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Destruction of lung elastin is critical for development of emphysema associated with chronic obstructive pulmonary disease (COPD). Lung macrophages release elastolytic enzymes, including matrix metalloproteinase (MMP)-9, along with tissue inhibitors of MMP (TIMP). We examined the production and activity of macrophage-derived MMP-9 and TIMP-1 from alveolar macrophages (AM) from smokers with COPD, healthy smokers (HS), and nonsmokers (NS). AM were stimulated with either lipopolysaccharide (LPS), interleukin (IL)-1 beta, or cigarette smoke-conditioned culture medium (CSM). AM from patients with COPD released greater amounts of MMP-9 with greater enzymatic activity than HS and NS. In contrast, AM from NS released more TIMP-1 than cells from HS and subjects with COPD. LPS and IL-1 beta caused a dose-dependent increase in MMP-9 release and activity, together with increased levels of TIMP-1. Dexamethasone prevented the increase in MMP-9 release, and increased TIMP-1 release. CSM increased MMP-9 and TIMP-1 release from AM of all groups. Dexamethasone decreased CSM-stimulated MMP-9 release, but had no effect on MMP-9 activity This study suggests that macrophages might be important in the development of COPD because these cells exhibit increased levels of elastolytic activity.

Original publication




Journal article


Am J Respir Cell Mol Biol

Publication Date





602 - 609


Aged, Bronchoalveolar Lavage Fluid, Cell Count, Cells, Cultured, Culture Media, Conditioned, Dexamethasone, Dose-Response Relationship, Drug, Enzyme Activation, Female, Glucocorticoids, Humans, Interleukin-1, Lipopolysaccharides, Macrophages, Alveolar, Male, Matrix Metalloproteinase 9, Middle Aged, Pulmonary Disease, Chronic Obstructive, Smoking, Tissue Inhibitor of Metalloproteinase-1, Tobacco Smoke Pollution