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World J Gastrointest Pharmacol Ther. Oct 6, 2010; 1(5): 107-111
Published online Oct 6, 2010. doi: 10.4292/wjgpt.v1.i5.107
Role of macrophages in the progression of acute pancreatitis
Sabrina Gea-Sorlí, Daniel Closa
Sabrina Gea-Sorlí, Daniel Closa, Department of Experimental Pathology, IIBB-CSIC-IDIBAPS-CIBEREHD, Barcelona 08036, Spain
Author contributions: Gea-Sorlí S wrote the sections on macrophages, macrophages and therapeutical target; Closa D wrote the sections on macrophage activation during acute pancreatitis, macrophage populations in pancreatitis, peritoneal macrophages, Kupffer cells and alveolar macrophages; Closa D and Gea-Sorlí S designed the figure.
Correspondence to: Dr. Daniel Closa, Department of Experimental Pathology, IIBB-CSIC, c/ Rosselló 161, 7°, Barcelona 08036, Spain.
Telephone: +34-93-3638307 Fax: +34-93-3638301
Received: February 26, 2010
Revised: July 30, 2010
Accepted: August 6, 2010
Published online: October 6, 2010

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.

Keywords: Pancreatitis, Macrophages, Inflammation, Systemic inflammatory response syndrome