Abstract
Under normal conditions, trypsin activity is properly suppressed in the pancreatic acinar cells. Small amount of trypsin can be inactivated by pancreatic secretory trypsin inhibitor (PSTI) thereby preventing damage to pancreatic acinar cells as a first line of defense. However, if trypsin activation exceeds the capacity of PSTI, a subsequent cascade of events leads to the activation of various proteases that damage cells. This can be interpreted as the main causative agent of pancreatitis onset.
Ischemia, autodigestion, and systemic inflammatory response syndrome (SIRS)/sepsis are the major aggravation mechanisms of acute pancreatitis. The role of trypsin, trypsin receptor (protease-activated receptor-2: PAR-2), pro-inflammatory cytokines, and endothelins are described as the key molecules for the aggravation of acute pancreatitis.
