Differences in innate immune signaling between alcoholic and non‐alcoholic steatohepatitis
Authors:
Open Access
- 15 July 2013
- journal article
- review article
- Published by Wiley in Journal of Gastroenterology and Hepatology
- Vol. 28 (S1) , 93-98
Abstract
Graphic The similar histopathological characteristics of alcoholic steatohepatitis (ASH) and non‐alcoholic steatohepatitis (NASH), and the crucial role of the innate immune response in both conditions may lead to the assumption that ASH and NASH represent the same pathophysiological entities caused by different risk factors. In this review paper, we elaborate on the pathophysiological differences between these two entities and highlight the disease‐specific involvement of signaling molecules downstream of the Toll‐like receptor 4, and the differential mechanism by which the inflammasome contributes to ASH versus NASH. Our findings emphasize that ASH and NASH have disease‐specific mechanisms and therefore represent distinct biological entities. Further studies are needed to dissect the emerging differences in pathogenesis of these two conditions.Keywords
Funding Information
- NIH (AA017729, DK075635)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK32520)
This publication has 76 references indexed in Scilit:
- Lack of interleukin-1α or interleukin-1β inhibits transformation of steatosis to steatohepatitis and liver fibrosis in hypercholesterolemic miceJournal of Hepatology, 2011
- Mitochondrial antiviral signaling protein defect links impaired antiviral response and liver injury in steatohepatitis in miceHepatology, 2011
- Type I Interferons Protect From Toll-Like Receptor 9–Associated Liver Injury and Regulate IL-1 Receptor Antagonist in MiceGastroenterology, 2011
- An essential role for monocyte chemoattractant protein-1 in alcoholic liver injury: Regulation of proinflammatory cytokines and hepatic steatosis in miceHepatology, 2010
- Interferon regulatory factor 3 and type I interferons are protective in alcoholic liver injury in mice by way of crosstalk of parenchymal and myeloid cellsHepatology, 2010
- The InflammasomesCell, 2010
- An early complement-dependent and TLR-4–independent phase in the pathogenesis of ethanol-induced liver injury in mice #Hepatology, 2009
- Probiotics restore bowel flora and improve liver enzymes in human alcohol-induced liver injury: a pilot studyAlcohol, 2008
- The critical role of toll‐like receptor (TLR) 4 in alcoholic liver disease is independent of the common TLR adapter MyD88†Hepatology, 2008
- Toll-like receptor-4 signaling and Kupffer cells play pivotal roles in the pathogenesis of non-alcoholic steatohepatitisJournal of Hepatology, 2007