Pseudomonas aeruginosa and the hyperlipidaemia of sepsis.

Pathophysiological alterations of liver sinusoidal endothelial cells (LSECs) impact liver and metabolism. LSEC fenestrations are pores facilitating lipoproteins and macromolecule transfer between blood and hepatocytes. The Gram negative bacterium Pseudomonas aeruginosa is one of the most common opportunistic nosocomial pathogens, especially in post-liver transplant recipients. Gram negative bacterial endotoxin (lipopolysaccharide, LPS) and the P. aeruginosa toxin, pyocyanin, have marked effects on LSECs, including loss of porosity (defenestration). Currently proposed mechanisms for sepsis-hyperlipidaemia, an important response to Gram negative bacterial sepsis, include tissue lipoprotein-lipase inhibition and increased hepatic triglyceride production. Owing to the well-substantiated role of LSECs in liver-allograft rejection and hyperlipidaemia, we propose defenestration of the LSEC is an additional cellular mechanism for sepsis-hyperlipidaemia, including pseudomonal sepsis post-liver transplantation.