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Updated: Aug 17, 2026

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
Published on: May 10, 2024
Potential new therapies for the treatment of acute pancreatitis
1Department of Surgery, MDC 16, University of South Florida, 12901 Bruce B. Downs Blvd, Tampa, FL 33612, USA. edenham@com1.med.usf.edu
Abstract:
The treatment of acute pancreatitis has remained virtually unchanged for the past 50 years, in large part due to a poor understanding of the initial intracellular events. Furthermore, there is a lack of knowledge regarding the mediator(s) responsible for the progression of the disease from local pancreatic inflammation to a systemic inflammatory disease, as well as the mediator(s) responsible for distant organ dysfunction and failure. With recent advances in the pathophysiology of pancreatitis, in particular the role of the inflammatory mediators interleukin-1 beta, tumour necrosis factor alpha and platelet-activating factor, the potential for new effective therapies has been realised. At present, a number of inflammatory mediator antagonists are being tested in humans, with the hope that we may soon develop a specific treatment for a disease, which thus far, has none.
Insights
Acute pancreatitis treatment lacks progress due to poor understanding of its intracellular events and inflammatory mediators. New therapies targeting key mediators like interleukin-1 beta show promise for effective treatment.
Area of Science:
- Gastroenterology and Immunology
- Pathophysiology of Inflammatory Diseases
Background:
- Acute pancreatitis treatment has seen minimal advancement over 50 years.
- Understanding of initial intracellular events and disease progression mediators is limited.
- Systemic inflammation and distant organ failure mechanisms in pancreatitis are poorly understood.
Purpose of the Study:
- To review the current understanding of acute pancreatitis pathophysiology.
- To highlight the role of specific inflammatory mediators in disease progression.
- To explore the potential for novel therapies targeting these mediators.
Main Methods:
- Review of recent advances in pancreatitis pathophysiology.
- Focus on the role of inflammatory mediators such as interleukin-1 beta, tumor necrosis factor alpha, and platelet-activating factor.
- Examination of ongoing clinical trials for inflammatory mediator antagonists.
Main Results:
- Inflammatory mediators like interleukin-1 beta, tumor necrosis factor alpha, and platelet-activating factor are implicated in pancreatitis progression.
- Advances in understanding these mediators open avenues for targeted therapies.
- Several inflammatory mediator antagonists are currently under human testing.
Conclusions:
- A deeper understanding of pancreatitis pathophysiology is crucial for developing effective treatments.
- Targeting specific inflammatory mediators offers a promising strategy for acute pancreatitis.
- The development of specific therapies for acute pancreatitis may be imminent with ongoing research.
Related Concept Videos
Acute Pancreatitis II: Clinical Manifestations and Management
Chronic Pancreatitis II: Collaborative Care
Assessment:
Acute Pancreatitis I: Introduction
Acute Pancreatitis I: Introduction
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
Acute Pancreatitis II: Pathophysiology
Chronic Pancreatitis I: Introduction

