Todetermine whether markers of mucus secretion can be quantified in airway lining fluid from asthmatic and from healthy subjects, we measured levels of a mucin-like glycoprotein (MLG) and lactoferrin in sputum induced by inhalation of hypertonic (3%) saline in 18 asthmatic and in 10 healthy subjects. Because DNA, like mucin, contributes to the viscosity of airway secretions, we also measured DNA levels in the induced sputum samples. Tocontrol for the presence of saliva in sputum, we also analyzed saliva samples from all subjects. The entire sputum sample and the saliva sample were reduced using dithiotreitol, and biochemical analysis was performed on supernatants obtained after centrifugation. We found that induced sputum from asthmatic subjects had higher levels of MLG [2,574.4±907.8 (mean±SEM) versus 562.2±90.5~ g/ml, p< 0.007] and DNA (7.1±1.6versus 3.6±0.6 J, lg/ml, p< 0.05), but the difference in lactoferrin levels failed to reach statistical significance. However, in the subgroup of asthmatic subjects who gave a history of sputum production (n= 9), lactoferrin levels were higher than in the healthy control SUbjects (118.9±46.3 versus 35.2±6.5 J, lg/ml, p< 0.05). The very low levels of MLG, DNA, and lactoferrin measured in saliva were not significantly different in asthmatic subjects from those in healthy subjects. We conclude that measurement of markers of mucus secretion in induced sputum is feasible in asthmatic and healthy subjects, and it reveals abnormally high markers of mucus secretion in subjects with stable asthma. In these asthmatic patients the sputum DNA levels were much lower than those reported in sputum from patients with cystic fibrosis or bronchiectasis.

Asthma is characterized clinically not only by episodic wheeze and reversible airflow obstruction but also by excessive airway secretions. Oppenshaw and Turner-Warwick (1) found that 77% of asthmatic subjects questioned in the outpatient setting reported sputum production as a prominent symptom. In addition, mucus plugging of the airways is a documented feature of the pathophysiology of acute severe asthma (2-5). Despite these observations, little is known about the cause of increased mucus production in asthma. Goblet cell hyperplasia and submucosal gland cell hyperplasia have been found on examination of airways from patients who died in status asthmaticus (4-6), and goblet cell hyperplasia has been demonstrated in patients with less severe asthma (7, 8-10). Biochemical and rheologic studies of asthmatic sputum have demonstrated no consistent differences between the viscosity of sputum from asthmatic subjects and that from healthy SUbjects or from subjects with other forms of airway disease (11-13), and no significant differences have been found from healthy sputum