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Published ahead of print on August 27, 2004, doi:10.1165/rcmb.2004-0193OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 6, December 2004, 626-632

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Submitted on June 17, 2004
Revised on August 25, 2004

Acute allergen-induced airway remodeling in atopic asthma

Simon Phipps1, Farid Benyahia1, Tsan-Teng Ou1, Julia Barkans1, Douglas S Robinson2, and A.Barry Kay1*

1 Departments of Allergy and Clinical Immunology, Imperial College, National Heart and Lung Institute, London, United Kingdom, 2 Departments of Allergy and Clinical Immunology, Imperial College, National Heart and Lung Institute, London, United Kingdom; Leukocyte Biology Section, Biomedical Sciences Division, Imperial College London, London, United Kingdom

* To whom correspondence should be addressed. E-mail: a.b.kay{at}imperial.ac.uk, j.m.mitchell@imperial.ac.uk.

Studies in animals and in human atopic skin suggest that allergen challenge may activate acute tissue remodeling changes via TGF-{beta} pathways. We determined whether inhalational allergen challenge in mild asthmatics induces similar acute changes to the airway epithelial mesenchymal trophic unit (EMTU). Endobronchial mucosal biopsies obtained before and 24 h after challenge were examined by confocal microscopy for extracellular matrix (ECM) deposition in the reticular basement membrane (RBM). Cells actively involved in ECM synthesis were identified as immunoreactive to HSP47, a chaperone of collagen synthesis. IL-4/13 and TGF-{beta} activated cells were identified by specific Ab to phosphorylated (phospho-) STAT6 and phospho-Smad2 respectively. After allergen challenge there was a significant increase in the numbers of HSP47 positive airway fibroblasts (p=0.003) and in the thickness of tenascin in the RBM (p=0.031). There were also increases in the number of phospho-Smad2+ epithelial cells (p=0.04) and nuclear phospho-Smad2+ fibroblasts (p=0.03) as well as phospho-STAT6+ epithelial cells (p=0.03), post-allergen challenge. Thus, allergen challenge in mild asthmatics induces activation of epithelial cells and fibroblasts in the EMTU as well as increased tenascin deposition within the RBM. Airway remodeling in asthma may, in part, result from repeated acute activation of the EMTU by allergen exposure.




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