Macrophages, reactive nitrogen species, and lung injury.

Evidence has accumulated over the past several years demonstrating that lung injury following inhalation of irritants like ozone is due, not only to direct effects of the chemical, but also indirectly to the actions of inflammatory mediators released by infiltrating macrophages. Among the mediators involved in the cytotoxic process, reactive nitrogen species (RNS) are of particular interest because of their well-documented cytotoxic potential. Findings that macrophage suppression blocks RNS production and ozone-induced toxicity provide strong support for a role of these cells and inflammatory mediators in lung injury. Recent investigations have focused on understanding pathways by which macrophages become activated to release RNS. One protein that has attracted considerable attention is caveolin-1, a membrane scaffolding molecule that functions to negatively regulate cell signaling. The fact that expression of caveolin-1 is down-regulated in macrophages after ozone inhalation suggests a mechanism controlling the release of cytotoxic mediators by these inflammatory cells.
AuthorsDebra L Laskin, Vasanthi R Sunil, Ladan Fakhrzadeh, Angela Groves, Andrew J Gow, Jeffrey D Laskin
JournalAnnals of the New York Academy of Sciences (Ann N Y Acad Sci) Vol. 1203 Pg. 60-5 (Aug 2010) ISSN: 1749-6632 [Electronic] United States
PMID20716284 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
Chemical References
  • Caveolin 1
  • Reactive Nitrogen Species
  • Tumor Necrosis Factor-alpha
  • Animals
  • Caveolin 1 (antagonists & inhibitors, biosynthesis, physiology)
  • Humans
  • Lung Injury (immunology, metabolism, pathology)
  • Macrophages (immunology, pathology, secretion)
  • Reactive Nitrogen Species (physiology, secretion)
  • Signal Transduction (immunology)
  • Tumor Necrosis Factor-alpha (metabolism, physiology)

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