Macrophages and the various inflammatory mediators they release have been implicated in lung injury induced by a number of different pulmonary toxicants. Exposure of humans or experimental animals to toxic doses of xenobiotics such as ozone, bleomycin, or mineral dusts results in an accumulation of macrophages in the lung. These cells are activated to release increased amounts of proinflammatory and cytotoxic mediators such as hydrogen peroxide, nitric oxide, peroxynitrite, bioactive lipids, interleukin-1, and tumor necrosis factor-α. Each of these mediators has the capacity to induce tissue injury directly and/or augment the inflammatory response. When animals are treated with agents that block macrophage functioning and/or mediator release, pulmonary injury induced by agents such as ozone or endotoxin is abrogated. Conversely, treatment of animals with macrophage activators enhances toxicant-induced lung damage. These data provide direct support for a role of macrophages and inflammatory mediators in pulmonary toxicity.
|Original language||English (US)|
|Number of pages||10|
|Journal||Methods: A Companion to Methods in Enzymology|
|State||Published - Aug 1996|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Biochemistry, Genetics and Molecular Biology(all)