Alveolar macrophage function and inflammatory stimuli in smokers with and without obstructive lung disease.

Abstract

To explore possible cofactors in the development of chronic obstructive pulmonary disease (COPD) in smokers, we performed bronchoalveolar lavage in 6 smokers with normal pulmonary function, 6 smokers with COPD (FEV1/FVC less than or equal to 65%) matched for smoking history and age, and 9 age-matched nonsmoking control subjects. Elastase release by macrophages from smokers with COPD was significantly higher (p less than 0.016) than was elastase release by macrophages from normal smokers. There were no differences between chemoattractiveness of alveolar macrophage supernatants for one person's polymorphonuclear leukocytes among the groups of smokers and there was no detectable C5/C5a in these supernatants (limit of detection of C5a greater than 1 ng/ml). There were no significant differences in numbers or species of bacteria in aerobically and anaerobically cultured bronchial brushings. There was no difference in alveolar macrophage superoxide anion release with particulate or membrane-perturbing stimuli for the smokers. Alveolar macrophages from the 3 groups of subjects had similar limited microbicidal ability for the obligate intracellular protozoan, Toxoplasma gondii, and similar numbers of elastase receptors and affinity for elastase.