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NLRC4 inflammasome activation regulated by TNF-α promotes inflammatory responses in nonalcoholic fatty liver disease.

Abstract：

:The prevalence of nonalcoholic fatty liver disease (NAFLD) is high and increasing throughout the world. The intense sterile inflammation stemming from steatosis plays a significant role in the development of NAFLD, but the mechanism is unclear. We found that the NLRC4 inflammasome was activated in an in vitro cell model of NAFLD, and that the secretion of inflammatory factors IL-18, IL-1β, and tumor necrosis factor α (TNF-α) increased during this process and pyroptosis is triggered. In this study, we used NLRC4-targeting siRNA and an NLRC4-encoding plasmid to demonstrate that the increases in IL-18 and IL-1β are mainly attributable to the activation of the NLR family CARD domain-containing protein 4 (NLRC4) inflammasome, which stimulates cellular pyroptosis. NLRC4 inflammasome activation is regulated by TNF-α and accompanies the translocation of NLRC4 from the cytoplasm into the mitochondria, but the specific mechanism is unclear. In summary, the increase in TNF-α during NAFLD promotes the activation of the NLRC4 inflammasome, which increases the production of IL-18 and IL-1β and triggers pyroptosis. These exacerbate inflammation and promote disease development.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Chen Y,Ma K

doi

10.1016/j.bbrc.2019.02.099

subject

Has Abstract

pub_date

2019-04-09 00:00:00

pages

524-530

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)30300-6

journal_volume

511

pub_type

杂志文章

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