Release and Activity of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-1 by Alveolar Macrophages from Patients with Chronic Obstructive Pulmonary Disease

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 acti...

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Veröffentlicht in:American journal of respiratory cell and molecular biology Jg. 26; H. 5; S. 602 - 609
Hauptverfasser: Russell, Richard E. K, Culpitt, Sarah V, DeMatos, Carmen, Donnelly, Louise, Smith, Michael, Wiggins, John, Barnes, Peter J
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States Am Thoracic Soc 01.05.2002
Schlagworte:
Aged
Bronchoalveolar Lavage Fluid - cytology
Cell Count
Cells, Cultured
Culture Media, Conditioned - pharmacology
Dexamethasone - pharmacology
Dose-Response Relationship, Drug
Enzyme Activation - drug effects
Female
Glucocorticoids - pharmacology
Humans
Interleukin-1 - pharmacology
Lipopolysaccharides - pharmacology
Macrophages, Alveolar - cytology
Macrophages, Alveolar - drug effects
Macrophages, Alveolar - metabolism
Male
Matrix Metalloproteinase 9 - biosynthesis
Middle Aged
Pulmonary Disease, Chronic Obstructive - metabolism
Pulmonary Disease, Chronic Obstructive - pathology
Smoking - metabolism
Smoking - pathology
Tissue Inhibitor of Metalloproteinase-1 - biosynthesis
Tobacco Smoke Pollution
ISSN:1044-1549, 1535-4989
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Zusammenfassung: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.
Bibliographie:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ISSN:1044-1549
1535-4989
DOI:10.1165/ajrcmb.26.5.4685