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Published ahead of print on January 30, 2004, doi:10.1165/rcmb.2003-0373OC
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American Journal of Respiratory Cell and Molecular Biology. Vol. 30, pp. 830-836, 2004
© 2004 American Thoracic Society
DOI: 10.1165/rcmb.2003-0373OC

Interleukin-1 Receptor Antagonist Attenuates Airway Hyperresponsiveness Following Exposure to Ozone

Jung-Won Park, Christian Taube, Christina Swasey, Taku Kodama, Anthony Joetham, Annette Balhorn, Katsuyuki Takeda, Nobuaki Miyahara, Corrie B. Allen, Azzeddine Dakhama, Soo-Hyun Kim, Charles A. Dinarello and Erwin W. Gelfand

Department of Pediatrics, National Jewish Medical and Research Center, Denver; and Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado

Address correspondence to: Erwin W. Gelfand, M.D., Department of Pediatrics, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206. E-mail: gelfande{at}njc.org

The role of an interleukin (IL)-1 receptor antagonist (IL-1Ra) on the development of airway hyperresponsiveness (AHR) and airway inflammation following acute O3 exposure in mice was investigated. Exposure of C57/BL6 mice to O3 at a concentration of 2.0 ppm or filtered air for 3 h resulted in increases in airway responsiveness to inhaled methacholine (MCh) 8 and 16 h after the exposure, and an increase in neutrophils in the bronchoalveolar lavage (BAL) fluid. IL-1ß expression, assessed by gene microarray, was increased 2-fold 4 h after O3 exposure, and returned to baseline levels by 24 h. Levels of IL-1ß in lung homogenates were also increased 8 h after O3 exposure. Administration of (human) IL-1Ra before and after O3 exposure prevented development of AHR and decreased BAL fluid neutrophilia. Increases in chemokine levels in lung homogenates, tumor necrosis factor-{alpha}, MIP-2, and keratinocyte chemoattractant following O3 exposure were prevented by IL-1Ra. Inhalation of dexamethasone, an inhibitor of IL-1 production, blocked the development of AHR, BAL fluid neutrophilia, and decreased levels of IL-1 following O3 exposure. In summary, acute exposure to O3 induces AHR, neutrophilic inflammation, epithelial damage, and IL-1. An IL-1Ra effectively prevents the development of altered airway function, inflammation, and structural damage.

Abbreviations: airway hyperresponsiveness, AHR • bronchoalveolar lavage, BAL • cyclooxygenase 2, COX-2 • enzyme-linked immunosorbent assay, ELISA • interleukin, IL • inducible nitric oxide synthase, iNOS • macrophage inflammatory protein, MIP • tumor necrosis factor-{alpha}, TNF-{alpha}




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