Systemic haemodynamic changes in patients with cystic fibrosis with and without chronic liver disease

Williams, Simon G.; Samways, Jack; Innes, J A; Guz, A.; Geddes, Duncan M.; Hodson, M E; Westaby, David

doi:10.1016/s0168-8278(96)80295-9

Cited by 3 publications

(1 citation statement)

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“…Acute liver failure is a complex and life‐threatening syndrome resulting from severe acute liver injury, which causes sudden and massive liver cell death and liver dysfunction, thereby leading to multiple organ failure . The sepsis‐induced inflammatory response mediated by dysregulated innate immunity is associated with direct hepatocyte injury by inducing cellular apoptosis .…”

Section: Introductionmentioning

confidence: 99%

Deletion of caveolin‐1 attenuates LPS/GalN‐induced acute liver injury in mice

Tsai

Tam

Chen

et al. 2018

J Cellular Molecular Medi

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Acute hepatic injury caused by inflammatory liver disease is associated with high mortality. This study examined the role of caveolin‐1 (Cav‐1) in lipopolysaccharide (LPS) and D‐galactosamine (GalN)‐induced fulminant hepatic injury in wild type and Cav‐1‐null (Cav‐1−/−) mice. Hepatic Cav‐1 expression was induced post‐LPS/GalN treatment in wild‐type mice. LPS/GalN‐treated Cav‐1−/− mice showed reduced lethality and markedly attenuated liver damage, neutrophil infiltration and hepatocyte apoptosis as compared to wild‐type mice. Cav‐1 deletion significantly reduced LPS/GalN‐induced caspase‐3, caspase‐8 and caspase‐9 activation and pro‐inflammatory cytokine and chemokine expression. Additionally, Cav‐1−/− mice showed suppressed expression of Toll‐like receptor 4 (TLR4) and CD14 in Kupffer cells and reduced expression of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 in liver cells. Cav‐1 deletion impeded LPS/GalN‐induced inducible nitric oxide synthase expression and nitric oxide production and hindered nuclear factor‐κB (NF‐κB) activation. Taken together, Cav‐1 regulated the expression of mediators that govern LPS‐induced inflammatory signalling in mouse liver. Thus, deletion of Cav‐1 suppressed the inflammatory response mediated by the LPS‐CD14‐TLR4‐NF‐κb pathway and alleviated acute liver injury in mice.

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Section: Introductionmentioning

confidence: 99%