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Pancreas: healing response in critical illness
David J Bentrem1, Raymond J Joehl
1Department of Surgery, Northwestern University Feinberg School of Medicine, and Surgical Service, VA Chicago Health Care System, Illinois, USA.
Critical Care Medicine
|August 9, 2003
Summary
Acute pancreatitis involves pancreatic cell injury and inflammation, driven by cytokines. Understanding these inflammatory mediators and the pancreatic healing response may lead to new treatments for this condition.
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Acute pancreatitis stems from diverse issues causing pancreatic inflammation.
- It involves acinar cell injury and inflammatory responses, with cytokines driving systemic effects and morbidity.
Purpose of the Study:
- To summarize pancreatic injury mechanisms in acute pancreatitis.
- To elucidate the role of cytokines in pathogenesis.
- To describe the pancreatic healing response.
Main Methods:
- A comprehensive literature review was conducted.
- Experimental and clinical pancreatitis reports were analyzed, focusing on cytokine involvement and healing.
Main Results:
- Histamine, bradykinin, and cytokines (TNF-α, IL-6, IL-1) are key in acute pancreatic inflammation.
- Inhibiting these mediators benefits experimental animals.
- Pancreatic fibrosis, including collagen deposition and cell atrophy, is a major histologic response.
Conclusions:
- Inflammatory mediators cause systemic effects and organ dysfunction in acute pancreatitis.
- Pancreatic repair involves reduced inflammation and inflammatory cell infiltration.
- Myofibroblast proliferation contributes to extracellular matrix production, suggesting novel treatment avenues.