Secondary Logo

Institutional members access full text with Ovid®

Molecular regulation of plasma lipid levels during systemic inflammation and sepsis

Trinder, Marka,b; Boyd, John H.a,b,c; Brunham, Liam R.a,b,c

Current Opinion in Lipidology: April 2019 - Volume 30 - Issue 2 - p 108–116
doi: 10.1097/MOL.0000000000000577

Purpose of review Sepsis is a common syndrome of multiorgan system dysfunction caused by a dysregulated inflammatory response to an infection and is associated with high rates of mortality. Plasma lipid and lipoprotein levels and composition change profoundly during sepsis and have emerged as both biomarkers and potential therapeutic targets for this condition. The purpose of this article is to review recent progress in the understanding of the molecular regulation of lipid metabolism during sepsis.

Recent findings Patients who experience greater declines in high-density lipoprotein during sepsis are at much greater risk of succumbing to organ failure and death. Although the causality of these findings remains unclear, all lipoprotein classes can sequester and prevent the excessive inflammation caused by pathogen-associated lipids during severe infections such as sepsis. This primordial innate immune function has been best characterized for high-density lipoproteins. Most importantly, results from human genetics and preclinical animal studies have suggested that several lipid treatment strategies, initially designed for atherosclerosis, may hold promise as therapies for sepsis.

Summary Lipid and lipoprotein metabolism undergoes significant changes during sepsis. An improved understanding of the molecular regulation of these changes may lead to new opportunities for the treatment of sepsis.

aCentre for Heart Lung Innovation

bDepartment of Experimental Medicine Program

cDepartment of Medicine, University of British Columbia, Vancouver, British Columbia, Canada

Correspondence to Liam R. Brunham, MD, PhD, Centre for Heart Lung Innovation, Room 166–1081 Burrard Street, Vancouver, BC V6Z 1Y6, Canada. Tel: +604 682 2344, ext. 63929; fax: +604 806 9274; e-mail:

Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.