Abstract
It has been generally accepted that pathogenic intra-acinar trypsinogen activation followed by auto-digestion of the pancreas plays a critical role in the development of acute pancreatitis. However, recent studies suggest that auto-digestion by activated trypsin alone cannot fully account for the pathogenesis of acute pancreatitis since experimental acute pancreatitis is successfully induced even without the full-activation of trypsinogen. Although intra-acinar trypsinogen activation followed by auto-digestion of the pancreas is an initial step of acute pancreatitis, pathogenic immune reactions are involved in the sustained pancreatic inflammation. In this regard, recent studies highlight the importance of innate immune responses mediated by intestinal microflora translocated into the pancreas and by endogenous auto-antigens released from the necrotic pancreatic tissue.
