Acute-phase gene expression correlates with intrahepatic tumor necrosis factor-alpha abundance but not with plasma tumor necrosis factor concentrations during sepsis/systemic inflammatory response syndrome in the rat

Abstract

The changes in TNF-alpha-dependent hepatic gene expression that accompany an animal model of the systemic inflammatory response syndrome correlate with intrahepatic, and not circulating, TNF-alpha concentrations and reflect paracrine, and not endocrine, activity. Therefore, plasma concentrations of TNF-alpha do not appropriately reflect hepatocellular responses during the systemic inflammatory response syndrome.