Alveolar macrophages (AM) participate actively in the inflammatory response that characterises chronic obstructive pulmonary disease (COPD). The present study investigated potential changes in AM phenotypes in patients with COPD.Using flow cytometry, the surface expression of receptors implicated in phagocytosis (CD44, CD36, CD51, CD61, CD14), antigen-presenting capacity (human leukocyte antigen (HLA)-DR), costimulatory molecules (CD80, CD86, CD40) and complement receptor type 3 were assessed in AM from 18 patients with COPD, 14 smokers with normal lung function and nine nonsmokers.When compared to smokers with normal lung function and nonsmokers, the surface expression of HLA-DR and CD80 was lower in AM of patients with COPD. In addition, these patients had a higher percentage of AM with a low level surface expression of CD44. There did not appear to be any difference in the other receptors studied in AM between the three groups. The expression of all these receptors in peripheral blood monocytes also did not differ between groups.In conclusion, these observations suggest that the cell-mediated immune function of alveolar macrophages can be reduced in chronic obstructive pulmonary disease, and that this is a local rather than a systemic event.

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The present study tested the hypothesis that alveolar macrophages (AM) from patients with chronic obstructive pulmonary disease (COPD) release more pro-inflammatory and/ or less anti-inflammatory mediators than those from smokers with normal lung function and neversmokers.AM were sorted by flow cytometry from bronchoalveolar lavage fluid in 13 patients with COPD (mean¡SEM 67¡2 yrs, forced expiratory volume in one second (FEV1) 61¡4% reference), 16 smokers with normal lung function (55¡2 yrs, FEV1 97¡4% reference) and seven never-smokers (67¡7 yrs, FEV1 94¡4% reference). After sorting, AM were cultured (with and without lipopolysaccharide stimulation) after 4 h and 24 h, and the concentrations of leukotriene B 4 (LTB 4 ), transforming growth factor (TGF)-b 1 and tissue inhibitor of metalloproteinase (TIMP)-1 were quantified in the supernatant by ELISA. The production of reactive oxygen intermediates (ROI) in freshly isolated AM was determined by flow cytometry.LTB 4 secretion and ROI production were not different between groups. In contrast, AM from COPD patients released significantly less TGF-b 1 and TIMP-1 than those from smokers with normal lung function and nonsmokers.In conclusion, these observations are compatible with reduced anti-inflammatory and antielastolytic capacity in chronic obstructive pulmonary disease, which is likely to contribute to the pathogenesis of the disease.

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