Published ahead of print on June 15, 2007, doi:10.1165/rcmb.2006-0315OC Am. J. Respir. Cell Mol. Biol., Volume 37, Number 4, October 2007, 477-484 A more recent version of this article appeared on October 1, 2007
Submitted on August 25, 2006 Type I Interleukin-1 Receptor is Required for Pulmonary Responses to Subacute Ozone Exposure in MiceRichard A Johnston1*,1 Department of Environmental Health, Harvard School of Public Health, Molecular and Integrative Physiological Sciences Program, Boston, MA, USA * To whom correspondence should be addressed. E-mail: rajohnst{at}utmb.edu.
Interleukin (IL)-1, a pro-inflammatory cytokine, is expressed in the lung following ozone (O3) exposure. IL-1 mediates its effects through the type I IL-1 receptor (IL-1RI), the only signaling receptor for both IL-1
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and IL-1
. The purpose of this study was to determine the role of IL-1RI in pulmonary responses to O3. To that end, wildtype, C57BL/6 (IL-1RI+/+) mice and IL-1RI-deficient (IL-1RI-/-) mice were exposed to O3 either subacutely (0.3 ppm for 72 h) or acutely (2 ppm for 3 h). Subacute O3 exposure increased bronchoalveolar lavage fluid (BALF) protein, IP-10, 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 O3 exposure increased IL-6 mRNA expression in IL-1RI+/+, but not IL-1RI-/- mice. Acute (2 ppm) O3 exposure increased BALF protein, IL-6, eotaxin, KC, MIP-2, IP-10, MCP-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 h 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 O3-induced pulmonary inflammation during subacute O3 exposure, but plays a more minor role during acute O3 exposure. In addition, these results suggest that the induction of IL-6 via IL-1RI may be important in mediating the effects of O3 during subacute exposure.
