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Interleukin-1 receptor antagonist attenuates airway hyperresponsiveness following exposure to ozone.
Am J Respir Cell Mol Biol 2004; 30(6):830-6AJ

Abstract

The role of an interleukin (IL)-1 receptor antagonist (IL-1Ra) on the development of airway hyperresponsiveness (AHR) and airway inflammation following acute O(3) exposure in mice was investigated. Exposure of C57/BL6 mice to O(3) 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-1beta expression, assessed by gene microarray, was increased 2-fold 4 h after O(3) exposure, and returned to baseline levels by 24 h. Levels of IL-1beta in lung homogenates were also increased 8 h after O(3) exposure. Administration of (human) IL-1Ra before and after O(3) 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 O(3) 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 O(3) exposure. In summary, acute exposure to O(3) induces AHR, neutrophilic inflammation, epithelial damage, and IL-1. An IL-1Ra effectively prevents the development of altered airway function, inflammation, and structural damage.

Authors+Show Affiliations

Department of Pediatrics, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

14754758

Citation

Park, Jung-Won, et al. "Interleukin-1 Receptor Antagonist Attenuates Airway Hyperresponsiveness Following Exposure to Ozone." American Journal of Respiratory Cell and Molecular Biology, vol. 30, no. 6, 2004, pp. 830-6.
Park JW, Taube C, Swasey C, et al. Interleukin-1 receptor antagonist attenuates airway hyperresponsiveness following exposure to ozone. Am J Respir Cell Mol Biol. 2004;30(6):830-6.
Park, J. W., Taube, C., Swasey, C., Kodama, T., Joetham, A., Balhorn, A., ... Gelfand, E. W. (2004). Interleukin-1 receptor antagonist attenuates airway hyperresponsiveness following exposure to ozone. American Journal of Respiratory Cell and Molecular Biology, 30(6), pp. 830-6.
Park JW, et al. Interleukin-1 Receptor Antagonist Attenuates Airway Hyperresponsiveness Following Exposure to Ozone. Am J Respir Cell Mol Biol. 2004;30(6):830-6. PubMed PMID: 14754758.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-1 receptor antagonist attenuates airway hyperresponsiveness following exposure to ozone. AU - Park,Jung-Won, AU - Taube,Christian, AU - Swasey,Christina, AU - Kodama,Taku, AU - Joetham,Anthony, AU - Balhorn,Annette, AU - Takeda,Katsuyuki, AU - Miyahara,Nobuaki, AU - Allen,Corrie B, AU - Dakhama,Azzeddine, AU - Kim,Soo-Hyun, AU - Dinarello,Charles A, AU - Gelfand,Erwin W, Y1 - 2004/01/30/ PY - 2004/2/3/pubmed PY - 2004/6/30/medline PY - 2004/2/3/entrez SP - 830 EP - 6 JF - American journal of respiratory cell and molecular biology JO - Am. J. Respir. Cell Mol. Biol. VL - 30 IS - 6 N2 - The role of an interleukin (IL)-1 receptor antagonist (IL-1Ra) on the development of airway hyperresponsiveness (AHR) and airway inflammation following acute O(3) exposure in mice was investigated. Exposure of C57/BL6 mice to O(3) 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-1beta expression, assessed by gene microarray, was increased 2-fold 4 h after O(3) exposure, and returned to baseline levels by 24 h. Levels of IL-1beta in lung homogenates were also increased 8 h after O(3) exposure. Administration of (human) IL-1Ra before and after O(3) 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 O(3) 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 O(3) exposure. In summary, acute exposure to O(3) induces AHR, neutrophilic inflammation, epithelial damage, and IL-1. An IL-1Ra effectively prevents the development of altered airway function, inflammation, and structural damage. SN - 1044-1549 UR - https://www.unboundmedicine.com/medline/citation/14754758/Interleukin_1_receptor_antagonist_attenuates_airway_hyperresponsiveness_following_exposure_to_ozone_ L2 - http://www.atsjournals.org/doi/full/10.1165/rcmb.2003-0373OC?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -