Related Experiment Video
Updated: Jun 1, 2026

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
Published on: May 10, 2024
Role of macrophages in the progression of acute pancreatitis
Sabrina Gea-Sorlí1, Daniel Closa
1Sabrina Gea-Sorlí, Daniel Closa, Department of Experimental Pathology, IIBB-CSIC-IDIBAPS-CIBEREHD, Barcelona 08036, Spain.
Abstract:
In addition to pancreatic cells, other inflammatory cell populations contribute to the generation of inflammatory mediators during acute pancreatitis. In particular, macrophages could be activated by mediators released during pancreatitis by a damaged pancreas. It has been reported that peritoneal macrophages, alveolar macrophages and Kupffer cells become activated in different stages of severe acute pancreatitis. However, macrophages display remarkable plasticity and can change their physiology in response to environmental cues. Depending on their microenvironmental stimulation, macrophages could follow different activation pathways resulting in marked phenotypic heterogeneity. This ability has made these cells interesting therapeutical targets and several approaches have been assayed to modulate the progression of inflammatory response secondary to acute pancreatitis. However, despite the recent advances in the modulation of macrophage function in vivo, the therapeutical applications of these strategies require a better understanding of the regulation of gene expression in these cells.
Insights
Macrophages are key inflammatory cells in acute pancreatitis. Understanding their gene expression regulation is crucial for developing new therapies targeting pancreatic inflammation.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Acute pancreatitis involves inflammatory mediators from damaged pancreas.
- Macrophages, including peritoneal, alveolar, and Kupffer cells, are activated during pancreatitis.
- Macrophages exhibit plasticity, with diverse activation pathways and phenotypes based on microenvironmental cues.
Purpose of the Study:
- To explore the role of macrophages in acute pancreatitis.
- To investigate the therapeutic potential of modulating macrophage function.
- To highlight the need for understanding gene expression regulation in macrophages for therapeutic development.
Main Methods:
- Review of existing literature on macrophage activation in acute pancreatitis.
- Analysis of macrophage plasticity and phenotypic heterogeneity.
- Discussion of therapeutic strategies targeting macrophage function.
Main Results:
- Macrophages are significant contributors to inflammatory mediator generation in acute pancreatitis.
- Macrophage activation and heterogeneity are influenced by the pancreatic microenvironment.
- Current therapeutic strategies show promise but require deeper understanding.
Conclusions:
- Macrophages are critical players in the inflammatory response during acute pancreatitis.
- Targeting macrophage plasticity offers therapeutic potential for pancreatitis.
- Further research into macrophage gene expression is essential for effective in vivo therapies.
Related Concept Videos
Acute Pancreatitis II: Pathophysiology
Chronic Pancreatitis I: Introduction
Chronic Pancreatitis I: Introduction
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
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 I: Introduction
Chronic Pancreatitis II: Pathophysiology

