25 Citations (Scopus)

Abstract

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 languageEnglish (US)
Pages (from-to)61-70
Number of pages10
JournalMethods: A Companion to Methods in Enzymology
Volume10
Issue number1
DOIs
StatePublished - Jan 1 1996

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Macrophages
Lung Injury
Lung
Animals
Ozone
Peroxynitrous Acid
Poisons
Bleomycin
Xenobiotics
Dust
Interleukin-1
Endotoxins
Hydrogen Peroxide
Minerals
Toxicity
Nitric Oxide
Tumor Necrosis Factor-alpha
Tissue
Lipids
Wounds and Injuries

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Molecular Biology

Cite this

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title = "Macrophages, inflammatory mediators, and lung injury",
abstract = "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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Macrophages, inflammatory mediators, and lung injury. / Laskin, Debra; Laskin, Jeffrey.

In: Methods: A Companion to Methods in Enzymology, Vol. 10, No. 1, 01.01.1996, p. 61-70.

Research output: Contribution to journalArticle

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