PRTN3 and bronchiectasis: The release of inflammatory effectors from neutrophils contributes toward the inflammatory environment of the lung [9], and an imbalance between neutrophil-derived serine proteases (NSPs; neutrophil elastase [NE], proteinase 3 [PR3] and cathepsin G [CatG]) and their endogenous inhibitors has been documented in patients with chronic inflammatory respiratory diseases, including bronchiectasis [10–14].