1. Some bronchiectatic patients persistently expectorate purulent secretions containing many polymorphonuclear leucocytes (PMN) and bacteria, suggesting ineffective microbial clearing from the lung. We have therefore studied several aspects of PMN recruitment to the lung by chemotaxis. 2. Circulating PMN from patients with bronchiectasis show a variable chemotactic response to the synthetic peptide N -formyl- l -methionyl- l -leucyl- l -phenylalanine. This is similar to the response of PMN from healthy controls and suggests that failure to clear microbial organisms is not due to defective chemotaxis as measured here. 3. Purulent sputum solphase demonstrates chemotactic activity against control PMN. This activity is greater ( P < 0.001) than that found with mucoid sputum solphase, which is consistent with the neutrophil content of the secretions in vivo. 4. Successful antibiotic therapy reduces the chemotactic activity of purulent sputum solphase from a median value of 183 (range 28–201) cells/high power field to 33.5 (range 0.7–64) cells/high power field ( P < 0.0025). This indicates that the chemotactic activity is largely associated with bacterial load.

1. Anti-elastase function in sputum sol-phase from patients with α 1 -proteinase inhibitor (α 1 PI) deficiency was compared with sol-phase from patients with cigarette smoke-induced bronchitis and emphysema. 2. Both α 1 PI (2 P < 0.01) and anti-leucoprotease (ALP) (2 P < 0.01) concentrations were lower in sol-phase from the α 1 PI-deficient group, although α 2 -macroglobulin (α 2 M) levels were similar. 3. There was no difference in α 1 PI function between the two groups, but the inhibitor was only ≃ 30% active. 4. The absolute neutrophil elastase (NE) inhibitory capacity was similar in both groups (median 185 μg of NE inhibited/ml of sputum, range 80–480, for the α 1 PI-deficient group; median 175, range 80–300, for the bronchitic group). A substantial proportion of NE inhibition in secretions could not be accounted for by the amount of α 1 PI, ALP and α 2 M present (median 74.8%, range 43.2–97.4, for α 1 PI-deficient sol-phase; median 50.0%, range 0–80.8, for bronchitic sol-phase). 5. Gel filtration of sol-phase demonstrated the presence of NE inhibition in the low molecular weight fractions which was markedly sensitive to changes in substrate concentration and ionic strength, in contrast to purified α 1 PI and ALP. 6. Sputum sol-phase from both groups failed to prevent hydrolysis of elastin–fluorescein or succinyltrialanyl- p -nitroanilide by NE completely during prolonged incubation in the presence of an excess of functional inhibitors. This was more apparent in secretions from subjects with α 1 PI deficiency and may explain why such patients have a more rapidly progressive form of emphysema.