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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Published in:	American journal of respiratory cell and molecular biology Vol. 26; no. 5; pp. 602 - 609
Main Authors:	Russell, Richard E. K, Culpitt, Sarah V, DeMatos, Carmen, Donnelly, Louise, Smith, Michael, Wiggins, John, Barnes, Peter J
Format:	Journal Article
Language:	English
Published:	United States Am Thoracic Soc 01.05.2002
Subjects:	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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Abstract	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.
AbstractList	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. 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.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.
Author	Barnes, Peter J Donnelly, Louise Wiggins, John Russell, Richard E. K DeMatos, Carmen Culpitt, Sarah V Smith, Michael
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/11970913$$D View this record in MEDLINE/PubMed
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References	B20 B21 B22 B23 Church D. F. (B28) 1985; 11 B24 B25 B26 B27 B29 Stone P. J. (B6) 1995; 151 Mead J. (B4) 1971; 64 B30 B31 B10 B32 B11 B33 B12 B34 B13 B14 B15 B16 B17 B18 B19 B1 B2 B3 B5 B7 B8 B9
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SubjectTerms	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
Title	Release and Activity of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-1 by Alveolar Macrophages from Patients with Chronic Obstructive Pulmonary Disease
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