[Frontiers in Bioscience 14, 2042-2050, January 1, 2009]

Acute pancreatitis as a model of SIRS

Madhav Bhatia

Department of Pharmacology, National University of Singapore, Yong Loo Lin School of Medicine, Centre for life Sciences, 28 Medical Drive, Singapore 117456

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Animal Models of Acute Pancreatitis and Associated SIRS
3.1. Secretagogue-Induced Pancreatitis
3.2. Choline-Deficient Ethionine Supplement Diet-Induced Pancreatitis
3.3. Duct Obstruction-Induced Pancreatitis
3.4. Duct Infusion-Induced Pancreatitis
3.5. Arginine-Induced Pancreatitis
4. Mediators of Acute Pancreatitis-Associated SIRS Identified Using Animal Models
4.1. TNF-a and IL-1b
4.2. IL-6
4.3. IL-10
4.4. PAF
4.5. CD40L
4.6. ICAM-1
4.7. C5a
4.8. Chemokines
4.9. Substance P
4.10. H2S
5. Summary and Perspective
6. Acknowledgement
7. References

1. ABSTRACT

Acute pancreatitis is a common clinical condition. Excessive systemic inflammatory response syndrome (SIRS) in acute pancreatitis leads to distant organ damage and multiple organ dysfunction syndrome (MODS), which is the primary cause of morbidity and mortality in this condition. Development of in vivo experimental models of acute pancreatitis and associated systemic organ damage has enabled us to study the role played by inflammatory mediators in the pathogenesis of acute pancreatitis and associated systemic organ damage. Using these models, recent studies by us and other investigators have established the critical role played by inflammatory mediators such as TNF-a, IL-1b, IL-6, PAF, IL-10, CD40L, C5a, ICAM-1, chemokines, substance P and hydrogen sulfide in acute pancreatitis and the resultant MODS. This chapter intends to present an overview of different experimental animal models of acute pancreatitis and associated MODS and the role of inflammatory mediators in the pathogenesis of this condition.