Macrophage stimulation and the inflammatory response to asbestos.
Chrysotile fibers injected into the peritoneal cavity of mice elicit a cellular exudate. Macrophages appearing in this exudate produce high levels of the neutral protease, plasminogen activator, when compared with the resident peritoneal macrophage population. In contrast, the levels of lysozyme and two lysosomal enzymes are the same for the two macrophage types. The asbestos-induced macrophages producing the plasminogen activator appear to have descended from recently divided precursors. Low concentrations of anti-inflammatory glucocorticoids inhibit macrophage plasminogen activator synthesis. Preliminary experiments indicate that different asbestos types induce hyperemia in skin, and also shorten the partial thromboplastin time of plasma and generate the release of kinins. These observations could be interrelated and are suggested as representing some aspects of the inflammatory response of the host to asbestos exposure.
D000118:Acetylglucosaminidase / Q000378:metabolism; D000818:Animals; D001194:Asbestos / Q000633:toxicity*; D001202:Ascitic Fluid / Q000166:cytology; D003907:Dexamethasone / Q000494:pharmacology; D005342:Fibrinolysis / Q000187:drug effects; D007249:Inflammation / Q000209:etiology*; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D010960:Plasminogen Activators / Q000378:metabolism; D001616:beta-Galactosidase / Q000378:metabolism
D001194:Asbestos; D003907:Dexamethasone; D001616:beta-Galactosidase; D000118:Acetylglucosaminidase; D010960:Plasminogen Activators