Apolipoproteins such as apoE and apoAI may be responsible for the protective effects of lipoproteins against the inflammatory response to lipopolysaccharide in sepsis.
Do apolipoproteins modulate the inflammatory response to lipopolysaccharide and protect against sepsis?
Apolipoproteins, rather than the lipid moieties of lipoproteins, appear responsible for attenuating the inflammatory response to LPS and protecting against sepsis in preclinical models.
An increasing body of evidence demonstrates a close interplay between lipoprotein metabolism and sepsis. Sepsis results in an increase of plasma triglycerides within VLDL as a consequence of an enhanced hepatic VLDL production and/or inhibited peripheral and hepatic VLDL clearance. In contrast, sepsis decreases plasma cholesterol within LDL and mainly HDL. The decrease in HDL is accompanied by a loss of mainly apoAI-containing particles, an almost total loss of apoCI, and an increase in apoE-containing HDL, as related to the effect of LPS on a wide range of apolipoproteins, plasma enzymes, lipid transfer factors, and receptors that are involved in HDL metabolism. Reciprocally, all lipoprotein classes have been shown to bind LPS and to attenuate the biological response to LPS in vitro and in rodents. Moreover, triglyceride-rich lipoproteins protect rodents against death from LPS and bacterial sepsis. Accumulating evidence indicates that apolipoproteins such as apoE and apoAI, and not the lipid moieties of the particles, may be responsible for these protective effects of lipoproteins. Therefore, to increase our understanding of the complex interaction between lipoprotein metabolism and sepsis, further studies that address the specific roles of apolipoproteins in sepsis are warranted.
Berbée et al. (2005) conducted a review in Sepsis. Apolipoproteins was evaluated. Apolipoproteins such as apoE and apoAI may be responsible for the protective effects of lipoproteins against the inflammatory response to lipopolysaccharide in sepsis.