Published online Feb 8, 2016. doi: 10.4254/wjh.v8.i4.207
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
Processing time: 372 Days and 0.4 Hours
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.
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.