Fatty acid and endotoxin activate inflammasomes in mouse hepatocytes that release danger signals to stimulate immune cells
T Csak, M Ganz, J Pespisa, K Kodys, A Dolganiuc… - Hepatology, 2011 - journals.lww.com
The pathogenesis of nonalcoholic steatohepatitis (NASH) and inflammasome activation
involves sequential hits. The inflammasome, which cleaves pro–interleukin-1β (pro–IL-1β)
into secreted IL-1β, is induced by endogenous and exogenous danger signals.
Lipopolysaccharide (LPS), a toll-like receptor 4 ligand, plays a role in NASH and also
activates the inflammasome. In this study, we hypothesized that the inflammasome is
activated in NASH by multiple hits involving endogenous and exogenous danger signals …
involves sequential hits. The inflammasome, which cleaves pro–interleukin-1β (pro–IL-1β)
into secreted IL-1β, is induced by endogenous and exogenous danger signals.
Lipopolysaccharide (LPS), a toll-like receptor 4 ligand, plays a role in NASH and also
activates the inflammasome. In this study, we hypothesized that the inflammasome is
activated in NASH by multiple hits involving endogenous and exogenous danger signals …