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World J Gastrointest Pharmacol Ther. Feb 6, 2010; 1(1): 15-20
Published online Feb 6, 2010. doi: 10.4292/wjgpt.v1.i1.15
Inflammatory role of the acinar cells during acute pancreatitis
Isabel De Dios
Isabel De Dios, Department of Physiology and Pharmacology, University of Salamanca, Salamanca 37007, Spain
Author contributions: De Dios I contributed solely to this review.
Supported by A grant from Insituto de Salud Carlos III, Spain, PI08/0035
Correspondence to: Isabel De Dios, PhD, Department of Physiology and Pharmacology, University of Salamanca, Salamanca 37007, Spain.
Telephone: +34-923-294673 Fax: +34-923-294673
Received: November 18, 2009
Revised: January 7, 2010
Accepted: January 14, 2010
Published online: February 6, 2010

Pancreatic acinar cells are secretory cells whose main function is to synthesize, store and finally release digestive enzymes into the duodenum. However, in response to noxious stimuli, acinar cells behave like real inflammatory cells because of their ability to activate signalling transduction pathways involved in the expression of inflammatory mediators. Mediated by the kinase cascade, activation of Nuclear factor-κB, Activating factor-1 and Signal transducers and activators of transcription transcription factors has been demonstrated in acinar cells, resulting in overexpression of inflammatory genes. In turn, kinase activity is down-regulated by protein phosphatases and the final balance between kinase and phosphatase activity will determine the capability of the acinar cells to produce inflammatory factors. The kinase/phosphatase pair is a redox-sensitive system in which kinase activation overwhelms phosphatase activity under oxidant conditions. Thus, the oxidative stress developed within acinar cells at early stages of acute pancreatitis triggers the activation of signalling pathways involved in the up-regulation of cytokines, chemokines and adhesion molecules. In this way, acinar cells trigger the release of the first inflammatory signals which can mediate the activation and recruitment of circulating inflammatory cells into the injured pancreas. Accordingly, the role of acinar cells as promoters of the inflammatory response in acute pancreatitis may be considered. This concept leads to amplifying the focus from leukocyte to acinar cells themselves, to explain the local inflammation in early pancreatitis.

Keywords: Acinar cells, Inflammatory mediators, Signal pathways, Acute pancreatitis