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Articles in PresS, published online ahead of print September 6, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00105.2002
Submitted on April 10, 2002
Accepted on August 30, 2002
1 Department of Asthma, Allergy and Respiratory Science, The Guy's, King's and St. Thomas' School of Medicine, King's College London, London, United Kingdom
2 Department of Thoracic Medicine, National Heart and Lung Institute at the Imperial College School of Medicine, London, United Kingdom
3 Department of Asthma, Allergy and Respiratory Science, The Guy's, King's and St. Thomas' School of Medicine, King's College London, London, United Kingdom; Department of Thoracic Medicine, National Heart and Lung Institute at the Imperial College School of Medicine, London, United Kingdom
* To whom correspondence should be addressed. E-mail: stuart.hirst{at}kcl.ac.uk.
Repeated ovalbumin (OA) or saline exposure of sensitized Brown Norway rats was examined on agonist reactivity, airway smooth muscle (ASM) content and contractile protein expression in small bronchioles at 24h, 7d, and 35d after challenge. OA increased ASM content (p<0.05 versus saline) at 24h, which resolved by 7d. Maximum developed tension (Tmax) to carbachol, KCl and 4ß-PDBu was increased (p<0.05) by OA in bronchioles at 24h, but was abrogated after correction for ASM. Differences in Tmax were not present at 7d. In contrast, at 35d Tmax was increased (p<0.05) after correction for ASM. Smooth muscle (sm)-
-actin, sm-myosin heavy chain (MHC)isoform 1, calponin, smoothelin-A, sm-myosin light chain kinase(sm-MLCK) expression was reduced (p<0.05) by OA at 24h in bronchioles, but not in trachealis. Consistent with contraction findings, no difference in expression of these proteins was detected at 7d. At 35d, however, with the exception of sm--actin, their abundance was again reduced (p<0.05) by OA. Non-muscle MHC and ß-actin were unchanged throughout by OA. These findings indicate persistent changes in contractile protein content, consistent with ASM phenotypic modulation in vivo, occur in response to repeated OA inhalation. Thus, OA exposure induces structural changes in bronchiole ASM content and in agonist responsiveness ex vivo that resemble remodeling in asthma.
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