Review
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World J Gastroenterol. Feb 7, 2013; 19(5): 616-630
Published online Feb 7, 2013. doi: 10.3748/wjg.v19.i5.616
Controversial role of toll-like receptors in acute pancreatitis
Juan Vaz, Hamid Akbarshahi, Roland Andersson
Juan Vaz, Hamid Akbarshahi, Roland Andersson, Department of Surgery, Clinical Sciences Lund, Skåne University Hospital Lund, Lund University, SE-221 85 Lund, Sweden
Author contributions: Vaz J and Akbarshahi H collected the underlying material, wrote the initial draft of the manuscript; Andersson R, Vaz J and Akbarshahi H designed the outline of the paper; Andersson R finalized and revised the manuscript; all authors have read and approved the final version of the manuscript.
Correspondence to: Roland Andersson, MD, PhD, Department of Surgery, Clinical Sciences Lund, Skåne University Hospital, Lund University, SE-221 85 Lund, Sweden. roland.andersson@med.lu.se
Telephone: +46-222-46172359 Fax: +46-222-46172335
Received: November 1, 2012
Revised: December 19, 2012
Accepted: January 11, 2013
Published online: February 7, 2013
Processing time: 96 Days and 18.6 Hours
Abstract

Acute pancreatitis (AP) is a common clinical condition with an incidence of about 300 or more patients per million annually. About 10%-15% of patients will develop severe acute pancreatitis (SAP) and of those, 10%-30% may die due to SAP-associated complications. Despite the improvements done in the diagnosis and management of AP, the mortality rate has not significantly declined during the last decades. Toll-like receptors (TLRs) are pattern-recognition receptors that seem to play a major role in the development of numerous diseases, which make these molecules attractive as potential therapeutic targets. TLRs are involved in the development of the systemic inflammatory response syndrome, a potentially lethal complication in SAP. In the present review, we explore the current knowledge about the role of different TLRs that have been described associated with AP. The main candidate for targeting seems to be TLR4, which recognizes numerous damage-associated molecular patterns related to AP. TLR2 has also been linked with AP, but there are only limited studies that exclusively studied its role in AP. There is also data suggesting that TLR9 may play a role in AP.

Keywords: Acute pancreatitis; Severe acute pancreatitis; Pathophysiological mechanism; Toll-like receptors; Intervention