Background: Smoking alters the inflammatory cell balance in the airways, often leading to repeated respiratory infections and, eventually, chronic obstructive pulmonary disease (COPD) in susceptible individuals.
Objective: It was the aim of this study to evaluate alterations in the airway inflammatory balance caused by chronic cigarette smoke exposure.
Methods: We compared results of biopsy and bronchoalveolar lavage (BAL) samples from non-smoking (n = 8) and smoking (n = 5; pack years 25.06 +/- 11.75, range 7.13-36.8) subjects without COPD.
Results: In BAL samples, we found a significantly higher number of total cells (353 +/- 96 million vs. 114 +/- 52 million; p = 0.003) and macrophages (331 +/- 100 million vs. 84 +/- 36 million; p = 0.002) in asymptomatic smoking subjects in comparison with never-smokers. Macrophages correlated negatively with the forced expiratory volume in 1 s as percent of the predicted value (rho = -0.75, p = 0.003). Of 23 mediators examined, mRNA expression of cytokines interleukin (IL)-6, interferon-gamma, tumor necrosis factor-beta, IL-13 and chemokines CCL5, CCL3, CCL4 and CCL20 was significantly lowered in BAL cells of smokers compared with never-smokers and was negatively correlated with macrophages and positively correlated with the forced expiratory volume in 1 s as percent of the predicted value. Differential cell counts were similar between smokers and never-smokers in the bronchial biopsies.
Conclusion: We conclude that in a susceptible population, smoking suppresses inflammatory defense by inhibiting expression of inflammatory mediators in the airways on a large scale.
(c) 2008 S. Karger AG, Basel.