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Published ahead of print on January 19, 2007, doi:10.1165/rcmb.2006-0083OC

Am. J. Respir. Cell Mol. Biol., Volume 36, Number 5, May 2007, 625-632

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Submitted on February 23, 2006
Revised on January 16, 2007

Comparison of Airway Remodeling in Acute, Subacute and Chronic Models of Allergic Airways Disease

Natasha R Locke1, Simon G Royce1, Jacquetta S Wainewright1, Chrishan S Samuel2, and Mimi L Tang1*

1 Department of Allergy and Immunology, The Royal Children's Hospital, Murdoch Children's Research Institute, Parkville, Victoria, Australia, 2 The University of Melbourne, Howard Florey Institute of Experimental Physiology and Medicine, Parkville, Victoria, Australia

* To whom correspondence should be addressed. E-mail: mimi.tang{at}rch.org.au.

The relationship between airway inflammation and structural changes of airway remodeling, and their relative effects on airway function are poorly understood. Remodeling is thought to result from chronic repetitive injury to the airway wall caused by airway inflammation, however the mechanisms regulating remodeling changes have not been clearly defined. We examined the sequence of events in remodeling using three commonly-used mouse models of allergic airways disease in which mice are exposed to nebulised OVA for 4 consecutive days (acute), 7 consecutive days (subacute) or 3 times a week for 6 weeks (chronic). Surprisingly, we found that a very short period of exposure to OVA was sufficient to elicit early changes of remodeling. Goblet cell hyperplasia and epithelial thickening were evident after just 4 days. In chronically-challenged mice, these changes persisted and, in addition, subepithelial collagen deposition was significantly increased. This collagen deposition was associated with a failure to upregulate MMP-2, in conjunction with increased TGF-{beta} and MMP9 expression. The relationship between inflammation, remodeling changes and airway hyperresponsiveness (AHR) were examined. The acute and subacute models exhibited marked airway inflammation, whereas the chronic model had very modest inflammation. Conversely, airway fibrosis was only evident in the chronic model. AHR was present in all three models, however was significantly higher in the chronic model compared to the acute (p<0.05) and subacute (p<0.05) models. These data demonstrate that both airway inflammation and airway fibrosis may contribute to AHR, with airway fibrosis leading to the greatest increases in AHR.




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