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Role of interleukin-6 in murine airway responses to ozone.

Abstract

This study sought to examine the role of interleukin-6 (IL-6) in ozone (O(3))-induced airway injury, inflammation, and hyperresponsiveness (AHR). Subacute (72 h) exposure to 0.3 ppm O(3) 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 O(3) 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 O(3) exposure in IL-6(-/-) mice. Increases in BALF neutrophils induced by O(3) (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 O(3). Acute O(3) exposure caused AHR in both groups of mice, but there was no genotype-related difference in the magnitude of O(3)-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 O(3) exposure, but has no effect on O(3)-induced AHR.

Authors+Show Affiliations

Bldg. 1, Rm. 1304A, Physiology Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115-6021, USA. rajohnst@hsph.harvard.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15516495

Citation

Johnston, Richard A., et al. "Role of Interleukin-6 in Murine Airway Responses to Ozone." American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 288, no. 2, 2005, pp. L390-7.
Johnston RA, Schwartzman IN, Flynt L, et al. Role of interleukin-6 in murine airway responses to ozone. Am J Physiol Lung Cell Mol Physiol. 2005;288(2):L390-7.
Johnston, R. A., Schwartzman, I. N., Flynt, L., & Shore, S. A. (2005). Role of interleukin-6 in murine airway responses to ozone. American Journal of Physiology. Lung Cellular and Molecular Physiology, 288(2), pp. L390-7.
Johnston RA, et al. Role of Interleukin-6 in Murine Airway Responses to Ozone. Am J Physiol Lung Cell Mol Physiol. 2005;288(2):L390-7. PubMed PMID: 15516495.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of interleukin-6 in murine airway responses to ozone. AU - Johnston,Richard A, AU - Schwartzman,Igor N, AU - Flynt,Lesley, AU - Shore,Stephanie A, Y1 - 2004/10/29/ PY - 2004/11/2/pubmed PY - 2005/2/12/medline PY - 2004/11/2/entrez SP - L390 EP - 7 JF - American journal of physiology. Lung cellular and molecular physiology JO - Am. J. Physiol. Lung Cell Mol. Physiol. VL - 288 IS - 2 N2 - This study sought to examine the role of interleukin-6 (IL-6) in ozone (O(3))-induced airway injury, inflammation, and hyperresponsiveness (AHR). Subacute (72 h) exposure to 0.3 ppm O(3) 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 O(3) 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 O(3) exposure in IL-6(-/-) mice. Increases in BALF neutrophils induced by O(3) (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 O(3). Acute O(3) exposure caused AHR in both groups of mice, but there was no genotype-related difference in the magnitude of O(3)-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 O(3) exposure, but has no effect on O(3)-induced AHR. SN - 1040-0605 UR - https://www.unboundmedicine.com/medline/citation/15516495/Role_of_interleukin_6_in_murine_airway_responses_to_ozone_ L2 - http://www.physiology.org/doi/full/10.1152/ajplung.00007.2004?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -