis in vivo [119]. However, the results clearly show that there is a close relation between viral replication and iNOS expression or peaks of plasma nitrate in the absence of any opportunistic infections, in either in macaques or infected patients [119, 122, 123]. [Pg.21]

Hallett, M. B., Campbell, A. K. (1983). Two distinct mechanisms for stimulation of oxygen-radical production by polymorphonuclear leucocytes. Biochem. J. 216, 459-65. [Pg.232]

Invasion of the tissues by an infective agent initiates an inflammatory response in the animal. This is non-specific and is mediated primarily by substances released from tissues that are damaged as a result of either trauma or the toxic effects of the infective agent. The major mediator is the vasoactive amine histamine, which causes an increased local blood flow and capillary permeability, resulting in local oedema. A major aspect of the inflammatory response is the involvement of large numbers of phagocytic cells, particularly the polymorphonuclear leucocytes. These are chemotactically attracted to the inflamed tissues and are mainly responsible for the elimination of particulate material. This often results in the destruction of many of these cells and the formation of pus. [Pg.228]

In polymorphonuclear leucocytes (PMNL, neutrophils), secretory responses measured as vitamin B -binding protein release were inhibited by feverfew extract when the response was induced by the chemotactic peptide FMLP or arachidonic acid but not when the calcium ionophore A23187 was... [Pg.229]

Toxicity by metabolism is not confined to the liver since oxidative systems occur in many organs and cells. Amodiaquine is a 4-aminoquinoline antimalarial that has been associated with hepatitis and agranulocytosis. Both side-effects are probably triggered by reactive metabolites produced in the liver or in other sites of the body. For instance polymorphonuclear leucocytes can oxidize amodiaquine. It appears that amodiaquine is metabolized to a quinone imine by the same pathway as that seen in... [Pg.104]

Mancini GM, Hu P, Verheijen FW, van Diggelen OP, Janse HC, Kleijer WJ, Beemer FA, Jen-nekens FG (1992) Salla disease variant in a Dutch patient. Potential value of polymorphonuclear leucocytes for heterozygote detection. Eur J Pediatr 151 590-595... [Pg.350]

Watson, D. L. 1976. The effect of cytophilic IgG2 on phagocytosis by polymorphonuclear leucocytes. Immunology 31, 159-165. [Pg.168]

Ellipsometry can follow the interactions between two types of biological macromolecules, the first of those two bound physically to the surface, the other acting from the solution. The binding of conconavalin A to adsorbed mannan 180) and of cholera toxin to adsorbed ganglioside t83) are examples. The adsorption of complement factors to an antibody-coated surface was monitored by ellipsometry and a modification of the same method was used for quantification of migration inhibition of human polymorphonuclear leucocytes 182). Interaction of proteins and cells with affinity ligands covalently coupled to silicon surfaces has been also studied 183). [Pg.54]

Camkl8 Brain (Hippocampus, cortex, amygdala, spinal cord) Granulocytes (Polymorphonuclear leucocytes) (Verploegen et al., 2000 Sakagami et al., 2005)... [Pg.172]

Ikei, S., Ogawa, M., and Yamaguchi, Y., Blood concentrations of polymorphonuclear leucocyte elastase and interleukin-6 are indicators for the occurrence of multiple organ failures at early stage of acute pancreatitis. J. Gastroenterol. Hepatol. 13,1274-1283 (1993). [Pg.74]

A. Baici, P. Salgam, K. Fehr, and A. BonL Inhibition from polymorphonuclear leucocytes by gold sodium thiomalate and pentoaaiie polysulfate (SPL54). Blochem. Pharmacol 50 703 (1981). [Pg.334]

Korhonen, H.J. and Reiter, B. 1983. Production of H2O2 by bovine blood and milk polymorphonuclear leucocytes. Acta Microbiol. Pol. 32, 53-64. [Pg.259]

Squadrito F, Altavilla D, Squadrito G, Saitta A, Deodato B, Arlotta M, et al. Tacrolimus limits polymorphonuclear leucocyte accumulation and protects against myocardial ischaemia-reperfusion injury. J Mol Cell Cardiol 2000 32 429 140. [Pg.41]

Crude extracts of the ascidian Didemnum candidum exhibit strong inhibitory effects against phospholipase A2 in vitro. A search for the active component led to the discovery of ascidiatrienolide A 33 (20), an eicosatetraene derivative that is closely related to the didemnilactones 34-36 derived from the tunicate Didemnum moseley (27). The latter are endowed with high affinity to the leukotriene B4 receptor of human polymorphonuclear leucocyte membrane fractions. These fatty acid derivatives of marine origin provided yet another opportunity to validate our strategy for ( ,Z)-control outlined in the previous chapter based upon proper matching of the reactivity of the metathesis catalyst with the conformational preferences of a constrained substrate (22). [Pg.8]


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