Protease Inhibitors Extracted from Caesalpinia echinata Lam. Affect Kinin Release during Lung Inflammation

Figure 4

Potential sources of kinin in LPS-induced lung inflammation model. Kinin may be generated in lung via kininogen hydrolysis and is rapidly degraded by kininases. This peptide can be released into the alveolar space through distinct pathways: (a) in neutrophil-bound kininogen cleavage by plasma kallikrein, (b) kininogen hydrolysis by NE and PR3, or (c) diffusion from the lung interstitium to the alveolar space. In the plasma, pK, PR3, and NE all release kinin. Additionally, kinin might be exchanged between plasma, lung, and alveolar space. K: kininogen (high-molecular-weight, low-molecular-weight, and/or T-kininogen); pK: plasma kallikrein; NE: neutrophil elastase; PR3: proteinase 3; BALF: bronchoalveolar lavage fluid; LKT: leukotrienes; PAF: platelet activator factor.