Protease inhibitors are added to prevent:
Innate immunity balances protease mediated tissue remodeling with protective antiproteases preventing autodamage. Neutrophils recruited to injury sites degranulate releasing azurophilic granules containing serine protease neutrophil elastase capable of degrading elastin collagen, cathepsin G, proteinase 3, and specific granules releasing matrix metalloproteases MMP8 collagenase and MMP9 gelatinase facilitating migration through basement membrane. Uncontrolled release would destroy cartilage and lung parenchyma causing emphysema in alpha-1 antitrypsin deficiency. Plasma contains defensive inhibitors: serpins alpha-1 antitrypsin AAT 52 kDa irreversible suicide substrate forming covalent complex with elastase, alpha-1 antichymotrypsin inhibiting cathepsin G, inter-alpha-trypsin inhibitor, and broad spectrum alpha-2 macroglobulin 720 kDa tetramer trapping proteases via bait region cleavage induced conformational change from expanded to compact enclosing enzyme inside physical cage sterically blocking large substrates, and tissue inhibitors metalloproteases TIMP-1 to TIMP-4 forming 1:1 complex with MMP zinc. This mechanistic insight supports diagnostic and therapeutic applications while reinforcing core immunological and cell biology principles taught in advanced curricula.
Ref: Lodish Molecular Cell Biology serpin α1 antitrypsin α2 macroglobulin; Alberts MBoC protease inhibitors serum protection lysis cocktail.