Antibiotic therapy is thought to improve lung function in patients with cystic fibrosis (CF) by decreasing neutrophil-derived inflammation. We investigated the origin and clinical significance of lactate in the chronically inflamed CF lung.

Methods
Lactate was measured in sputa of 18 exacerbated and 25 stable CF patients via spectrophotometry and gaschromatography. Lung function was assessed via spirometry. Seven patients with chronic obstructive pulmonary disease (COPD) and three patients with acute lung inflammation served as control groups. Neutrophil and bacterial lactate production was assessed under aerobic and anaerobic conditions.

Results
In sputum specimens of patients with respiratory exacerbations lactate concentrations decreased significantly (p < 0.005) from 3.4 ± 2.3 mmol/L to 1.4 ± 1.4 mmol/L after 2–3 weeks of intravenous antibiotics. Successful treatment was reflected in 16 patients (88.9%) by FVC increase associated with lactate decrease (p < 0.05). In every single sputum lactate was detectable (3.0 ± 3.1 mmol/L, range 0.2–14.1 mmol/L). Lactate was lower (1.6 ± 0.8 mmol/L) in sputa from seven COPD patients, and it was below the detection limit in three patients with acute lung inflammation. Neutrophil lactate production accumulated up to 10.5 mmol/L after 4 days, whereas bacterial lactate production did not appear to contribute substantially to sputum lactate concentrations.

Conclusions
Successful antibiotic therapy is reflected by a decrease in lactate concentrations. Neutrophils are the most likely source for lactate in sputum of CF patients. Therefore lactate may be used to monitor responses to antibiotic therapy as an adjunct to lung function measurements.