TY - JOUR
T1 - Macrophages, inflammatory mediators, and lung injury
AU - Laskin, Debra L.
AU - Laskin, Jeffrey D.
N1 - Funding Information:
This work was supported by USPHS National Institutes of Health Grants ES04738 and ES05022. Dr. Debra Laskin is a Burroughs Wellcome Scholar. This work was also supported in part by a grant from the Burroughs Wellcome Fund.
PY - 1996/8
Y1 - 1996/8
N2 - 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.
AB - 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.
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U2 - 10.1006/meth.1996.0079
DO - 10.1006/meth.1996.0079
M3 - Article
AN - SCOPUS:0030221126
SN - 1046-2023
VL - 10
SP - 61
EP - 70
JO - Methods: A Companion to Methods in Enzymology
JF - Methods: A Companion to Methods in Enzymology
IS - 1
ER -