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Smoking cessation improves both direct and indirect airway hyperresponsiveness in COPD
B W M Willemse1, N H T ten Hacken, B Rutgers
1University Hospital Groningen, Dept of Pathology, Hanzeplein 1, 9713 GZ, Groningen, the Netherlands. b.w.m.willemse@path.azg.nl
The European Respiratory Journal
|September 11, 2004
Summary
Smoking causes chronic obstructive pulmonary disease (COPD). Airway hyperresponsiveness (AHR) to direct and indirect stimuli is linked to lower lung function in COPD. Smoking cessation improves AHR, but not lung function or sputum inflammation.
Area of Science:
- Pulmonary Medicine
- Respiratory Physiology
Background:
- Smoking is a primary cause of chronic obstructive pulmonary disease (COPD).
- Airway hyperresponsiveness (AHR) and inflammation are key features of COPD.
- The impact of smoking cessation on AHR and sputum inflammation in COPD remains incompletely understood.
Purpose of the Study:
- To investigate the association between AHR (direct and indirect) and lung function/sputum inflammation in smokers with COPD.
- To assess the effects of 1-year smoking cessation on AHR, lung function, and sputum inflammatory cells in COPD patients.
Main Methods:
- Cross-sectional study of 33 smokers with COPD assessing AHR to methacholine and adenosine-5'-monophosphate (AMP), lung function, and sputum inflammatory cells.
- Prospective assessment of changes in these parameters in 14 smokers who quit for 1 year.
Main Results:
- AHR to both methacholine and AMP was associated with reduced lung function but not with sputum inflammation.
- One year of smoking cessation significantly improved AHR to both stimuli.
- Smoking cessation led to increased neutrophils and epithelial cells in sputum, but did not significantly alter lung function or overall sputum inflammation.
Conclusions:
- Direct and indirect AHR are linked to lower lung function in COPD, independent of sputum inflammation.
- Smoking cessation improves AHR in COPD patients, suggesting mechanisms beyond reduced sputum inflammation, potentially involving irritant receptor stimulation or airway remodeling.