Abstract
Acute pancreatitis (AP) is a severe disease associated with high morbidity and mortality. Clinical studies can provide some data concerning the etiology, pathophysiology, and outcomes of this disease. However, the study of early events and new targeted therapies cannot be performed on humans due to ethical reasons. Experimental murine models can be used in the understanding of the pancreatic inflammation, because they are able to closely mimic the main features of human AP, namely their histologic glandular changes and distant organ failure. These models continue to be important research tools for the reproduction of the etiological, environmental, and genetic factors associated with the pathogenesis of this inflammatory pathology and the exploration of novel therapeutic options. This review provides an overview of several murine models of AP. Furthermore, special focus is made on the most frequently carried out models, the protocols used, and their advantages and limitations. Finally, examples are provided of the use of these models to improve knowledge of the mechanisms involved in the pathogenesis, identify new biomarkers of severity, and develop new targeted therapies.
Highlights
Acute pancreatitis (AP), especially severe cases, is a major clinical and financial burden, representing over 320,000 hospital admissions in the United States in 2012 [1]
The failure to reproduce acute pancreatitis reflects the human condition, and it is necessary to take into account an additional sensitizing factor or a genetic predisposition regarding the development of alcoholic AP
This model was used by several researchers to study the pathogenesis [143] and target therapies [144,145], and was developed in an attempt to mimic the clinical situation of a gallstone that oIbnt.sJt
Summary
Acute pancreatitis (AP), especially severe cases, is a major clinical and financial burden, representing over 320,000 hospital admissions in the United States in 2012 [1]. An ideal model should be simple and reproducible, with the ability to produce controlled severity in order to mimic human disease and answer the experimental question [13]. When performing these models, the researcher should be based on the elevation of pancreatic enzymes, such as amylase and lipase, in order to confirm the induction of AP, taking into account that these enzymes do not reflect the degree of severity. Pancreatitis severity can be assessed by significant histological changes such as interstitial edema, acinar cell death, parenchymal loss, hemorrhage, inflammatory cell infiltration, and vacuolization, and the evaluation of local or systemic complications, with the lung being the organ most involved [14]. Examples of the use of these models with the objective of improving the knowledge of the mechanisms involved in the pathogenesis, identifying new biomarkers of severity, and developing new targeted therapies are provided
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