IL1B and Sepsis: In combination with IL-1β and TNF-α, IL-6 markedly enhances gene expression of acute-phase proteins (APP) via transcriptional activation.[14] IL-18, secreted by KCs, could activate both TNF-α and Fas ligand-mediated hepatocytotoxic pathways in LPS-induced liver injury.[15] Lastly, increased levels of ROS have been demonstrated in different models of sepsis and this disturbance may lead to DNA, protein, or lipid damage resulting in apoptosis and necrosis followed by cell death.