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: Type I interleukin-1 receptor is required for pulmonary responses to subacute ozone exposure in mice.

Authors: Johnston, Richard A; Mizgerd, Joseph P; Flynt, Lesley; Quinton, Lee J; Williams, Erin S; Shore, Stephanie A

Published In Am J Respir Cell Mol Biol, (2007 Oct)

Abstract: Interleukin (IL)-1, a proinflammatory cytokine, is expressed in the lung after ozone (O(3)) exposure. IL-1 mediates its effects through the type I IL-1 receptor (IL-1RI), the only signaling receptor for both IL-1alpha and IL-1beta. The purpose of this study was to determine the role of IL-1RI in pulmonary responses to O(3.) To that end, wild-type, C57BL/6 (IL-1RI(+/+)) mice and IL-1RI-deficient (IL-1RI(-/-)) mice were exposed to O(3) either subacutely (0.3 ppm for 72 h) or acutely (2 ppm for 3 h). Subacute O(3) exposure increased bronchoalveolar lavage fluid (BALF) protein, interferon-gamma-inducible protein (IP)-10, soluble tumor necrosis factor receptor 1 (sTNFR1), and neutrophils in IL-1RI(+/+) and IL-1RI(-/-) mice. With the exception of IP-10, all outcome indicators were reduced in IL-1RI(-/-) mice. Furthermore, subacute O(3) exposure increased IL-6 mRNA expression in IL-1RI(+/+), but not IL-1RI(-/-) mice. Acute (2 ppm) O(3) exposure increased BALF protein, IL-6, eotaxin, KC, macrophage inflammatory protein (MIP)-2, IP-10, monocyte chemotactic protein-1, sTNFR1, neutrophils, and epithelial cells in IL-1RI(+/+) and IL-1RI(-/-) mice. For IL-6, eotaxin, MIP-2, and sTNFR1, there were small but significant reductions of these outcome indicators in IL-1RI(-/-) versus IL-1RI(+/+) mice at 6 hours after exposure, but not at other time points, whereas other outcome indicators were unaffected by IL-1RI deficiency. These results suggest that IL-1RI is required for O(3)-induced pulmonary inflammation during subacute O(3) exposure, but plays a more minor role during acute O(3) exposure. In addition, these results suggest that the induction of IL-6 via IL-1RI may be important in mediating the effects of O(3) during subacute exposure.

PubMed ID: 17575079 Exiting the NIEHS site

MeSH Terms: Animals; Bronchoalveolar Lavage Fluid/cytology; Cell Count; Female; Gene Expression Regulation/drug effects; Inflammation; Intercellular Adhesion Molecule-1/genetics; Intercellular Adhesion Molecule-1/metabolism; Interleukin-1alpha/genetics; Interleukin-1alpha/metabolism; Interleukin-1beta/genetics; Interleukin-1beta/metabolism; Interleukin-6/genetics; Interleukin-6/metabolism; Lung/drug effects*; Lung/metabolism*; Lung/pathology; Male; Mice; Mice, Inbred C57BL; Ozone/pharmacology*; RNA, Messenger/genetics; RNA, Messenger/metabolism; Receptors, Interleukin-1 Type I/deficiency; Receptors, Interleukin-1 Type I/metabolism*; Respiration/drug effects

Back
to Top