Airway Inflammation in Smokers with Nonobstructive and Obstructive Chronic Bronchitis

Abstract

To assess the manifestation and location of airway inflammation in smokers with chronic bronchitis (CB) or chronic obstructive pulmonary disease (COPD), we lavaged the airways of 12 smokers with CB and 11 smokers with COPD and coexisting CB (OCB). For comparison, the airways of 5 asymptomatic smokers (AS) and 10 healthy nonsmokers (HNS) were lavaged. In all cases, the first lavage aliquot, labeled "bronchial lavage" (BL), was processed separately from the four subsequent aliquots, which were combined and labeled "bronchoalveolar lavage" (BAL). The composition of BL and BAL fluids indicate an ongoing inflammatory process in the airways of all three groups of smokers. CB patients with obstruction had significantly lower concentrations of inflammatory cells in the BL and BAL fluids compared with subjects with nonobstructed CB. Furthermore, airway obstruction, indicated by a reduced FEV1, was significantly correlated with the concentrations of glutathione (p < 0.001), myeloperoxidase (MPO; p < 0.01), and eosinophil cationic protein (ECP; p < 0.01) in BAL fluids. Taken together, these findings suggest that the manifestations of inflammation present in the airways of smokers with CB are different in those who have developed obstruction compared with those who have not.

Enhanced detection of myeloperoxidase activity in deep tissues through luminescent excitation of near-infrared nanoparticles

“…The pathogenesis of COPD is characterized by neutrophil infiltration of pulmonary tissues and elevated concentrations of MPO in bronchoalveolar lavage fluids 18 . MPO is the only enzyme in the body that is known to produce hypochlorous acid, which oxidizes lipids, proteins and DNA 3,4 .…”

Oxidative stress and regulation of glutathione in lung inflammation

“…These studies suggest that GSH plays a critical role in maintaining epithelial membrane integrity and may protect epithelial cells against the inflammatory response produced by either inhaled or endogenous oxidants/free radicals. Furthermore, LINDEN and coworkers [204,205] demonstrated that airway obstruction, measured by means of the forced expiratory volume in one second (FEV1) in patients with COPD, correlated significantly with the concentration of GSH in BALF; the higher the BALF GSH, the lower the FEV1. It may be that the BALF GSH levels were influenced by the recent smoking history of these patients [24].…”

Association of current smoking with airway inflammation in chronic obstructive pulmonary disease and asymptomatic smokers

“…For example, higher numbers of neutrophils, macrophages and CD8 positive T-cells in the peripheral airways of COPD patients were found as compared to smokers [10,[17][18][19], whereas others did not [10,19,20]. Two studies showed a higher percentage of neutrophils and higher IL-8 levels in broncho-alveolar lavage of COPD patients [13,21], whereas Linden et al found no differences [7]. A few studies showed higher numbers of neutrophils [22], CD3, CD4 [23] CD8 positive T-cells [23,24] in bronchial biopsies, whereas other studies found no differences in neutrophils [24], CD3, CD4 [22,24] and CD8 positive T-cels [22], macrophages, eosinophils and mast cells [22,24].…”

“…For example, higher numbers of CD8 positive T-cells, macrophages, neutrophils, and mast cells, both in central and peripheral airways have been found in COPD patients, irrespective whether these patients were current smokers or ex-smokers [4][5][6][7][8][9][10]. In addition, the percentage of neutrophils and IL-8 levels in sputum and broncho-alveolar lavage of COPD patients were higher [7,[11][12][13][14][15][16]. As compared to healthy smokers, the differences with COPD patients are less clear cut.…”