Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

National Institute of Environmental Health Sciences

Use this QR code to view the newest version of this document
Use this QR code to view the newest version of this document

Your Environment. Your Health.

Publication Detail

Title: Enhanced production of interleukin-1, tumor necrosis factor-alpha, and fibronectin by rat lung phagocytes following inhalation of a pulmonary irritant.

Authors: Pendino, K J; Shuler, R L; Laskin, J D; Laskin, D L

Published In Am J Respir Cell Mol Biol, (1994 Sep)

Abstract: Interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and fibronectin are macrophage-derived mediators thought to be important in the pathogenesis of lung injury, inflammation, and fibrosis. In the present studies, we examined the effects of acute exposure of rats to the pulmonary irritant, ozone (O3), on production of these mediators by lung phagocytes. Cells were isolated from lungs 48 h after exposure of rats to air or O3 (2 ppm, 3 h). We found that cells from O3-exposed rats released 2- to 3-fold more IL-1 and TNF-alpha into the culture medium than did cells from air-exposed rats. These effects were time dependent, reaching a maximum at 2 and 24 h for IL-1, and 2 to 4 h for TNF-alpha. We also found that alveolar macrophages from O3-treated rats produced increased amounts of fibronectin, both alone and in response to transforming growth factor-beta, lipopolysaccharide, and interferon-gamma when compared with cells from control rats. Examination of immunohistochemically stained tissue sections indicated increased IL-1, TNF-alpha, and fibronectin in lungs from O3-exposed animals when compared with control animals. IL-1 and TNF-alpha were localized in lung macrophages, whereas fibronectin was associated with blood vessel walls and the lung interstitium. These results demonstrate that lung phagocyte production of these inflammatory mediators is elevated following O3 exposure and suggest that they may play a role in oxidant-induced pulmonary inflammation and injury.

PubMed ID: 8086166 Exiting the NIEHS site

MeSH Terms: Administration, Inhalation; Animals; Female; Fibronectins/biosynthesis*; Interferon Type II/pharmacology; Interleukin-1/biosynthesis*; Lipopolysaccharides/pharmacology; Lung/cytology; Lung/immunology*; Macrophages, Alveolar/drug effects; Macrophages, Alveolar/immunology; Ozone/administration & dosage; Ozone/pharmacology*; Phagocytes/drug effects; Phagocytes/immunology*; Rats; Rats, Sprague-Dawley; Specific Pathogen-Free Organisms; Transforming Growth Factor beta/pharmacology; Tumor Necrosis Factor-alpha/biosynthesis*

Back
to Top