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World J Gastrointest Pathophysiol. Feb 15, 2016; 7(1): 108-116
Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.108
Mechanisms of interleukin-22’s beneficial effects in acute pancreatitis
Chongmin Huan, Daniel Kim, Peiqi Ou, Antonio Alfonso, Albert Stanek
Chongmin Huan, Daniel Kim, Antonio Alfonso, Albert Stanek, Department of Surgery, Downstate Medical Center, State University of New York, Brooklyn, NY 11203, United States
Peiqi Ou, Program of Molecular and Cellular Biology, School of Graduate Studies, Downstate Medical Center, State University of New York, Brooklyn, NY 11203, United States
Albert Stanek, Department of Pathology, Downstate Medical Center, State University of New York, Brooklyn, NY 11203, United States
Author contributions: Huan C and Kim D contributed equally to this work; Huan C wrote the manuscript and directed the acute pancreatitis study; Kim D generated and analyzed the major sources of data; Ou P measured IL-22 mRNA levels; Alfonso A contributed to the writing of the manuscript; Stanek A assisted the direction of the study, performed histology study, and made important revisions of the manuscript.
Conflict-of-interest statement: The authors declare no conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Chongmin Huan, MD, PhD, Assistant Professor, Department of Surgery, Downstate Medical Center, State University of New York, 450 Clarkson Avenue, Brooklyn, NY 11203, United States. chongmin.huan@downstate.edu
Telephone: +1-718-2706772 Fax: +1-718-2216132
Received: August 11, 2015
Peer-review started: August 11, 2015
First decision: September 28, 2015
Revised: November 11, 2015
Accepted: November 17, 2015
Article in press: November 25, 2015
Published online: February 15, 2016
Processing time: 173 Days and 2.8 Hours
Abstract

Acute pancreatitis (AP) is a disorder characterized by parenchymal injury of the pancreas controlled by immune cell-mediated inflammation. AP remains a significant challenge in the clinic due to a lack of specific and effective treatment. Knowledge of the complex mechanisms that regulate the inflammatory response in AP is needed for the development of new approaches to treatment, since immune cell-derived inflammatory cytokines have been recognized to play critical roles in the pathogenesis of the disease. Recent studies have shown that interleukin (IL)-22, a cytokine secreted by leukocytes, when applied in the severe animal models of AP, protects against the inflammation-mediated acinar injury. In contrast, in a mild AP model, endogenous IL-22 has been found to be a predominantly anti-inflammatory mediator that inhibits inflammatory cell infiltration via the induction of Reg3 proteins in acinar cells, but does not protect against acinar injury in the early stage of AP. However, constitutively over-expressed IL-22 can prevent the initial acinar injury caused by excessive autophagy through the induction of the anti-autophagic proteins Bcl-2 and Bcl-XL. Thus IL-22 plays different roles in AP depending on the severity of the AP model. This review focuses on these recently reported findings for the purpose of better understanding IL-22’s regulatory roles in AP which could help to develop a novel therapeutic strategy.

Keywords: Interleukin-22; Acute pancreatitis; Cytokine; Inflammatory response; Acinar cell

Core tip: Interleukin (IL)-22 has been recognized as a potential therapeutic agent for acute pancreatitis (AP) treatment due to its discovered beneficial effects in inflammatory diseases. However, according to recent publications and our results, IL-22 appears to have differential effects in AP depending on the severity of the disorder. In this review we discuss the different regulatory mechanisms of IL-22 in mild and severe AP models in order to promote development of an effective and efficient therapeutic approach.