PATHOGENETIC ASPECTS OF ACUTE PANCREATITIS AT THE SUB-CELLULAR LEVEL

Abstract

The pathogenesis of acute pancreatitis (AP) is based on a cascade of reactions of immunological
inflammation due to dysfunction of important structures at the subcellular level. At an early stage of AP,
excessive activation of leukocytes and the subsequent release of an inflammatory mediator are crucial for
the development of early organ failure. Regardless of the cause, trigger events lead to premature activation
of pancreatic proteases simultaneously with the activation of lysosomal enzymes. The initiating events of
pancreatic necrosis, including zymogen activation and cell death, occur in the pancreatic acinar cells (PAC),
where the earliest immune response is also noted in the form of activation of circulating immune cells,
which triggers a systemic inflammatory response. Further in-depth study of pathophysiological disorders
at the subcellular level is necessary for targeted and effective therapy of AP.