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Sterile inflammatory response in acute pancreatitis
Rafaz Hoque1, Ahsan F Malik, Fred Gorelick
1Section of Digestive Diseases, Yale University, New Haven, CT 06520-8019, USA.
Pancreas
|March 15, 2012
Summary
Sterile injury in acute pancreatitis releases damage-associated molecular patterns (DAMPs), triggering inflammation. Targeting DAMP receptors offers novel therapeutic strategies for pancreatitis.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Acute pancreatitis begins with sterile injury and acinar cell necrosis.
- Released intracellular contents act as damage-associated molecular patterns (DAMPs), initiating inflammation.
- DAMPs are crucial in determining pancreatic injury severity, remote organ damage, and disease outcomes.
Purpose of the Study:
- To investigate the role of DAMPs and their receptors in acute pancreatitis.
- To identify potential therapeutic targets within DAMP-mediated inflammatory pathways.
Main Methods:
- Review of experimental models of acute pancreatitis.
- Analysis of DAMPs (e.g., HMGB1, ATP, HSP70) and their receptors (e.g., TLR4, TLR9, P2X7).
- Examination of downstream signaling molecules (e.g., NLRP3, caspase-1, IL-1β, IL-18).
Main Results:
- Several DAMPs are implicated in experimental pancreatitis and are found in human cases.
- Specific DAMP receptors (TLR4, TLR9, P2X7) and downstream components (NLRP3, caspase-1, IL-1β, IL-18) are essential for pancreatitis.
- Genetic deletion and pharmacologic antagonism confirm the role of these pathways.
Conclusions:
- DAMP-mediated sterile inflammation is a central mechanism in acute pancreatitis.
- DAMP receptors and downstream signaling molecules represent promising therapeutic targets.
- Antagonists of DAMP receptors offer potential treatment strategies for acute pancreatitis.
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