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pubmed:abstractText |
Activation of the pro-inflammatory cytokine cascade, including tumor necrosis factor alpha (TNF-alpha) is considered to play an important role in the pathophysiology and clinical outcome of severe liver injury. Kupffer cells, resident macrophages of the liver, have a transmembrane protein Toll-like receptor 4 (TLR4), which recognizes endotoxin (lipopolysaccharide; LPS) or LPS-CD14 complex and mediates macrophage activation and pro-inflammatory cytokine release. D-Galactosamine (GalN), a hepatocyte-specific inhibitor of RNA synthesis, is known to sensitize animals to the lethal effects of LPS and TNF-alpha. In the present study we seek to address TLR4-signaling in the development of GalN-induced acute hepatic failure (AHF) and explore the expression of TLR4 mRNA as compared to TNF-alpha mRNA and CD14 mRNA in the liver, spleen and lung of rats with GalN-induced hepatitis.
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