Pathogenesis of the hyperlipidemia of Gram-negative bacterial sepsis may involve pathomorphological changes in liver sinusoidal endothelial cells.

摘要: The Gram-negative bacterium Pseudomonas aeruginosa is one of the most common opportunistic pathogens, especially after liver transplantation. Pathophysiological alterations sinusoidal endothelial cells (LSECs) have far-reaching repercussions on and metabolism. LSECs are perforated with fenestrations, pores that facilitate transfer lipoproteins macromolecules between blood hepatocytes. bacterial endotoxin (lipopolysaccharide, LPS) P. toxin, pyocyanin, marked effects LSECs. Initial loss LSEC porosity (defenestration) induced by pyocyanin LPS may confer subsequent immune tolerance to circulating antigens toxins. This review collates known responses toxins, a focus Hyperlipidemia an important response sepsis. mechanisms proposed for sepsis-associated hyperlipidemia include tissue lipoprotein lipase inhibition upregulated hepatic triglyceride production. In this review, we propose defenestration toxins as additional mechanism Given role in allograft rejection, changes including significant clinical implications.