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Am J Physiol Lung Cell Mol Physiol (October 29, 2004). doi:10.1152/ajplung.00007.2004
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Submitted on January 13, 2004
Accepted on October 22, 2004

ROLE OF INTERLEUKIN-6 IN MURINE AIRWAY RESPONSES TO OZONE

Richard A. Johnston1*, Igor N. Schwartzman1, Lesley Flynt1, and Stephanie A. Shore1

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.

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 wildtype, C57BL/6 (IL-6+/+) mice; however, all four outcome indicators were significantly reduced in IL-6 deficient (IL-6-/-) compared to IL-6+/+ mice. Acute O3 exposure (2 ppm for 3 h) increased BALF protein, KC, 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-/- versus IL-6+/+ mice. Airway responsiveness to methacholine was measured by whole-body plethysmography prior to 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.




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