Airway inflammation and bronchial microbial patterns in patients with stable chronic obstructive pulmonary disease

The effect of bacterial colonization of the bronchi on the progress of airf low limitation is not web known. Therefore, the pattern of airway inflammat ion in smokers and patients with stable chronic obstructive pulmonary disea se (COPD) and its relation to bronchial microbial colonization was assessed . Eight nonsmoking and 18 smoking controls as well as 52 patients with COPD ( 28 mild, 11 moderate and 13 severe) were studied. All subjects were investi gated by means of flexible bronchoscopy including protected specimen brush and bronchoalveolar lavage (BAL) sampling. Differential cell counts, cytoki ne (interleukin (IL)-1 beta, IL-6, IL-8, IL-10 and tumour necrosis factor-a lpha (TNF-alpha) concentrations and microbial patterns were determined in B AL fluid. Forced expiratory volume in one second (FEV1) % of the predicted value was inversely correlated with pack-yrs of cigarette smoking (r=0.47, p<0.0001), the percentage of neutrophil (rho=-0.56, p<0.0001) and IL-6 (rho=-0.37, p= 0.01) and IL-8 concentration (rho=-0.43, p=0.004) in BAL fluid. Accordingly , pk-yrs of cigarette smoking (rho=0.39, p=0.01) and IL-8 (rho=0.69, p<0.00 01) and TNF alpha (rho=0.4, p<0.005) were positively correlated with the pe rcentage of neutrophils in BAL fluid. Smoking controls and COPD patients we re mainly colonized in the bronchial tree (33%) by community endogenous pot entially pathogenic micro-organisms (PPMs). Colonization rates and patterns of PPMs were not affected by severity of airflow obstruction. The presence of PPMs was significantly associated with higher percentages of neutrophil s (33.2+/-10.4% versus 10.1+/-3.5%, p=0.02) and TNF-alpha concentration (29 .9+/-10.8 versus 6.3+/-2.1 pg.mL(-1), p=0.01) in BAL fluid. In conclusion, bronchial neutrophilia is a key inflammatory pattern in chro nic obstructive pulmonary disease patients. Bronchial colonization with pot entially pathogenic micro-organisms may represent an independent stimulus f or additional airway inflammation.