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Background: Airway bacterial colonization by potentially pathogenic microorganisms occurs in a proportion of patients with Chronic Obstructive Pulmonary Disease (COPD). It increases airway inflammation and influences outcomes negatively. Yet, its diagnosis in clinical practice is not straightforward. The electronic nose is a new non-invasive technology capable of distinguishing volatile organic compound (VOC) breath-prints in exhaled breath. We aim to explore if an electronic nose can reliably discriminate COPD patients with and without airway bacterial colonization., Methods: We studied 37 clinically stable COPD patients (67.8 ± 5.2 yrs, FEV1 41 ± 10% ref.) and 13 healthy controls (62.8 ± 5.2 yrs, FEV1 99 ± 10% ref.). The presence of potentially pathogenic microorganisms in the airways of COPD patients (n = 10, 27%) was determined using quantitative bacterial cultures of protected specimen brush. VOCs breath-prints were analyzed by discriminant analysis on principal component reduction, resulting in cross-validated accuracy values. Area Under Receiver Operating Characteristics (AUROC) was calculated using multiple logistic regression., Results: Demographic, functional and clinical characteristics were similar in colonized and non-colonized COPD patients but their VOC breath-prints were different (accuracy 89%, AUROC 0.92, p > 0.0001). Likewise, VOCs breath-prints from colonized (accuracy 88%, AUROC 0.98, p < 0.0001) and non-colonized COPD patients (accuracy 83%, AUROC 0.93, p < 0.0001) were also different from controls., Conclusions: An electronic nose can identify the presence of airway bacterial colonization in clinically stable patients with COPD., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Background: Chronic obstructive pulmonary disease (COPD) is characterized by an enhanced and persistent innate and acquired immune response to tobacco smoking. Myeloid-derived suppressor cells (MDSCs) modulate T-cell responses by down-modulating the T cell receptor ζ chain (TCR ζ) through the catabolism of l-arginine. The effects of smoking on MDSCs and their potential participation in COPD immunopathogenesis have not been explored so far., Methods: To investigate it, we compared the level of circulating Lineage-/HLA-DR-/CD33+/CD11b+ MDSCs, the serum concentration of arginase I (ARG I) and the expression of peripheral T-cell receptor ζ chain (TCR ζ) in never smokers, smokers with normal spirometry and COPD patients. Flow cytometry was used to quantify circulating MDSCs and TCR ζ expression. Serum ARG I levels were determined by ELISA., Results: The main findings of this study were that: (1) current smoking upregulates and activates circulating MDSCs both in smoker controls and COPD patients; and, (2) at variance with the smokers with normal spirometry, in patients with COPD this effect persists after quitting smoking and is accompanied by a significant and specific down-regulation of the TCR ζ chain expression in circulating T lymphocytes., Conclusion: Smoking modulates circulating MDSCs. Their regulation appears altered in patients with COPD., (Copyright © 2013 Elsevier Ltd. All rights reserved.)