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.
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.
Authors: R B Gonçalves; R D Coletta; K G Silvério; L Benevides; M Z Casati; J S da Silva; F H Nociti Journal: Inflamm Res Date: 2011-02-05 Impact factor: 4.575
Authors: Sharon A McGrath-Morrow; Thomas Lauer; J Michael Collaco; Min Yee; Michael O'Reilly; Wayne Mitzner; Enid Neptune; Robert Wise; Shyam Biswal Journal: Am J Respir Cell Mol Biol Date: 2011-01-14 Impact factor: 6.914
Authors: Marian C Aldhous; Kimberley Soo; Lesley A Stark; Agata A Ulanicka; Jennifer E Easterbrook; Malcolm G Dunlop; Jack Satsangi Journal: PLoS One Date: 2011-09-12 Impact factor: 3.240