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Proteolytic action of NSPs is controlled endogenously by the serpin (serine proteinase inhibitor) superfamily of proteins (e.g., alpha1-antitrypsin (AAT), alpha1antichymotrypsin, monocyte NE inhibitor) and the chelonianin family of canonical inhibitors (elafin, secretory leukocyte protease inhibitor) ( 3.1 Inflammatory respiratory diseases NSPs are released in the airways of patients with multiple types of chronic pulmonary diseases such as COPD, AATD, bronchiectasis, and CF, and have been implicated as key mediators of chronic inflammation and disease progression ( 3.1.1 Chronic obstructive pulmonary disease COPD is characterized by persistent neutrophilic inflammation of the airway lumen and destruction of the lung parenchyma, leading to progressive deterioration of lung function ( Multiple lines of evidence point to NSPs as primary mediators of COPD-associated pulmonary tissue damage and clinical decline ( NE has generally been regarded as the principal NSP contributing to the pathophysiology of COPD, but more recent data indicate that PR3 and CatG also have significant roles ( 3.1.2 Alpha-1 antitrypsin deficiency AAT is the archetypal member of the serpin superfamily ( AATD is an underrecognized genetic condition characterized by low circulating AAT levels that may lead to lung and liver disease

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These proteins trigger the formation of new blood vessels, a process known as angiogenesis