The best-studied mechanism of tissue damage in COPD is that of protease-antiprotease imbalance. Proteases are enzymes that degrade matrix proteins. Elastin is an important target, but collagen, proteoglycans, laminin and fibronectin are also degraded [41-43].
The most potent proteases are the neutrophil elastase, cathepsin G and proteinase 3 and matrix metalloproteinases [44,45]. Neutrophils are the major providers of the above proteases, but other cells such as macrophages and airway epithelial cells may also contribute. The elastolytic activity of proteases is balanced by the antiproteases, such as a1-antitrypsin. a1-Antitrypsin is the major endogenous tissue antiprotease (plasma/lung parenchyma), and secretory leucoprotease inhibitor (SLPI) is the major antiprotease in the airways [41,46]. Clearly, in COPD there is an imbalance in the protease-antiprotease system in favour of proteases .
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