The precise mechanisms involved in the pathophysiology of acute pancreatitis (AP) are still far from clear. Several earlier studies have focused mainly on pancreatic enzyme activation as the key intracellular perturbation in the pancreatic acinar cells. For decades, the trypsin-centered hypothesis has remained the focus of the intra-acinar events in acute pancreatitis. Recent advances in basic science research have lead to the better understanding of various other mechanisms such as oxidative and endoplasmic stress, impaired autophagy, mitochondrial dysfunction, etc. in causing acinar cell injury. Despite all efforts, the clinical outcome of patients with AP has not changed significantly over the years. This suggests that the knowledge of the critical molecular pathways in the pathophysiology of AP is still limited. The mechanisms through which the acinar cell injury leads to local and systemic inflammation are not well understood. The role of inflammatory markers and immune system activation is an area of much relevance from the point of view of finding a target for therapeutic intervention. Some data are available from experimental animal models but not much is known in human pancreatitis. This review intends to highlight the current understanding in this area.
Keywords: Acute pancreatitis; Damage associated molecular pattern; Inflammation; Pathophysiology; Trypsin.