Showing papers by "William G. Austen published in 2001"
TL;DR: SCR1sLe(x) is more effective than sCR1 in moderating skeletal muscle reperfusion injury, by antagonizing neutrophil endothelial selectin interaction and complement activation.
Abstract: The role of the sialyl Lewisx (sLex)-decorated version of soluble complement receptor type 1 (sCR1) in moderating skeletal muscle reperfusion injury, by antagonizing neutrophil endothelial selectin...
45 citations
TL;DR: Data indicate that mast cells mediate complement activation, via chymase degranulation, after acid aspiration, and this mast cell activity likely is regulated by the release of substance P.
Abstract: A significant role for the alternative complement pathway in acid aspiration has been demonstrated by the observation that C3 but not C4 genetic knockout mice are protected from permeability edema. Using mast cell-deficient mice (W/W v ), we tested the hypothesis that mast cells mediate complement activation after acid aspiration. Tracheostomy tubes were placed in anesthetized mice and 2 mUkg 0.1 N HCL was instilled in the trachea. After 4 h, extravasation of 125 I-albumin was used to calculate lung vascular permeability. The serum alternative complement pathway hemolytic activity was examined, and lung immunohistochemistry was performed. Lung permeability in W/W v mice was 62% less than that of mast cell sufficient (+/+) animals and similar to +/+ mice treated with the chymase inhibitor chymostatin (65% decrease). Treatment of +/+ mice with D-PRO 2 , D-TRP 7,9 -Substance P, an antagonist to the neuropeptide substance P, reduced injury by 66%. Serum complement hemolytic activity was intact in injured W/W v mice and +/+ animals treated with chymostatin or dpdt-sp, but was decreased to 65% in the injured untreated +/+ group. Alveolar C3 deposition was intense in injured untreated +/+ mice but absent in the other groups. We interpret these data to indicate that mast cells mediate complement activation, via chymase degranulation, after acid aspiration. This mast cell activity likely is regulated by the release of substance P.
11 citations
TL;DR: It is concluded that sCR1sLe(x) moderates permeability by antagonizing complement activation and neutrophil adhesion and delayed complement and neutrophic antagonism significantly reduces injury.
Abstract: The potentially enhanced anti-inflammatory effects of the sialyl Lewisx(sLex)-decorated version of soluble complement receptor type 1 (sCR1) in moderating acid aspiration injury are examined. HCl w...
11 citations