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1 Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: rajohnst{at}hsph.harvard.edu.
Ozone (O3), a common air pollutant, induces airway inflammation and airway hyperresponsiveness. In mice, the neutrophil chemokines KC and macrophage inflammatory protein-2 (MIP-2) are expressed in the lungs following O3 exposure. The purpose of this study was to determine whether CXCR2, the receptor for these chemokines, is essential to O3-induced neutrophil recruitment, injury to the lungs, and increases in respiratory system responsiveness to methacholine (MCh). O3 exposure (1 ppm for 3 h) increased the number of neutrophils in the bronchoalveolar lavage fluid (BALF) of wildtype (BALB/c) and CXCR2-deficient mice. However, CXCR2-deficient mice had significantly fewer emigrated neutrophils than did wildtype mice. The numbers of neutrophils in the blood and concentrations of BALF KC and MIP-2 did not differ between genotypes. Altogether, these data suggest CXCR2 is essential for maximal chemokine-directed migration of neutrophils to the airspaces. In wildtype mice, O3 exposure increased BALF epithelial cell numbers and total protein levels, two indirect measures of lung injury. In contrast, in CXCR2-deficient mice, the number of BALF epithelial cells was not increased by O3 exposure. Responses to inhaled MCh were measured by whole-body plethysmography using enhanced pause as the outcome indicator. O3 exposure increased responses to inhaled MCh in both wildtype and CXCR2-deficient mice 3 h after O3 exposure. However, at 24 h after exposure, responses to inhaled MCh were elevated in wildtype but not CXCR2-deficient mice. These results indicate that CXCR2 is essential for maximal neutrophil recruitment, epithelial cell sloughing, and persistent increases in MCh responsiveness after an acute O3 exposure.
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