Table of Contents
Journal of Allergy
Volume 2012, Article ID 403059, 7 pages
http://dx.doi.org/10.1155/2012/403059
Research Article

Combined Beta-Agonists and Corticosteroids Do Not Inhibit Extracellular Matrix Protein Production In Vitro

1Division of Cell Biology, Woolcock Institute of Medical Research, Sydney, P.O. Box M77, Missenden Road, NSW 2050, Australia
2Discipline of Pharmacology, The University of Sydney, Sydney, NSW 2006, Australia

Received 7 July 2011; Accepted 31 October 2011

Academic Editor: Peter Borger

Copyright © 2012 Qi Ge et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Persistent asthma is characterized by airway remodeling. Whereas we have previously shown that neither β2-agonists nor corticosteroids inhibit extracellular matrix (ECM) protein release from airway smooth muscle (ASM) cells, the effect of their combination is unknown and this forms the rationale for the present study. Methods. ASM cells from people with and without asthma were stimulated with TGFβ1 (1 ng/ml) with or without budesonide (10-8 M) and formoterol (10-10 and 10-8 M), and fibronectin expression and IL-6 release were measured by ELISA. Bronchial rings from nonasthmatic individuals were incubated with TGFβ1 (1 ng/ml) with or without the drugs, and fibronectin expression was measured using immunohistochemistry. Results. Budesonide stimulated fibronectin deposition, in the presence or absence of TGFβ1, and this was partially reversed by formoterol (10-8 M) in both asthmatic and nonasthmatic cells. Budesonide and formoterol in combination failed to inhibit TGFβ-induced fibronectin in either cell type. A similar pattern of expression of fibronectin was seen in bronchial rings. TGFβ1-induced IL-6 release was inhibited by the combination of drugs. Conclusion. Current combination asthma therapies are unable to prevent or reverse remodeling events regulated by ASM cells.