Evidence for airway remodeling in chronic asthma.
OBJECTIVE
This review focuses on recent findings in relation to potential functional consequences of structural changes in the asthmatic airway.


RESULTS
Increases in smooth muscle mass have been shown to be an early finding in childhood asthma, related to clinical severity and predictive of greater airflow obstruction. Both hyperplasia and hypertrophy contribute to the increase in smooth muscle mass. A phenotypic shift in the epithelium of asthmatic airways related to stress and injury is suggested by recent data, with likely direct transformation of epithelial cells into mesenchymal cells. Fibrocyte in-migration from the vasculature may be an additional source of increased smooth muscle mass. The increased smooth muscle may contribute to neovascularization via vascular endothelial growth factor. Computed tomography studies continue to show some correlations between wall thickness and airway physiology. Exacerbations are predictive of greater lung function decline and hence remodeling.


CONCLUSIONS
On balance, recent evidence continues to show that structural changes contribute to asthma persistence, airflow obstruction, lung function decline, and clinical severity, though there is increased recognition of the heterogeneity of asthma and in some phenotypes inflammatory cell influx or vascular effects may be more important than structural effects.
UBC James Hogg Research Centre, Providence Heart and Lung Institute, St Paul's Hospital and Department of Medicine, University of British Columbia, Vancouver, Canada. tbai@mrl.ubc.ca
Tony R
TR
Bai
D000402:Airway Obstruction; D056151:Airway Remodeling; D000818:Animals; D001249:Asthma / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology*; D002471:Cell Transformation, Neoplastic; D002675:Child, Preschool; D006801:Humans; D006965:Hyperplasia; D032389:Myocytes, Smooth Muscle / Q000473:pathology*; D009389:Neovascularization, Pathologic; D011379:Prognosis; D020545:Respiratory Mucosa / Q000098:blood supply / Q000473:pathology*