Abstract
BackgroundSmoking is associated with a mixed inflammatory infiltrate in the airways. We evaluated whether airway inflammation in smokers is related to lung function parameters and inflammatory markers in exhaled breath.MethodsThirty-seven smokers undergoing lung resection for primary lung cancer were assessed pre-operatively by lung function testing including single-breath-nitrogen washout test (sb-N2-test), measurement of fractional exhaled nitric oxide (FeNO) and pH/8-isoprostane in exhaled breath condensate (EBC). Lung tissue sections containing cancer-free large (LA) and small airways (SA) were stained for inflammatory cells. Mucosal (MCT) respectively connective tissue mast cells (MCTC) and interleukin-17A (IL-17A) expression by mast cells was analysed using a double-staining protocol.ResultsThe median number of neutrophils, macrophages and mast cells infiltrating the lamina propria and adventitia of SA was higher than in LA. Both MCTC and MCT were higher in the lamina propria of SA compared to LA (MCTC: 49 vs. 27.4 cells/mm2; MCT: 162.5 vs. 35.4 cells/mm2; P<0.005 for both instances). IL-17A expression was predominantly detected in MCTC of LA. Significant correlations were found for the slope of phase III % pred. of the sb-N2-test (rs= -0.39), for the FEV1% pred. (rs= 0.37) and for FEV1/FVC ratio (rs=0.38) with MCT in SA (P<0.05 for all instances). 8-isoprostane concentration correlated with the mast cells in the SA (rs=0.44), there was no correlation for pH or FeNO with cellular distribution in SA.ConclusionsNeutrophils, macrophages and mast cells are more prominent in the SA indicating that these cells are involved in the development of small airway dysfunction in smokers. Among these cell types, the best correlation was found for mast cells with lung function parameters and inflammatory markers in exhaled breath. Furthermore, the observed predominant expression of IL-17A in mast cells warrants further investigation to elucidate their role in smoking-induced lung injury, despite the lack of correlation with lung function and exhaled breath parameters.
Highlights
Tobacco smoke is the most important risk factor for the development of chronic obstructive pulmonary disease (COPD) [1,2]
Significant correlations were found for the slope of phase III % pred. of the sbN2-test, for the FEV1% pred. and for FEV1/FVC ratio with MCT in small airways (SA) (P
Neutrophils, macrophages and mast cells are more prominent in the SA indicating that these cells are involved in the development of small airway dysfunction in smokers
Summary
Tobacco smoke is the most important risk factor for the development of chronic obstructive pulmonary disease (COPD) [1,2]. Smoking induces an inflammatory response along the trachea-bronchial tree, the lung parenchyma and pulmonary vasculature. Compared to non-smokers, smokers have increased numbers of mast cells in the large airways [7]. Mast cells are composed of mucosal (MCT) and connective tissue mast cells (MCTC) [8]. Smoking and especially the development of COPD seems to induce a shift in mast cell phenotype with an increase in the percentage of MCTC [6]. We evaluated whether airway inflammation in smokers is related to lung function parameters and inflammatory markers in exhaled breath
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