Increased sputum IL-8 and IL-5 in asymptomatic nonspecific airway hyperresponsiveness

Since asymptomatic, nonspecific airway hyperresponsiveness (BHR) may be due to an enhanced local inflammatory response, we studied molecular markers o f inflammation in induced sputum from subjects with asymptomatic BHR (n = 1 4) compared with control subjects (n = 13) and patients with chronic obstru ctive pulmonary disease (COPD) (n = 10). Pulmonary lung function parameters were measured by spirometry and body plethysmography. Hyperresponsiveness was defined based on histamine challenge. Induced sputum samples were colle cted and the solid phase was isolated and analyzed for leukocyte numbers an d differential and for cytokines (ELISA). IL-8 was 2.4-fold increased (p = 0.036) in the sputum of subjects with asymptomatic BHR (24.8 +/- 22.0 ng/mL ; +/- SD) and 11.2-fold enhanced in patients with COPD (117.8 +/- 106.3 ng/ mL) as compared with control subjects (10.5 +/- 7.7 ng/mL). In control subj ects, no IL-5 was measured, however, sputum of those with asymptomatic BHR contained IL-5 at 0.044 +/- 0.090 ng/mL fluid and COPD patients at 1.00 +/- 2.01 ng/mL. GM-CSF could not be detected in sputum samples of any subjects investigated. Number of total leukocytes was higher in those with asymptom atic BHR and COPD (with BHR: 9.4 +/- 10.8 x 10(5); COPD: 83.5 +/- 182.5 x 1 0(5)) compared with persons without BHR (2.9 +/- 3.4 x 10(5)). PMN were inc reased in patients with asymptomatic BHR (4.1 +/- 5.3 x 10(5)) (38.8 +/- 24 .7%) and COPD (32.9 +/- 71.0 x 10(5)) (75.4 +/- 18.6%) compared with contro ls (0.7 +/- 0.9 x 10(5)) (25.8 +/- 25.7%). In contrast to PMN counts in tho se with asymptomatic BHR (0.06 +/- 0.11 x 10(5)) (1.5 +/- 3.7%), eosinophil counts were only slightly increased compared with control subjects (0.01 /- 0.02 x 10(5)) (0.6 +/- 0.9%). This study supports the hypothesis that BH R in asymptomatic people is associated with airway inflammation that may pr edispose to development of chronic diseases such as COPD.