University of Hertfordshire

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COX-1, and not COX-2 activity, regulates airway function : Relevance to aspirin-sensitive asthma. / Harrington, L.S.; Lucas, R.; McMaster, S.K.; Moreno, L.; Scadding, G.; Mitchell, J.A.; Warner, T.D.

In: FASEB Journal, Vol. 22, No. 11, 01.11.2008, p. 4005-4010.

Research output: Contribution to journalArticle

Harvard

Harrington, LS, Lucas, R, McMaster, SK, Moreno, L, Scadding, G, Mitchell, JA & Warner, TD 2008, 'COX-1, and not COX-2 activity, regulates airway function: Relevance to aspirin-sensitive asthma', FASEB Journal, vol. 22, no. 11, pp. 4005-4010. https://doi.org/10.1096/fj.08-107979

APA

Harrington, L. S., Lucas, R., McMaster, S. K., Moreno, L., Scadding, G., Mitchell, J. A., & Warner, T. D. (2008). COX-1, and not COX-2 activity, regulates airway function: Relevance to aspirin-sensitive asthma. FASEB Journal, 22(11), 4005-4010. https://doi.org/10.1096/fj.08-107979

Vancouver

Harrington LS, Lucas R, McMaster SK, Moreno L, Scadding G, Mitchell JA et al. COX-1, and not COX-2 activity, regulates airway function: Relevance to aspirin-sensitive asthma. FASEB Journal. 2008 Nov 1;22(11):4005-4010. https://doi.org/10.1096/fj.08-107979

Author

Harrington, L.S. ; Lucas, R. ; McMaster, S.K. ; Moreno, L. ; Scadding, G. ; Mitchell, J.A. ; Warner, T.D. / COX-1, and not COX-2 activity, regulates airway function : Relevance to aspirin-sensitive asthma. In: FASEB Journal. 2008 ; Vol. 22, No. 11. pp. 4005-4010.

Bibtex

@article{13a5fc13999340ae97ea31b8671e090c,
title = "COX-1, and not COX-2 activity, regulates airway function: Relevance to aspirin-sensitive asthma",
abstract = "Cyclooxygenase (COX) -1 and COX-2 are expressed in airway cells, where their activities influence functions such as airway hyperreactivity. Clinical data show that mixed COX-1/COX-2 inhibitors such as aspirin, but not COX-2 selective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sensitive individuals. This anomaly has not yet been explained. Here, we have used tissue from genetically modified mice lacking functional COX-1 (COX-1 ), as well as airway tissue from {"}aspirin-sensitive{"} and control patients to address this issue. Bronchi from wild-type mice contained predominantly COX-1 immunoreactivity and contracted in vitro in response to acetylcholine and U46619. Bronchi from COX-1 mice were hyperresponsive to bronchoconstrictors. Inhibitors of COX (naproxen, diclofenac, or ibuprofen) increased bronchoconstriction in tissue from wild-type but not from COX-1 mice. Cells cultured from aspirin-sensitive or control human donors contained similar levels of COX-1 and COX-2 immunoreactivity. COX activity in cells from aspirin-sensitive or tolerant patients was inhibited by aspirin, SC560, which blocks COX-1 selectively, but not by rofecoxib, which is a selective inhibitor of COX-2. These observations show that despite the presence of COX-2, COX-1 is functionally predominant in the airways and explains clinical observations relating to drug specificity in patients with aspirin-sensitive asthma.",
author = "L.S. Harrington and R. Lucas and S.K. McMaster and L. Moreno and G. Scadding and J.A. Mitchell and T.D. Warner",
note = "MEDLINE{\textregistered} is the source for the MeSH terms of this document. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/us/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.",
year = "2008",
month = nov,
day = "1",
doi = "10.1096/fj.08-107979",
language = "English",
volume = "22",
pages = "4005--4010",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "FASEB",
number = "11",

}

RIS

TY - JOUR

T1 - COX-1, and not COX-2 activity, regulates airway function

T2 - Relevance to aspirin-sensitive asthma

AU - Harrington, L.S.

AU - Lucas, R.

AU - McMaster, S.K.

AU - Moreno, L.

AU - Scadding, G.

AU - Mitchell, J.A.

AU - Warner, T.D.

N1 - MEDLINE® is the source for the MeSH terms of this document. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/us/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

PY - 2008/11/1

Y1 - 2008/11/1

N2 - Cyclooxygenase (COX) -1 and COX-2 are expressed in airway cells, where their activities influence functions such as airway hyperreactivity. Clinical data show that mixed COX-1/COX-2 inhibitors such as aspirin, but not COX-2 selective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sensitive individuals. This anomaly has not yet been explained. Here, we have used tissue from genetically modified mice lacking functional COX-1 (COX-1 ), as well as airway tissue from "aspirin-sensitive" and control patients to address this issue. Bronchi from wild-type mice contained predominantly COX-1 immunoreactivity and contracted in vitro in response to acetylcholine and U46619. Bronchi from COX-1 mice were hyperresponsive to bronchoconstrictors. Inhibitors of COX (naproxen, diclofenac, or ibuprofen) increased bronchoconstriction in tissue from wild-type but not from COX-1 mice. Cells cultured from aspirin-sensitive or control human donors contained similar levels of COX-1 and COX-2 immunoreactivity. COX activity in cells from aspirin-sensitive or tolerant patients was inhibited by aspirin, SC560, which blocks COX-1 selectively, but not by rofecoxib, which is a selective inhibitor of COX-2. These observations show that despite the presence of COX-2, COX-1 is functionally predominant in the airways and explains clinical observations relating to drug specificity in patients with aspirin-sensitive asthma.

AB - Cyclooxygenase (COX) -1 and COX-2 are expressed in airway cells, where their activities influence functions such as airway hyperreactivity. Clinical data show that mixed COX-1/COX-2 inhibitors such as aspirin, but not COX-2 selective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sensitive individuals. This anomaly has not yet been explained. Here, we have used tissue from genetically modified mice lacking functional COX-1 (COX-1 ), as well as airway tissue from "aspirin-sensitive" and control patients to address this issue. Bronchi from wild-type mice contained predominantly COX-1 immunoreactivity and contracted in vitro in response to acetylcholine and U46619. Bronchi from COX-1 mice were hyperresponsive to bronchoconstrictors. Inhibitors of COX (naproxen, diclofenac, or ibuprofen) increased bronchoconstriction in tissue from wild-type but not from COX-1 mice. Cells cultured from aspirin-sensitive or control human donors contained similar levels of COX-1 and COX-2 immunoreactivity. COX activity in cells from aspirin-sensitive or tolerant patients was inhibited by aspirin, SC560, which blocks COX-1 selectively, but not by rofecoxib, which is a selective inhibitor of COX-2. These observations show that despite the presence of COX-2, COX-1 is functionally predominant in the airways and explains clinical observations relating to drug specificity in patients with aspirin-sensitive asthma.

U2 - 10.1096/fj.08-107979

DO - 10.1096/fj.08-107979

M3 - Article

AN - SCOPUS:55549128232

VL - 22

SP - 4005

EP - 4010

JO - FASEB Journal

JF - FASEB Journal

SN - 0892-6638

IS - 11

ER -