Role of NLRP3 inflammasome in the pathogenesis of alcoholic liver disease
10.3760/cma.j.issn.1007-3418.2019.07.019
- VernacularTitle: NLRP3炎症小体在酒精性肝病发病机制中的作用
- Author:
Xue BAI
1
;
Shuhong SUN
;
Junying ZHOU
Author Information
1. Department of Infectious Disease, the Third Hospital of Hebei Medical University, Shijiazhuang 050051, China
- Publication Type:Review
- Keywords:
Liver diseases, alcoholic;
Endotoxemia;
Uric acid;
Adenosine triphosphate;
NLRP3 inflammasome
- From:
Chinese Journal of Hepatology
2019;27(7):567-571
- CountryChina
- Language:Chinese
-
Abstract:
Chronic excess alcohol intake triggers the formation of enterogenic endotoxemia. TLR4 ligand localization activates nuclear transcription factor NF-κB by inducing the up-regulation of NLRP3 inflammasome and the biologically inactive IL-1β and IL-18 precursors to form initiation of pro-inflammatory signals. Under the influence of ethanol, the damaged hepatocyte release uric acid, and adenosine triphosphate and induces NLRP3 inflammasome assembly and functional activation in Kupffer cells to promote the release of inflammatory mediators, such as interleukin-1β and interleukin-18, that cascade mediates inflammation and drive alcoholic liver disease from steatosis to inflammation and fibrosis. The NLRP3 inflammasome acts as a ligand-sensing element and plays an important role in mediating the immune and inflammatory response in the course of alcoholic liver disease. Thus, exploring the activation mechanism of NLRP3 inflammasome and its pathogenic role may provide a new idea in the clinical treatment of alcoholic liver disease.
