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ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Research Article

ER Stress-induced Inflammasome Activation Contributes to Hepatic Inflammation and Steatosis

Jinyu Zhang1,2, Kezhong Zhang3, Zihai Li1,2, and Beichu Guo1,2*

1Department of Microbiology and Immunology, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425-5040, USA

2Hollings Cancer Center, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425, USA

3Department of Immunology and Microbiology, Center for Molecular Medicine & Genetics, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit,MI 48201, USA

*Corresponding Author:
Dr. Beichu Guo
Department of Microbiology and Immunology
Medical University of South Carolina (MUSC)
Hollings Cancer Center,HO-612D
86 Jonathan Lucas Street
Charleston, South Carolina 29425-5040
USA
Tel: (843)792-5708
Fax: (843)792-9588
E-mail: [email protected]

Received date: July 20, 2016; Accepted date: September 21, 2016; Published date: September 26, 2016

Citation: Zhang J, Zhang K, Li Z, Guo B (2016) ER Stress-induced Inflammasome Activation Contributes to Hepatic Inflammation and Steatosis. J Clin Cell Immunol 7: 457. doi:10.4172/2155-9899.1000457

Copyright: © 2016 Zhang J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Abstract

Endoplasmic reticulum (ER) stress functions as a protein folding and quality control mechanism to maintain cell homeostasis. Emerging evidence indicates that ER stress is also involved in metabolic and inflammatory diseases. However, the link between ER stress and inflammation remains not well characterized. In this study, we have demonstrated that ER stress-induced inflammasome activation plays a critical role in the pathogenesis of hepatic steatosis. By utilizing genetic and pharmacological agent-induced hepatic steatosis animal models, we found that hepatic steatosis was associated with inflammasome activation and ER stress. Our results show that caspase-1 ablation alleviated liver inflammation and injury. Liver tissues from caspase-1 KO mice had significantly reduced production of IL-1β under ER stress conditions. We also found that ER stress promoted inflammasome activation and IL-1β processing in both hepatocytes and Kupffer cells/macrophages. Moreover, lack of caspase-1 ameliorated cell death or pyropoptosis of hepatocytes induced by ER stress. Taken together, our findings suggest that ER stressinduced inflammasome activation and IL-1β production generate a positive feedback loop to amplify inflammatory response, eventually leading to liver steatosis and injury.

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