We aimed at comparing exhaled and non-exhaled non-invasive markers of respiratory inflammation in patients with COPD and healthy subjects and define their relationships with smoking habit. Forty-eight patients with stable COPD who were ex-smokers, 17 patients with stable COPD who were current smokers, 12 healthy current smokers and 12 healthy ex-smokers were included in a cross-sectional, observational study. Biochemical [prostaglandin (PG) E 2 , 15-F 2t -isoprostane, fraction of exhaled nitric oxide (F E NO)] and cellular (sputum cell counts) inflammatory outcomes and functional (spirometry) outcomes were measured in various biological matrices including exhaled breath condensate (EBC), exhaled breath, sputum supernatants, and urine. Sputum PGE 2 was elevated in both groups of smokers compared with ex-smoker counterpart (COPD: P < 0.02; healthy subjects: P < 0.03), whereas EBC PGE 2 was elevated in current (P = 0.0065) and ex-smokers with COPD (P = 0.0029) versus healthy exsmokers. EBC 15-F 2t -isoprostane, a marker of oxidative stress, was increased in current and exsmokers with COPD (P < 0.0001 for both) compared with healthy ex-smokers, whereas urinary 15-F 2t -isoprostane was elevated in both smoker groups (COPD: P < 0.01; healthy subjects: P < 0.02) versus healthy ex-smokers. F E NO was elevated in ex-smokers with COPD versus smoker groups (P = 0.0001 for both). These data suggest that the biological meaning of these inflammatory markers depends on type of marker and biological matrix in which is measured. An approach combining different types of outcomes can be used for assessing respiratory inflammation in patients with COPD. Large studies are required to establish the clinical utility of this strategy.Keywords: exhaled breath condensate, sputum, prostaglandin E 2 , 15-F 2t -isoprostane, fraction of exhaled nitric oxide, respiratory inflammation, chronic obstructive pulmonary disease Abstract word count: 252
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