Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Feb 8, 2016; 8(4): 207-210
Published online Feb 8, 2016. doi: 10.4254/wjh.v8.i4.207
Inflammasome activation in decompensated liver cirrhosis
José M González-Navajas
José M González-Navajas, FISABIO Biomedical Research Foundation, Hospital General Universitario de Alicante, 03010 Alicante, Spain
José M González-Navajas, Networked Biomedical Research Center for Hepatic and Digestive Disease (CIBERehd), Instituto de Salud Carlos III, 28029 Madrid, Spain
Author contributions: González-Navajas JM solely contributed to this article.
Supported by Grant PI13/00315 from the Instituto de Salud Carlos III (co-financed by FEDER funds); and grants UGP-14-123 and UGP-14-248 from FISABIO Research Foundation.
Conflict-of-interest statement: The author declares no conflict 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: José M González-Navajas, PhD, FISABIO Biomedical Research Foundation, Hospital General Universitario de Alicante, Av. Pintor Baeza, 12, 03010 Alicante, Spain. gonzalez_josnav@gva.es
Telephone: +34-965-913928 Fax: +34-965-913922
Received: January 19, 2015
Peer-review started: January 20, 2015
First decision: March 6, 2015
Revised: November 2, 2015
Accepted: January 16, 2016
Article in press: January 19, 2016
Published online: February 8, 2016

Inflammation participates in the pathogenesis of many liver diseases, including liver cirrhosis. Certain inflammatory citokines, such as interleukin (IL)-1β and IL-18, are produced after the activation of a multiprotein complex known as the inflammasome. Activation of the inflammasome has been documented in several liver diseases, but its role in the development and progression of liver cirrhosis or the complications associated with this disease is still largely unknown. We have recently studied the impact of the inflammasome in the sterile inflammatory response that takes place in the ascitic fluid of patients with decompensated cirrhosis, providing evidence that activation of the absent in melanoma 2 (AIM2) inflammasome is an important response in these patients. Ascitic fluid-derived macrophages were able to mount a very robust AIM2-mediated response even in the absence of a priming signal, which is usually required for the full activation of all the inflammasomes. In addition, high level of inflammasome activation in these patients was associated with a higher degree of liver disease and an increased incidence of spontaneous bacterial peritonitis. These results may help explain the exacerbated inflammatory response that usually occurs in patients with decompensated cirrhosis in the absence of detectable infections. Thus, inflammasomes should be considered as possible therapeutic targets in sterile inflammatory complications in patients with cirrhosis.

Keywords: Cirrhosis, Ascites, Inflammasome, Absent in melanoma 2, Interleukin-1β

Core tip: In this Editorial I discuss the involvement of the inflammasome in the inflammatory reactions that occur in patients with liver cirrhosis and ascites. I focus on a recent work in which we observed that the absent in melanoma 2 inflammasome is highly activated in the ascitic fluid of patients with advanced cirrhosis and that its activation is linked to the severity of liver disease. These findings are important for the understanding of the sterile inflammatory reactions in these patients, and could have important therapeutic implications.