RATIONALE: Inflammation is now recognized as an integral part of the pathogenesis of chronic obstructive pulmonary disease (COPD). In contrast to the sterile airways of normal lungs, bacterial pathogens are often isolated from the airways in stable COPD. This "colonization" of the tracheobronchial tree, currently believed to be innocuous, could serve as an inflammatory stimulus, independent of current tobacco smoke exposure. OBJECTIVE: To test the hypothesis that bacterial colonization is associated with airway inflammation in stable COPD. METHODS: Bronchoscopy with bronchoalveolar lavage (BAL) was performed in three groups of subjects: 26 ex-smokers with stable COPD (COPD), 20 ex-smokers without COPD (ex-smokers), and 15 healthy nonsmokers (nonsmokers). Quantitative bacterial cultures, cell counts, chemokine, cytokine, proteinase/antiproteinase, and endotoxin levels in the BAL fluid were compared. RESULTS: Potentially pathogenic bacteria were recovered at > or = 100 cfu/ml in 34.6% of COPD, 0% of ex-smokers, and in 6.7% of nonsmokers (p = 0.003). All values are expressed as median (interquartile range). Subjects with colonized COPD had significantly greater relative (12.0 [28.4] vs. 3.0 [7.8]%, p = 0.03) and absolute (4.98 [5.26] x 10(4)/ml vs. 3.04 [2.82] x 10(4)/ml, p = 0.02) neutrophil counts, interleukin 8 (33.8 [189.8] vs. 16.9 [20.1] pg/ml, p = 0.005), active matrix metalloproteinase-9 (2.16 [4.30] vs. 0.84 [0.99] U/ml, p = 0.03), and endotoxin (36.0 [72.6] vs. 3.55 [7.17] mEU/ml, p = 0.004) levels in the BAL than the subjects with noncolonized COPD. These inflammatory constituents of BAL were also significantly elevated in subjects with colonized COPD when compared with ex-smokers and nonsmokers. CONCLUSIONS: Bacterial colonization is associated with neutrophilic airway lumen inflammation in ex-smokers with COPD and could contribute to progression of airway disease in COPD.
RATIONALE: Inflammation is now recognized as an integral part of the pathogenesis of chronic obstructive pulmonary disease (COPD). In contrast to the sterile airways of normal lungs, bacterial pathogens are often isolated from the airways in stable COPD. This "colonization" of the tracheobronchial tree, currently believed to be innocuous, could serve as an inflammatory stimulus, independent of current tobacco smoke exposure. OBJECTIVE: To test the hypothesis that bacterial colonization is associated with airway inflammation in stable COPD. METHODS: Bronchoscopy with bronchoalveolar lavage (BAL) was performed in three groups of subjects: 26 ex-smokers with stable COPD (COPD), 20 ex-smokers without COPD (ex-smokers), and 15 healthy nonsmokers (nonsmokers). Quantitative bacterial cultures, cell counts, chemokine, cytokine, proteinase/antiproteinase, and endotoxin levels in the BAL fluid were compared. RESULTS: Potentially pathogenic bacteria were recovered at > or = 100 cfu/ml in 34.6% of COPD, 0% of ex-smokers, and in 6.7% of nonsmokers (p = 0.003). All values are expressed as median (interquartile range). Subjects with colonized COPD had significantly greater relative (12.0 [28.4] vs. 3.0 [7.8]%, p = 0.03) and absolute (4.98 [5.26] x 10(4)/ml vs. 3.04 [2.82] x 10(4)/ml, p = 0.02) neutrophil counts, interleukin 8 (33.8 [189.8] vs. 16.9 [20.1] pg/ml, p = 0.005), active matrix metalloproteinase-9 (2.16 [4.30] vs. 0.84 [0.99] U/ml, p = 0.03), and endotoxin (36.0 [72.6] vs. 3.55 [7.17] mEU/ml, p = 0.004) levels in the BAL than the subjects with noncolonized COPD. These inflammatory constituents of BAL were also significantly elevated in subjects with colonized COPD when compared with ex-smokers and nonsmokers. CONCLUSIONS: Bacterial colonization is associated with neutrophilic airway lumen inflammation in ex-smokers with COPD and could contribute to progression of airway disease in COPD.
Authors: Marie C Earley; Robert F Vogt; Howard M Shapiro; Francis F Mandy; Kathryn L Kellar; Ronald Bellisario; Kenneth A Pass; Gerald E Marti; Carleton C Stewart; W Harry Hannon Journal: Cytometry Date: 2002-10-15
Authors: P Saikku; M Leinonen; K Mattila; M R Ekman; M S Nieminen; P H Mäkelä; J K Huttunen; V Valtonen Journal: Lancet Date: 1988-10-29 Impact factor: 79.321
Authors: S R Rutgers; D S Postma; N H ten Hacken; H F Kauffman; T W van Der Mark; G H Koëter; W Timens Journal: Thorax Date: 2000-01 Impact factor: 9.139
Authors: L Von Hertzen; H Alakärppä; R Koskinen; K Liippo; H M Surcel; M Leinonen; P Saikku Journal: Epidemiol Infect Date: 1997-04 Impact factor: 2.451
Authors: Timothy F Murphy; Aimee L Brauer; Andrew T Schiffmacher; Sanjay Sethi Journal: Am J Respir Crit Care Med Date: 2004-04-29 Impact factor: 21.405
Authors: Francesco Cappello; Gaetano Caramori; Claudia Campanella; Chiara Vicari; Isabella Gnemmi; Andrea Zanini; Antonio Spanevello; Armando Capelli; Giampiero La Rocca; Rita Anzalone; Fabio Bucchieri; Silvestro Ennio D'Anna; Fabio L M Ricciardolo; Paola Brun; Bruno Balbi; Mauro Carone; Giovanni Zummo; Everly Conway de Macario; Alberto J L Macario; Antonino Di Stefano Journal: PLoS One Date: 2011-11-28 Impact factor: 3.240
Authors: Emily S Charlson; Kyle Bittinger; Andrew R Haas; Ayannah S Fitzgerald; Ian Frank; Anjana Yadav; Frederic D Bushman; Ronald G Collman Journal: Am J Respir Crit Care Med Date: 2011-06-16 Impact factor: 21.405
Authors: Meghan E Fitzpatrick; John R Tedrow; Maria E Hillenbrand; Lorrie Lucht; Thomas Richards; Karen A Norris; Yingze Zhang; Frank C Sciurba; Naftali Kaminski; Alison Morris Journal: Microbiol Immunol Date: 2014-03 Impact factor: 1.955
Authors: Mark T Dransfield; Andrew M Wilhelm; Brian Flanagan; Clifford Courville; Sherry L Tidwell; S Vamsee Raju; Amit Gaggar; Chad Steele; Li Ping Tang; Bo Liu; Steven M Rowe Journal: Chest Date: 2013-08 Impact factor: 9.410