Volume 149, Issue 7, Pages 1682-1685 (December 2015) Neutrophil Extracellular Traps Provide a Grip on the Enigmatic Pathogenesis of Acute Pancreatitis  Juha T. Korhonen  Gastroenterology  Volume 149, Issue 7, Pages 1682-1685 (December 2015) DOI: 10.1053/j.gastro.2015.10.027 Copyright © 2015 AGA Institute Terms and Conditions

Figure 1 Key intra-pancreatic events during acute pancreatitis. Pathologic stimulus leads to intra-acinar events leading to co-localization of zymogen and lysosomes which brings trypsinogen in contact with cathepsin B. In these co-localized organelles, cathepsin B activates trypsinogen to trypsin. Activated trypsin then aides in leakage of cathepsin B into the cytosol, which in turn activates the cell death pathways. Pathologic stimulus, besides causing co-localization, also activate nuclear factor-κB, which regulates the production of cytokines and chemokines, that in turn attract neutrophils to the site of injury. The infiltrating neutrophils also increase intra-acinar trypsinogen activation. These infiltrating neutrophils can also release neutrophil extracellular traps, which can contribute to intra-acinar trypsin activation and tissue damage. Gastroenterology 2015 149, 1682-1685DOI: (10.1053/j.gastro.2015.10.027) Copyright © 2015 AGA Institute Terms and Conditions