CHRONIC SMOKE EXPOSURE ALTERS THE PHENOTYPE PATTERN AND THE METABOLICRESPONSE IN HUMAN ALVEOLAR MACROPHAGES

Smoking induces a chronic inflammatory process in the lower respirator y tract, where the alveolar macrophages (AM) are the main phagocytes. In the present study, the expressions of different membrane glycoprote ins (CD11abc, CD71, CD54, CD14 and CD16) were determined by flow cytom etry in AM from smokers and non-smokers after quenching of the intrace llular autofluorescence. The metabolic activity of the AM was quantifi ed as a functional test. The expressions of CD11a, CD54 and CD71 were higher in non-smokers' AM than in smokers'. The expressions of CD11b a nd CD16 were similar between the groups, while the CD11c was higher in smokers' AM compared with non-smokers'. The expression of CD14 was we ak in both groups, therefore there was no clear-cut difference between the background and positively labelled cell populations. The metaboli c response after in vitro stimulation with the phorbol ester phorbol m yristate acetate (PMA) was higher in non-smokers' than in smokers' AM. Our results indicate that chronic exposure to tobacco smoke influence s both the expression of AM membrane antigens and the metabolic activi ty. AM from non-smokers express a phenotype more related to cell proli feration and an accessory function. In contrast, receptors reflecting adhesion and phagocytosis were unaltered or even increased in smokers' AM. The findings suggest a functional change in the AM population aft er chronic smoke exposure.