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Cited 3 time in webofscience Cited 3 time in scopus
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Loss of toll-like receptor 3 aggravates hepatic inflammation but ameliorates steatosis in mice

Authors
Lee, Young-SunKim, Do-YeonKim, Tae-JunKim, So YeonJeong, Jong-MinJeong, Won-IlJung, Jae-KwangChoi, Jae-KapYi, Hyon-SeungByun, Jin-Seok
Issue Date
18-Mar-2018
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Endocannabinoids; Nonalcoholic steatohepatitis; Necroinflammations; Lipogenesis
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.497, no.4, pp.957 - 962
Indexed
SCIE
SCOPUS
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
497
Number
4
Start Page
957
End Page
962
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/3747
DOI
10.1016/j.bbrc.2018.01.191
ISSN
0006-291X
Abstract
The importance of toll-like receptor (TLR) 4 in the pathogenesis of steatohepatitis has been well documented; however, little is known about the role of TLR3. In this study, we determined whether the depletion of TLR3 modulated hepatic injury in mice and further aimed to provide mechanistic insights into the TLR3-mediated modulation of diet-induced hepatic inflammation and fat accumulation. Hepatic steatosis and inflammatory response were induced by feeding wild-type (WT) or TLR3 knockout mice a high-fat diet for 8 weeks. Primary liver resident cells, including hepatocytes, Kupffer cells, and hepatic stellate cells (HSCs), were treated with palmitic acid. TLR3 knockout mice fed a high-fat diet showed severe hepatic inflammation accompanied by nuclear factor-kappa B and IRF3 activation, which is mainly induced by the activation of Kupffer cells. Decreased TLR4 expression was restored in hepatic mononuclear cells and Kupffer cells in TLR3 knockout mice compared to that in the WT. Moreover, hepatic steatosis was decreased in TLR3 knockout mice. Hepatocytes from TLR3 knockout mice exhibited reduced expression of cannabinoid receptors. HSCs from TLR3 knockout mice showed decreased expression of the enzymes involved in endocannabinoid synthesis. In conclusion, this study suggests that the selective modulation of TLR3 could be a novel therapeutic target for the treatment of hepatic inflammation and steatosis. (C) 2018 Elsevier Inc. All rights reserved.
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Lee, Young Sun
Guro Hospital (Department of Gastroenterology and Hepatology, Guro Hospital)
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