Review of experimental animal models of acute pancreatitis

Abstract

The underlying mechanisms involved in the pathogenesis of acute pancreatitis are ill understood. The mortality rate of this disease has not significantly improved over the past few decades. Current treatment options are limited, and predominantly aimed at supportive therapy. A key feature of severe acute pancreatitis is the presence of extensive tissue necrosis with both local and systemic manifestations of inflammatory response syndromes. A better understanding of the underlying pathophysiology of severe acute pancreatitis may lead to more targeted therapeutic options, potentially leading to improved survival. Animal models of acute pancreatitis are therefore an essential investigative tool for these aims to be achieved. This review discusses the suitability of recent non-invasive models of acute pancreatitis such as hormone-induced, alcohol-induced, immune-mediated, diet-induced, gene knockout and L-arginine; and invasive models including closed duodenal loop, antegrade pancreatic duct perfusion, biliopancreatic duct injection, combination of secretory hyperstimulation with minimal intraductal bile acid exposure, vascular-induced, ischaemia/reperfusion and duct ligation.

High Expression Levels of Trigger Receptor Expressed on Myeloid Cells-1 on Neutrophils Associated with Increased Severity of Acute Pancreatitis in Mice

“…21) Furthermore, the severity of AP induced by L-arginine is dose-and time-dependent, which is very useful for the investigation of early and late phases of the process of AP. [22][23][24] In addition, the course, severity, and histological changes of AP in this model are similar to those in humans.…”

Autophagy and pancreatitis

“…There are several widely used rodent models of nonalcoholic acute pancreatitis, such as pancreatitis induced in rats or mice by administration of high-dose caerulein (an analog of CCK-8), L-arginine, or bile acids and, in young mice, by feeding a choline-deficient, ethionine-supplemented diet (60,99). Models of alcoholic pancreatitis combine ethanol feeding with another stressor [low-dose caerulein (81) or LPS (24)], because alcohol alone does not cause pronounced pancreatic damage in rodents.…”

Time-course proteomic analysis of taurocholate-induced necrotizing acute pancreatitis

“…This mechanism of disease induction yields a significantly different phenotype than the cerulein model explored in previously published proteomic studies on AP. Taurocholate-induced AP is indeed characterized by a more severe disease with, in particular, severe pancreatic necrosis and systemic inflammation [2,9]. The objectives of this study were to highlight changes in the pancreas proteome occurring in the early steps of the experimental disease, to determine the kinetics of functionally related proteins, and to correlate these results with parameters classically used to assess disease severity and with proteomic data previously obtained from the cerulein model.…”