Display options
Share it on

World J Hepatol. 2016 Feb 08;8(4):207-10. doi: 10.4254/wjh.v8.i4.207.

Inflammasome activation in decompensated liver cirrhosis.

World journal of hepatology

José M González-Navajas

Affiliations

  1. José M González-Navajas, FISABIO Biomedical Research Foundation, Hospital General Universitario de Alicante, 03010 Alicante, Spain.

PMID: 26855691 PMCID: PMC4733463 DOI: 10.4254/wjh.v8.i4.207

Abstract

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

References

  1. J Gen Virol. 2012 Feb;93(Pt 2):235-46 - PubMed
  2. J Hepatol. 2012 Sep;57(3):642-54 - PubMed
  3. Nature. 2012 Feb 01;482(7384):179-85 - PubMed
  4. Nature. 2012 Jan 18;481(7381):278-86 - PubMed
  5. J Hepatol. 2001 Jan;34(1):32-7 - PubMed
  6. Nat Immunol. 2012 Mar 19;13(4):333-42 - PubMed
  7. Cell. 2010 Mar 19;140(6):821-32 - PubMed
  8. Nature. 2009 Mar 26;458(7237):514-8 - PubMed
  9. Curr Allergy Asthma Rep. 2010 Jul;10 (4):229-35 - PubMed
  10. Infect Immun. 2009 May;77(5):1981-91 - PubMed
  11. J Clin Invest. 2009 Feb;119(2):305-14 - PubMed
  12. Nat Rev Microbiol. 2009 Feb;7(2):99-109 - PubMed
  13. Hepatology. 2008 Dec;48(6):1924-31 - PubMed
  14. J Hepatol. 2008 Jan;48(1):61-7 - PubMed
  15. Nature. 2009 Mar 26;458(7237):509-13 - PubMed
  16. Mol Cell. 2002 Aug;10(2):417-26 - PubMed
  17. J Hepatol. 2015 Jan;62(1):64-71 - PubMed
  18. J Hepatol. 2011 Nov;55(5):1086-94 - PubMed
  19. Hepatology. 2008 Mar;47(3):978-85 - PubMed

Publication Types