|
 |
|
|||||||
|
|||||||||
© 2005 The American Thoracic Society
The Role of Airway Smooth Muscle in the Pathogenesis of Airway Wall Remodeling in Chronic Obstructive Pulmonary Disease
National Heart and Lung Institute, Imperial College and Royal Brompton Hospital, London, United Kingdom
Correspondence and requests for reprints should be addressed to Kian Fan Chung, M.D., D.Sc., F.R.C.P., National Heart and Lung Institute, Imperial College, Dovehouse Street, London SW3 6LY, UK. E-mail: f.chung{at}imperial.ac.uk
Airway wall remodeling processes are present in the small airways of patients with chronic obstructive pulmonary disease, consisting of tissue repair and epithelial metaplasia that contribute to airway wall thickening and airflow obstruction. With increasing disease severity, there is also increased mucous metaplasia and submucosal gland hypertrophy, peribronchial fibrosis, and an increase in airway smooth muscle mass. Apart from its contractile properties, airway smooth muscle produces inflammatory cytokines, proteases, and growth factors, which may contribute to the remodeling process and induce phenotypic changes of the muscle. Airflow limitation responds minimally to ß-agonists and corticosteroid therapy, unlike asthma, perhaps because of alterations in ß-receptor or glucocorticoid receptor numbers, alterations in receptor signaling, or the constrictive limitation imposed by peribronchial fibrosis. Better response is observed with the combination of inhaled long-acting ß-agonists and corticosteroids. This could result from effects at the level of airway smooth muscle. Airway wall remodeling may involve the release of growth factors from inflammatory or resident cells. The influence of smoking cessation or of current therapies on airway wall remodeling is unknown. Specific therapies for airway wall remodeling may be necessary, together with noninvasive methods of imaging small airway wall remodeling to assess responses.
Key Words: corticosteroids • emphysema • long-acting ß-agonists • matrix metalloproteases • transforming growth factor-ß
This article has been cited by other articles:
|
|
 |
|
  K. M. Kassel, N. A. Schulte, and M. L. Toews Modulation of epidermal growth factor receptor binding to human airway smooth muscle cells by glucocorticoids and {beta}2-adrenergic receptor agonists Am J Physiol Lung Cell Mol Physiol, April 1, 2009; 296(4): L693 - L699. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Thompson, S. McMahon, Y. Bosse, C. M. Dubois, J. Stankova, and M. Rola-Pleszczynski Leukotriene D4 Up-Regulates Furin Expression through CysLT1 Receptor Signaling Am. J. Respir. Cell Mol. Biol., August 1, 2008; 39(2): 227 - 234. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. F. Chung and I. M. Adcock Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction Eur. Respir. J., June 1, 2008; 31(6): 1334 - 1356. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Tliba and Y. Amrani Airway Smooth Muscle Cell as an Inflammatory Cell: Lessons Learned from Interferon Signaling Pathways Proceedings of the ATS, January 1, 2008; 5(1): 106 - 112. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-F. Cordier Challenges in pulmonary fibrosis {middle dot} 2 : Bronchiolocentric fibrosis Thorax, July 1, 2007; 62(7): 638 - 649. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Roviezzo, A. Di Lorenzo, M. Bucci, V. Brancaleone, V. Vellecco, M. De Nardo, D. Orlotti, R. De Palma, F. Rossi, B. D'Agostino, et al. Sphingosine-1-Phosphate/Sphingosine Kinase Pathway Is Involved in Mouse Airway Hyperresponsiveness Am. J. Respir. Cell Mol. Biol., June 1, 2007; 36(6): 757 - 762. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
