Matrix metalloproteinase expression and production by alveolar macrophages in emphysema.

  title={Matrix metalloproteinase expression and production by alveolar macrophages in emphysema.},
  author={G A Finlay and L. R. O’Driscoll and K. J. Russell and E M D'arcy and James B. Masterson and Muiris X. FitzGerald and Clare M. O'connor},
  journal={American journal of respiratory and critical care medicine},
  volume={156 1},
The aim of this study was to examine the hypothesis that alveolar macrophages represent a significant source of matrix-degrading proteinases in the emphysematous lung. Macrophages from bronchoalveolar lavage fluid of 10 patients with emphysema and 10 normal volunteers were maintained in vitro for 24 h and assessed semiquantitatively for mRNA transcript levels of the matrix metalloproteinases (MMPs) gelatinases A and B, macrophage metalloelastase (MME), and interstitial collagenase. Release of… 

Figures and Tables from this paper

Matrix Metalloproteinase Expression by Human Alveolar Macrophages in Relation to Emphysema

Results suggest that alveolar macrophage matrix metalloproteinase 1 and 12 may have a role in the lung structural changes leading to the development of emphysema, and provide evidence to support the concept that multiple proteinases, causing both elastin and collagen degradation, are important in the pathogenesis of pulmonary emphySEma.

Surfactant protein A increases matrix metalloproteinase-9 production by THP-1 cells.

Observations suggest the presence of a novel, locally controlled mechanism by which MMP-9 levels may be regulated in alveolar macrophages, and speculate that SP-A may influence the protease/antiprotease balance in the lungs of patients with quantitative and/or qualitative changes in surfactant constituents favoring an abnormal breakdown of extracellular matrix components.

Human collagenase (matrix metalloproteinase-1) expression in the lungs of patients with emphysema.

The lung is altered in emphysema such that the Type II pneumocyte secretes MMP-1 and the induction of a proteolytic enzyme within the Type 2 pneumocyte suggests that the cells within the lung itself are capable of producing degradative enzymes in this disease process.

Matrix metalloproteinases and tissue inhibitor of metalloproteinase-1 in sarcoidosis and IPF

The purpose of this study was to examine the role of interstitial collagenases, members of the family of matrix metalloproteinases, in the development of pulmonary fibrosis. The activity, levels and

Release and activity of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 by alveolar macrophages from patients with chronic obstructive pulmonary disease.

It is suggested that macrophage-derived MMP-9 and TIMP-1 from alveolar macrophages might be important in the development of COPD because these cells exhibit increased levels of elastolytic activity.

Matrix Metalloproteinase-12 and Cathepsin D Expression in Pulmonary Macrophages and Dendritic Cells of Cigarette Smoke-Exposed Mice

Results indicate that cigarette smoke increases the expression of MMP-12 and Cathepsin D in the lungs of mice, and that not only macrophages but also DCs produce M MP-12.

Balance of matrix metalloprotease-9 and tissue inhibitor of metalloprotease-1 from alveolar macrophages in cigarette smokers. Regulation by interleukin-10.

It is concluded that the release of proteases and antiproteases by airway macrophages is increased in cigarette smokers, and can be regulated by exogenous IL-10.

Red blood cells increase secretion of matrix metalloproteinases from human lung fibroblasts in vitro.

Tissue remodeling is an important process in many inflammatory and fibrotic lung disorders. RBC may in these conditions interact with extracellular matrix (ECM). Fibroblasts can produce and secrete

Increase in macrophage elastase (MMP-12) in lungs from patients with chronic obstructive pulmonary disease

It is demonstrated that COPD patients produce greater quantities of MMP-12 than controls, which may be a critical step in the pathogenesis of COPD and emphysema.



Elastin degradation by human alveolar macrophages. A prominent role of metalloproteinase activity.

A prominent role for metalloproteinase activity in elastin degradation by both human and murine macrophages is indicated and support the concept that events at the cell-substrate interface are critically important to macrophage-mediated elast in degradation.

Alveolar macrophage modulation of proteolysis by neutrophil elastase in extracellular matrix.

It is suggested that AM can release previously internalized NE in an enzymatically active form and that AM may enhance collagen degradation in matrix that was also exposed to NE.

Neutral metalloproteinases produced by human mononuclear phagocytes. Enzyme profile, regulation, and expression during cellular development.

The potential of macrophages to directly degrade extracellular matrix via secreted metalloproteinases in a manner that differs both qualitatively and quantitatively from that of fibroblasts is confirmed.

Elastolytic metalloproteinases produced by human mononuclear phagocytes. Potential roles in destructive lung disease.

  • S. Shapiro
  • Biology
    American journal of respiratory and critical care medicine
  • 1994
The most newly described member of the MMP family is human macrophage metalloelastase, a major product of human alveolar macrophages that is also an elastase.

Alveolar inflammation and its relation to emphysema in smokers.

The data suggest that as long as the inflammatory reaction is predominantly of neutrophils there is no destruction of the lung, and the extent of lung destruction becomes evident, and its extent is directly related to the number of alveolar macrophages and T-lymphocytes/mm3.

Excessive neutrophil elastase in bronchoalveolar lavage fluid in subclinical emphysema.

It is concluded that NE-alpha 1-PI complex in BALF is a factor that may differentiate smokers who are potentially developing emphysema from those who are not, and NE inhibitory activity measured by a spectrophotometric method did not show any significant difference between the two groups of current smokers.

The role of thiol proteases in tissue injury and remodeling.

Human lung macrophages express all four of the known lysosomal thiol proteases and recent studies of the differential expression of these cathepsins suggest they not only cooperate in terminal degradation of endocytized protein but also have specific functions such as proenzyme activation, antigen processing, and tissue remodeling, especially bone matrix resorption.

Degradation of connective tissue matrices by macrophages. III. Morphological and biochemical studies on extracellular, pericellular, and intracellular events in matrix proteolysis by macrophages in culture

Extracellular, pericellular, and lysosomal events each contribute to degradation of extracellular matrix macromolecules by inflammatory macrophages.

Elastin and collagen remodeling in emphysema. A scanning electron microscopy study.

The novel concept of increased collagen deposition and aberrant collagen remodeling in the pathogenesis of emphysema is supported by ultrastructural examination of elastin and collagen templates in an animal model of empysema and in human lungs.