ALVEOLAR MACROPHAGE FUNCTION AND INFLAMMATORY STIMULI IN SMOKERS WITH AND WITHOUT OBSTRUCTIVE LUNG-DISEASE

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Abstract
Possible cofactors in the development of chronic obstructive pulmonary disease (COPD) in smokers were studied by bronchoalveolar lavage in 6 smokers with normal pulmonary function, 6 smokers with COPD (FEV1/FVC [forced expiratory volume in 1 min/forced vital capacity] .ltoreq. 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 < 0.016) than was elastaserelease by macrophages from normal smokers. There were no diffferences between chemoattractiveness of alveolar macrophages supernatants for 1 person''s polymorphonuclear leukocytes among the groups of smokers and there was no detectable C5/C5a in these supernatants (limit of detectionof C5a greater than 1 ng/ml). There were no significant differences in numbers of 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.

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