Macrophages, reactive nitrogen species, and lung injury

Debra L. Laskin, Vasanthi R. Sunil, Ladan Fakhrzadeh, Angela Groves, Andrew J. Gow, Jeffrey D. Laskin

Research output: Chapter in Book/Report/Conference proceedingConference contribution

22 Citations (Scopus)

Abstract

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.

Original languageEnglish
Title of host publicationOxidative/Nitrosative Stress and Disease
Pages60-65
Number of pages6
Volume1203
DOIs
Publication statusPublished - Aug 2010
Externally publishedYes

Publication series

NameAnnals of the New York Academy of Sciences
Volume1203
ISSN (Print)00778923
ISSN (Electronic)17496632

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Keywords

  • caveolin
  • macrophages
  • nitric oxide
  • ozone
  • TNFα

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Laskin, D. L., Sunil, V. R., Fakhrzadeh, L., Groves, A., Gow, A. J., & Laskin, J. D. (2010). Macrophages, reactive nitrogen species, and lung injury. In Oxidative/Nitrosative Stress and Disease (Vol. 1203, pp. 60-65). (Annals of the New York Academy of Sciences; Vol. 1203). https://doi.org/10.1111/j.1749-6632.2010.05607.x