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What drives the peripheral lung-remodeling process in chronic obstructive pulmonary disease?
James C Hogg1, John E McDonough, John V Gosselink
1Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada. jhogg@mrl.ubc.ca
Proceedings of the American Thoracic Society
|December 17, 2009
Summary
Small airway remodeling in chronic obstructive pulmonary disease (COPD) involves narrowing and obliteration of terminal bronchioles. This process occurs before emphysematous destruction and involves altered tissue repair gene expression.
Area of Science:
- Pulmonary Medicine
- Respiratory Biology
- Pathology
Background:
- Small airways (<2 mm diameter) are a primary site of obstruction in chronic obstructive pulmonary disease (COPD).
- Understanding bronchiolar remodeling is crucial for managing COPD progression.
Purpose of the Study:
- To investigate the structural and molecular changes in small airways during COPD progression.
- To correlate small airway remodeling with disease severity and gene expression patterns.
Main Methods:
- Quantitative histology and micro-computed tomography (CT) were used to assess bronchiolar tissue volume, collagen content, and terminal bronchiolar structure in COPD patients.
- Gene expression analysis of tissue repair genes was performed using laser capture microdissection on paired airway and lung tissue samples.
Main Results:
- COPD progression was associated with decreased bronchiolar tissue volume, reduced total collagen, and an increased ratio of collagen-3 to collagen-1.
- Micro-CT revealed a significant reduction in the number and lumen area of terminal bronchioles.
- Expression of most tissue repair genes decreased with declining FEV(1), while eight COPD-associated genes showed increased expression in surrounding lung tissue.
Conclusions:
- Small airway remodeling in COPD is characterized by progressive narrowing and obliteration of terminal bronchioles.
- These structural changes precede emphysematous destruction and are linked to differential expression of tissue repair genes in airways and surrounding lung tissue.
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