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Am J Physiol Lung Cell Mol Physiol 288: L390-L397, 2005. First published October 29, 2004; doi:10.1152/ajplung.00007.2004
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Role of interleukin-6 in murine airway responses to ozone

Richard A. Johnston, Igor N. Schwartzman, Lesley Flynt, and Stephanie A. Shore

Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts

Submitted 13 January 2004 ; accepted in final form 22 October 2004

This study sought to examine the role of interleukin-6 (IL-6) in ozone (O3)-induced airway injury, inflammation, and hyperresponsiveness (AHR). Subacute (72 h) exposure to 0.3 ppm O3 significantly elevated bronchoalveolar lavage fluid (BALF) protein, neutrophils, and soluble TNF receptors (sTNFR1 and sTNFR2) in wild-type C57BL/6 (IL-6+/+) mice; however, all four outcome indicators were significantly reduced in IL-6-deficient (IL-6–/–) compared with IL-6+/+ mice. Acute O3 exposure (2 ppm for 3 h) increased BALF protein, KC, macrophage inflammatory protein(MIP)-2, eotaxin, sTNFR1, and sTNFR2 in IL-6+/+ mice. However, MIP-2 and sTNFR2 were not significantly increased following O3 exposure in IL-6–/– mice. Increases in BALF neutrophils induced by O3 (2 ppm for 3 h) were also significantly reduced in IL-6–/– vs. IL-6+/+ mice. Airway responsiveness to methacholine was measured by whole body plethysmography before and following acute (3 h) or subacute (72 h) exposure to 0.3 ppm O3. Acute O3 exposure caused AHR in both groups of mice, but there was no genotype-related difference in the magnitude of O3-induced AHR. AHR was absent in mice of either genotype exposed for 72 h. Our results indicate that IL-6 deficiency reduces airway neutrophilia, as well as the levels of BALF sTNFR1 and sTNFR2 following acute high dose and/or subacute low-dose O3 exposure, but has no effect on O3-induced AHR.

airway responsiveness; inflammation; injury; neutrophil; soluble tumor necrosis factor receptor


Address for reprint requests and other correspondence: R. A. Johnston, Bldg. 1, Rm. 1304A, Physiology Program, Dept. of Environmental Health, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115-6021 (E-mail: rajohnst{at}hsph.harvard.edu)




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