Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers

Abstract

Smoking cessation is the only treatment in patients with chronic obstructive pulmonary disease (COPD) effective in slowing down disease progression. Its effect on airway inflammation in COPD is unknown, although cross-sectional studies suggest ongoing inflammation in ex-smokers.In order to elucidate the effect of smoking cessation on airway inflammation, 28 smokers with COPD (mean age: 55 yrs; forced expiratory volume in one second: 71% predicted) and 25 asymptomatic smokers with normal lung function (aged 50 yrs) were included in a 1-yr smoking cessation programme. Effects of smoking cessation on airway inflammation were investigated in bronchial biopsies (baseline, 12 months) and sputum samples (baseline, 2, 6 and 12 months).In the 12 candidates with COPD who successfully ceased smoking, airway inflammation persisted in bronchial biopsies, while the number of sputum neutrophils, lymphocytes, interleukin (IL)-8 and eosinophilic-cationic-protein levels significantly increased at 12 months. In the 16 asymptomatic smokers who successfully quitted, inflammation significantly reduced (i.e. number of sputum macrophages, percentage of eosinophils and IL-8 levels) or did not change.The current authors suggest that the observed persistent airway inflammation in patients with chronic obstructive pulmonary disease is related to repair of tissue damage in the airways. It remains to be elucidated whether this reflects a beneficial or detrimental effect.

Transepithelial exit of leucocytes: inflicting, reflecting or resolving airway inflammation?

“…Further support for a role for transepithelial egression as a mode of ridding diseased bronchial tissues of inflammatory cells comes from smoking cessation studies. Thus, symptom improvement over several months following smoking cessation in COPD was associated with sputum neutrophilia 12 13 and increased sputum lymphocytes 12. Also, sputum eosinophilia has been associated with improved lung function in patients with asthma treated with β-agonists 14.…”

Ageing, smoking and oxidative stress

“…Potential explanations for these changes in COPD include persistent inflammation from infectious colonisation with bacteria or Pneumocystis, 9 latent adenovirus, 10 autoimmunity, 11 or repeated attempts at repair of airway damage. 12 Inflammation was present in the small airways of surgically resected lung specimens from individuals up to 9 years after smoking cessation, 7 and in induced sputum, BAL fluid, and mucosal biopsies in COPD patients who were not currently smoking. 13 Inflammatory changes following smoking cessation appear to be quite complex.…”

Decreased Sputum Mature Dendritic Cells in Healthy Smokers and Patients with Chronic Obstructive Pulmonary Disease

“…Specifically, reduced CD83 expression on DCs may suppress their ability to induce T cell responses [35]. Likewise, after smoking cessation in healthy smokers the observed return of mature DC numbers to the never-smoker levels may enhance the ability of pulmonary DCs to respond efficiently to infections and may attenuate airway inflammation [36]. …”