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In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure
Published on: October 22, 2019
Alveolar macrophage proteinase/antiproteinase expression in lung function and emphysema
Takeo Ishii1, Raja T Abboud, Alison M Wallace
1Institute for Heart and Lung Health, St. Paul's Hospital, Vancouver, BC.
The European Respiratory Journal
|August 1, 2013
Summary
Matrix metalloproteinases (MMPs) and cathepsins in alveolar macrophages are linked to chronic obstructive pulmonary disease (COPD) severity. Increased MMP12 and MMP1 expression may contribute to emphysema development in COPD patients.
Area of Science:
- Pulmonary Medicine
- Cellular Biology
- Immunology
Background:
- Alveolar macrophages are key players in chronic obstructive pulmonary disease (COPD) pathogenesis.
- Their production of matrix metalloproteinases (MMPs), cathepsins, and their inhibitors influences COPD phenotypes.
Purpose of the Study:
- To investigate how macrophage gene expression of MMPs and cathepsins relates to COPD phenotypes.
- To determine the influence of genetic variations on these molecular expressions.
Main Methods:
- Quantitative PCR and ELISAs/gelatine zymography were used to measure mRNA and protein levels.
- Analysis correlated molecular expression with genotype, pulmonary function (spirometry, DLCO), and emphysema extent.
Main Results:
- Basal MMP12 mRNA levels correlated inversely with lung diffusing capacity and FEV1/FVC.
- Stimulated MMP12 protein levels related inversely to lung diffusing capacity and positively to emphysema extent.
- Basal MMP1 mRNA correlated positively with emphysema, while Cathepsin L protein associated positively with FEV1% predicted.
Conclusions:
- Elevated MMP12 and MMP1 expression in alveolar macrophages may drive emphysema pathogenesis.
- Cathepsin L and MMP9 might be involved in the development of airflow limitation in COPD.
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