Effect of smoking cessation on airway inflammation in chronic bronchitis.

Abstract

To investigate the effect of smoking cessation on the airway inflammatory process present in nonatopic subjects with chronic bronchitis, we obtained bronchial biopsies from nine current smokers and seven exsmokers, all with symptoms of chronic bronchitis at the time of the study, and from seven healthy nonsmoking subjects. The exsmokers had stopped smoking on average 13 yr before the study, yet cough and production of sputum had persisted. Bronchial biopsies were assessed using immunohistochemical techniques to investigate the number of inflammatory cells, the markers of mononuclear cell activation, and the expression of endothelial adhesion molecules and cytokines in the subepithelium. Current smokers and exsmokers had an increased number of macrophages, IL-2R-positive cells, VLA-1-positive cells, ICAM-1-positive vessels, and E-selectin-positive vessels compared with normal nonsmoking subjects, but the number of cells positive for neutrophils, EG-2, CD3, CD4, CD8, TNF-alpha and IL-1 beta were similar among the three groups. No differences were observed between current smokers and exsmokers for any parameter examined. In conclusion, the inflammatory process present in the airway mucosa of current smokers may persist after smoking cessation in subjects who continue to have symptoms of chronic bronchitis.

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

“…This suggests an ongoing inflammatory process in the airways, in agreement with cross-sectional studies in smokers and exsmokers with COPD [3,4,9]. The presented sputum data also suggests that inflammation continues and even increases after smoking cessation.…”

“…Airway inflammation in bronchial biopsies and sputum did not differ between smokers and ex-smokers, except for some cytokines (interleukin (IL)-8, IL-6, soluble tumour necrosis factor-receptor (sTNF-R)75 and sTNF-R55) [3][4][5][6][7][8]. Furthermore, RUTGERS et al [9] showed that airway inflammation was more extensive in ex-smokers with COPD than in healthy ex-smokers.…”

The Importance of Chronic Bronchitis in Chronic Obstructive Pulmonary Disease

“…It is an independent risk factor for all cause mortality both in COPD (38), and in subjects with normal lung function, even when smoking has been accounted for (38)(39)(40). The overall ten year mortality following a diagnosis of chronic bronchitis is 50%, with respiratory failure following an acute exacerbation being the most frequent terminal event (41). Currently there are no clearly identified genetic risk factors for Chronic Bronchitis, however, twin studies have suggested that the heritability estimate for this condition is 40%, with only 14% of genetic influences shared with those related to smoking habits (42).…”

Cross-Sectional Study of Soluble Intercellular Adhesion Molecule-1 and Cardiovascular Risk Factors in Apparently Healthy Men

“…Immunohistochemical expression of ICAM-1 is significantly increased in peripheral pulmonary vessels of smokers compared with nonsmokers. 24,25 Experimental studies using cigarette smoke condensate indicate an increase in adherence of human monocytes to cultured endothelial cells, concomitantly with enhanced expression of ICAM-1 and ELAM-1. 26 Our results with regard to cigarette consumption reinforce the concept that the detrimental effects of smoking may be mediated, in part, by expression of adhesion molecules.…”