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Role of interleukin-6 in murine airway responses to ozone

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

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