Monday February 25th 2019

Airway inflammation following smoking

Studies of bronchial biopsy specimens of smokers and ex-smokers with moderate to severe COPD have also demonstrated no difference in mediators of inflammation associated with neutrophil and mononuclear cell recruitment, such as IL-8 and monocyte chemoattractant protein (MCP)-1, as well as the MCP-1 chemokine receptor 2, in the lung tissued Although cross-sectional studies of lung tissue in COPD demonstrate more consistent findings of persistent inflammation in ex-smokers, cross-sectional studies of sputum, blood, or BAL generally demonstrate reductions in biomarkers of inflammation or no difference in ex-smokers vs smokers. In the only longitudinal study of the effect of smoking cessation on airway inflammation in COPD, 12 subjects with COPD Canadian pharmacy viagra (defined by pulmonary function and not by CT scan) were found to have persistent airway inflammation in bronchial biopsy specimens and a significant increase in the number of sputum neutrophils and IL-8 levels at 1 year.

Although these studies have provided important information regarding the potential for continued airway inflammation following smoking cessation in COPD, the studies have mainly been cross-sectional and have focused on subjects with chronic bronchitis rather than subjects with -diagnosed COPD-emphysema (COPD-E). In addition, most studies have not used CT scan to define subjects as having emphysema as an entry criterion and have not used blood cotinine levels to verify smoking status. In this study we have performed a longitudinal assessment (at baseline and after 4 years of observation) of continued airway inflammation in a cohort of ex-smokers who had the diagnosis of COPD-E established based on the presence of significant emphysema on chest CT scan at the baseline visit. Our study demonstrates persistent increased levels of mediators of inflammation in sputum (myeloperoxidase [MPO], leukotriene B4 [LTB4], IL-8, MCP-1, matrix metalloprotease-9 [MMP-9]), which was associated with significant progression of COPD-E on chest CT scan in subjects with COPD-E who discontinued tobacco smoking for at least 4 years, as verified by blood cotinine levels.

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