Abstract
BackgroundChronic Obstructive Pulmonary Disease (COPD) is associated with bronchial epithelial changes, including squamous cell metaplasia and goblet cell hyperplasia. These features are partially attributed to activation of the epidermal growth factor receptor (EGFR). Whereas smoking cessation reduces respiratory symptoms and lung function decline in COPD, inflammation persists. We determined epithelial proliferation and composition in bronchial biopsies from current and ex-smokers with COPD, and its relation to duration of smoking cessation.Methods114 COPD patients were studied cross-sectionally: 99 males/15 females, age 62 ± 8 years, median 42 pack-years, no corticosteroids, current (n = 72) or ex-smokers (n = 42, median cessation duration 3.5 years), postbronchodilator FEV1 63 ± 9% predicted. Squamous cell metaplasia (%), goblet cell (PAS/Alcian Blue+) area (%), proliferating (Ki-67+) cell numbers (/mm basement membrane), and EGFR expression (%) were measured in intact epithelium of bronchial biopsies.ResultsEx-smokers with COPD had significantly less epithelial squamous cell metaplasia, proliferating cell numbers, and a trend towards reduced goblet cell area than current smokers with COPD (p = 0.025, p = 0.001, p = 0.081, respectively), but no significant difference in EGFR expression. Epithelial features were not different between short-term quitters (<3.5 years) and current smokers. Long-term quitters (≥3.5 years) had less goblet cell area than both current smokers and short-term quitters (medians: 7.9% vs. 14.4%, p = 0.005; 7.9% vs. 13.5%, p = 0.008; respectively), and less proliferating cell numbers than current smokers (2.8% vs. 18.6%, p < 0.001).ConclusionEx-smokers with COPD had less bronchial epithelial remodelling than current smokers, which was only observed after long-term smoking cessation (>3.5 years).Trial registrationNCT00158847
Highlights
Chronic Obstructive Pulmonary Disease (COPD) is associated with bronchial epithelial changes, including squamous cell metaplasia and goblet cell hyperplasia
The airway epithelium undergoes alterations, including squamous cell metaplasia, goblet and basal cell hyperplasia [2]. These findings are important for our understanding of the pathogenesis of COPD, since bronchial epithelial cells orchestrate an adequate maintenance of lung homeostasis by mucus production, ciliary beating, secretion of antimicrobial products and adequate immunological drive in response to noxious stimuli
In the present study, we demonstrated that long-term exsmokers with COPD had less bronchial epithelial mucin stores, proliferating cells, and squamous cell metaplasia than current smokers with COPD
Summary
Chronic Obstructive Pulmonary Disease (COPD) is associated with bronchial epithelial changes, including squamous cell metaplasia and goblet cell hyperplasia. The airway epithelium undergoes alterations, including squamous cell metaplasia, goblet and basal cell hyperplasia [2] These findings are important for our understanding of the pathogenesis of COPD, since bronchial epithelial cells orchestrate an adequate maintenance of lung homeostasis by mucus production, ciliary beating, secretion of antimicrobial products and adequate immunological drive in response to noxious stimuli. Goblet cell hyperplasia is more pronounced in smokers with COPD compared to those without, suggesting a role in the development of airflow limitation [3] It contributes to mucus hypersecretion, which is associated with morbidity and mortality in COPD [4,5]. Squamous cell metaplasia impairs mucociliary clearance and contributes to the increased risk of squamous cell carcinoma as observed in COPD [6]
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