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Neutrophil-mediated acute inflammation

A close association has been described for IL-8 and other CXCRl/2 ligands in acute inflammation, including neutrophil-mediated inflammatory diseases such as ischemia-reperfusion injury, bacterial pneumonia, adult respiratory distress syndrome, and other infectious diseases. Neutralization of IL-8 in rabbits has shown dramatic protection in several models of neutrophil-mediated acute inflammation (261,262). [Pg.161]

The time course of chemokine expression seems clearly associated with the time-dependent infiltration of different immune cells in the ischemic brain area. Particularly, early expression of CXC chemokines like CXCLl, CXCL2, CXCL3 and CINC [67-69] has been observed and precedes infiltration of neutrophils [70, 71]. CXCL8 is a potent neutrophil chemotactic and activating factor and most likely plays an important role in neutrophil-mediated acute inflammation [72]. In addition to... [Pg.155]

CXCL8/IL-8, and its murine homologue CXCLl/GRO-a, were initially characterized as neutrophil chemoattractants and as such have been shown to play an important role in neutrophil-mediated acute inflammation (Harada et al., 1994). However, it is now known to have much more wide-ranging effects on both non-leukocyte and leukocyte subtypes of cells (Harada et al., 1994). The CXCL8/CXCL1 receptor, CXCR2, is also expressed on the surface of monocytes (Moser et al., 1993 Chuntharapai et al.. [Pg.230]

N. Mukaida, T. Matsumoto, K. Yokoi, A. Harada, and K. Matsushima. Inhibition of Neutrophil-Mediated Acute Inflammatory Injury by an Antibody Against Interleukin-8(IL-8), Inflammation Research. 47(suppl 3) (1998) 151-157. [Pg.198]

Endogenous histamine has a modulating role in a variety of inflammatory and immune responses. Upon injury to a tissue, released histamine causes local vasodilation and leakage of plasma-containing mediators of acute inflammation (complement, C-reactive protein) and antibodies. Histamine has an active chemotactic attraction for inflammatory cells (neutrophils, eosinophils, basophils, monocytes, and lymphocytes). Histamine inhibits the release of lysosome contents and several T- and B-lymphocyte functions. Most of these actions are mediated by H2 or H4 receptors. Release of peptides from nerves in response to inflammation is also probably modulated by histamine, in this case acting through presynaptic H3 receptors. [Pg.348]

Many mediators of inflammation have been identified— cytokines IL-6, tumor necrosis factor alpha cell adhesion molecules intracellular adhesion molecule-1 (ICAM-I), P-selectin and acute phase reactants CR.R fibrinogen, serum amyloid A, and soluble CD40 (Fig. I) (3). Myeloperoxidase is an enzyme secreted from monocytes, neutrophils, and macrophages. A single measurement taken from patient with chest pain in the emergency department predicted the early risk of myocardial infarction and the risk of major cardiac of ends in the next 30 days to six months (15). [Pg.467]

Terui T, Ozawa M, Tagami Role of neutrophils in induction of acute inflammation in T-cell-mediated immune dermatosis, psoriasis A neutrophil-associated inflammation-boosting loop. Exp Dermatol 2000 9 1. [Pg.91]

During the initial acute inflammation phase, which is protective in nature, PUFA provide a steady supply of pro-inflammatory chemotactic lipid mediators such as prostaglandins and leukotrienes that help to recruit polymorphonuclear neutrophils... [Pg.173]


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See also in sourсe #XX -- [ Pg.230 ]




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