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Leukocyte polymorphonuclear

Eosinophils develop in the bone marrow where they also mature. They are then released into the blood followed by their migration into the tissue spaces. Eosinophils comprise 1-5% of blood leukocytes in nonatopic individuals. They are present in thymus, spleen, lymph nodes, uterus and lower GI tract. Under normal conditions, they are not present in the skin, lungs or esophagus. They can live up to 72 h in the tissue. Their migration to the site of inflammation or parasitic infection is directed by leukotriene B4 and chemokines eotaxin (CCL11) and RANTES (CCL5). They [Pg.17]

Eosinophils are attracted by proteins released by T cells, mast cells and basophils [eosinophil chemotactic factor of anaphylaxis (ECF-A)]. They bind schistosomulae coated with IgG or IgE, degranulate and release major basic protein, which is toxic. Eosinophils also release histaminase and aryl sulfatase, which inactivates histamine and Slow reacting substance of anaphylaxis (SRS-A). This results in antiinflammatory effects and inhibits migration of granulocytes to the site of injury. [Pg.18]


After insertion of an lUD, polymorphonuclear leukocytes and macrophages accumulate in the uterine cavity. These cells appear to phagocytize sperm and Hberate a blastotoxic toxin (92,93). Intrauterine devices also may create a hostile environment, perhaps because antibodies are produced that interfere with implantation of the fertilized ovum (93). [Pg.121]

Arnhold, J., Reichl, S., Peikovic, M., and Vocks, A. (2002). Pholasin luminescence of polymorphonuclear leukocytes. In Stanley, P. E., and Kricka, L. J. (eds.), Bioluminescence and Chemiluminescence, Progress and Current Applications, pp. 233-236. World Scientific, Singapore. [Pg.380]

Mice that are homozygous for a disrupted Bx or B2 receptor gene are healthy, fertile and normotensive. In Bx-deficient mice, bacterial lipopolysaccharide-induced hypotension is diminished and the recruitment of polymorphonuclear leukocytes to the sites of tissue injury is impaired, and the animals show signs of hypoalgesia. Deletion of the B2 gene in mice leads to salt-sensitive hypertension and altered nociception. [Pg.675]

Polychloromethylsulphonylbiphenyls, mass spectra of 154, 155 Polyenes, synthesis of 771 Polymerization, of sulphoxides 846 Polymer-supported reagents 928 Polymorphonuclear leukocytes 854 Poly(olefin sulphonejs, radiolysis of 916-922 Polysulphones, radiolysis of 913 Population analysis 14, 15, 21, 22 Propargylic sulphenates, rearrangement of 736-739... [Pg.1203]

Redmond, T., Zigmond, S.H. (1993). Distribution of F-actin elongation sites in lysed polymorphonuclear leukocytes parallels the distribution of endogenous F-actin. Cell Mot. Cytoskel. 26, 7-28. [Pg.105]

Schmalsteig, F.C, Rudloff, H.E., Hillman, G.R., Anderson, D.C. (1986). Two-dimensional and three-dimensional movement of human polymorphonuclear leukocytes Two fundamentally different mechanisms of locomotion. J. Leukocyte Biol. 40,677-691. [Pg.105]

Johansen, K.S., Berger, E.M., Repine, J.E. (1983). Effect of temperature on polymorphonuclear leukocyte function. Acta Pathol. Microbiol. Immunol. Scand. Sect C, Immunol. 91, 355-359. [Pg.455]

Liver, the major site of purine nucleotide biosynthesis, provides purines and purine nucleosides for salvage and utilization by tissues incapable of their biosynthesis. For example, human brain has a low level of PRPP amidotransferase (reaction 2, Figure 34-2) and hence depends in part on exogenous purines. Erythrocytes and polymorphonuclear leukocytes cannot synthesize 5-phosphoribosylamine (strucmre III, Figure 34-2)... [Pg.294]

Key PMN, polymorphonuclear leukocytes EC, endothelial cell lymphs, lymphocytes CD, cluster of differentiation iCAM, intercellular adhesion molecule LFA-1, lymphocyte function-associated antigen-1 PECAM-1, platelet endothelial cell adhesion cell molecule-1. [Pg.529]

Borregaard N, Cowland JB Granules of the human neutrophilic polymorphonuclear leukocyte. Blood 1997 89 3503. [Pg.625]

Au(CN)2] inhibits the oxidative burst of polymorphonuclear leukocytes and the proliferation of lymphocytes in vitro (both types of cells actively participate in the development and maintenance of inflammatory processes of rheumatoid disease) [71]. It is also far more toxic than gold(I) thiolates to bacteria, plants and animals. [Pg.295]

Thomas, M.J. (1992). Urate causes the human polymorphonuclear leukocyte to secrete superoxide. Free Rad. Biol. Med. 12, 89-91. [Pg.52]

Hallenbeck, J.M., Dutka, A.J., Tanishima, T., Kochanek, P.M., Kumaroo, K.K., Thompson, C.B., Obrenovitch, T.P. and Contreras, T.J. (1986). Polymorphonuclear leukocyte accumulation in brain regions with low blood flow during the early post ischemic period. Stroke 17, 246-253. [Pg.81]

Sola, P., Godessart, N., Vila, L., Puig, L. and Moragas, J.M. (1992). Epidermal cell-polymorphonuclear leukocyte cooperation in the formation of leukotriene B4 by transcellular biosynthesis. J. Invest. Dermatol. 98, 333-339. [Pg.124]

Levine, P.H., Hardin, J.C., Scoon, K.L. and Krinsky, N.I. (1981). Effect of corticosteroids on the production of superoxide and hydrogen peroxide and the appearance of chemiluminescence by phagocytosing polymorphonuclear leukocytes. Inflammation 5, 19-27. [Pg.167]

Molin, L. and Stendahl, O. (1979). The effect of sulfasalazine and its active components on human polymorphonuclear leukocyte function in relation to ulcerative colitis. Acta Med. Scand. 206, 451-457. [Pg.167]

Hatzelman, A. and Ullrich, V. (1987). Regulation of 5-lipoxygenase activity by the glutathione status in human polymorphonuclear leukocytes. Eur. J. Biochem. 169, 175-184. [Pg.229]

Biemond, P., Van Eijk, H.G., Swaak, A.J.G. and Koster, J.F. (1984). Iron mobilization from ferritin by superoxide derived from stimulated polymorphonuclear leukocytes. Possible mechanism in inflammation diseases. J. Clin. Invest. 73, 1576-1579. [Pg.256]

Doll, N.J., Stankus, R.P., Goldbach, S. and Salvaggio, J.E. (1982). In vitro effect of asbestos fibers on polymorphonuclear leukocyte function. Int. Arch. Allergy Appl. Immunol. 68, 17-21. [Pg.257]

Evans, P.H., Morgan, L.G., Yano, E. and Urano, N. (1992a), Chemiluminescent detection of free radical generation by stimulated polymorphonuclear leukocytes in vitro effect of nickel compounds. In Nickel and Human Health Current Perspectives (eds. E. Nieboer and J.O. Nriagu) pp. 363-373. Wiley, New York. [Pg.257]

Frenkel, K. and Chrzan, K. (1987). Hydrogen peroxide formation and DNA base modification by tumor promoter-activated polymorphonuclear leukocytes. Carcinogenesis 8, 455-460. [Pg.258]

Kensler, T.W. and Trush, M.A, (1983). Inhibition of oxygen radical metabolism in phorbol ester-activated polymorphonuclear leukocytes by an antitumor promoting copper complex with superoxide dismutase-mimetic activity. Biochem. Pharmacol. 32, 3485-3487. [Pg.259]

Thomas, M.J., Shirley, P.S., Hedrick, C.C. and DeChatelet, L.R. (1986). Role of free radical processes in stimulated human polymorphonuclear leukocytes. Biochemistry 25, 8042-8048. [Pg.261]

BUN, blood urea nitrogen IV, intravenous Na, sodium PMN polymorphonuclear leukocyte TIPS, transjugular intrahepatic portosystemic shunt. (From Chung RT, Podolsky DK. Cirrhosis and its complications. In Kasper DL, Braunwald E, Fauci AS, et a I, (eds.) Harrison s Principles of Internal Medicine. 16th ed. New York McGraw-Hill, 2005 1858-1869, with permission.)... [Pg.334]

Microscopic examination of stool is extremely useful and reveals multiple polymorphonuclear leukocytes and red blood cells. Diagnosis is usually confirmed by stool culture. [Pg.1118]

Lloyd AR, Biragyn A, Johnston JA, et al. Granulocyte-colony stimulating factor and lipopolysaccharide regulate the expression of interleukin 8 receptors on polymorphonuclear leukocytes. J Biol Chem 1995 270 28188-28192. [Pg.83]

Terashima T, English D, Hogg JC, van Eeden SF. Release of polymorphonuclear leukocytes from the bone marrow by interleukin-8. Blood 1998 92 1062-1069. [Pg.85]

Early infiltration of polymorphonuclear leukocytes and monocyte/macro-phages into the transplanted organ occurs soon after reperfusion of the transplant is initiated. In the context of transplantation, oxygen deprivation and general tissue stress of the graft leads to the activation of proinflammatory cytokines and the upregulation of the adhesion molecules required for leukocyte... [Pg.142]

El-Sawy T, Belperio JA, Strieter RM, Remick DG, Fairchild RL. Inhibition of polymorphonuclear leukocyte-mediated graft damage synergizes with short-term costimulatory blockade to prevent cardiac allograft rejection. Circulation 2005 112 320-331. [Pg.151]


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Polymorphonuclear leukocytes (PMN)

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