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Published ahead of print on November 24, 2004, doi:10.1165/rcmb.2004-0190OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 2, February 2005, 99-107

A more recent version of this article appeared on February 1, 2005
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Submitted on June 14, 2004
Revised on November 24, 2004

Epithelial expression of profibrotic mediators in a model of allergen-induced airway remodeling

Margaret M Kelly1*, Richard Leigh2, Philippe Bonniaud1, Russ Ellis2, Jennifer Wattie2, Mary Jo Smith1, Gail Martin1, Mohammed Panju1, Mark D Inman2, and Jack Gauldie1

1 Department of Pathology and Molecular Medicine and Centre for Gene Therapeutics, McMaster University, Hamilton, ON, Canada, 2 Firestone Institute for Respiratory Health and Department of Medicine, McMaster University, Hamilton, ON, Canada

* To whom correspondence should be addressed. E-mail: kellym{at}mcmaster.ca.

Airway remodeling, including subepithelial fibrosis, is a characteristic feature of asthma and likely contributes to the pathogenesis of airway hyperresponsiveness. We examined expression of genes related to airway wall fibrosis in a model of chronic allergen-induced airway dysfunction using laser capture microdissection and quantitative real-time PCR. BALB/c mice were sensitized and subjected to chronic ovalbumin exposure over a 12-week period after which they were rested and then harvested 2 and 8 weeks after the last exposure. Chronic allergen exposed mice had significantly increased indices of airway remodeling and airway hyperreactivity at all time points, although no difference in expression of fibrosis-related genes was found when mRNA extracted from whole lung was examined. In contrast, fibrosis-related gene expression was significantly up-regulated in mRNA obtained from microdissected bronchial wall at 2 weeks post chronic allergen exposure. In addition, when bronchial wall epithelium and smooth muscle were separately microdissected, gene expression of transforming growth factor-{beta}1 and plasminogen activating inhibitor-1 were significantly upregulated only in the airway epithelium. These data suggest that transforming growth factor-{beta}1 and other profibrotic mediators produced by airway wall, and specifically, airway epithelium, play an important role in the pathophysiology of airway remodeling.




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