High density lipoprotein (HDL) is an important component of the innate immune system, and contributes to pathogen clearance by sequestering and removing pathogen lipids from circulation. During sepsis, HDL cholesterol (HDL-C) levels drop, and lower HDL-C levels are associated with worse clinical outcomes, such as prolonged hospital admission and death.
In this study published in the American Journal of Respiratory and Critical Care Medicine, Mark Trinder, a PhD candidate at HLI in Dr. Brunham’s lab, and their team found that genetic variation in cholesteryl ester transferase protein (CETP) influences HDL-C levels and clinical outcomes during sepsis. More specifically, the team found that elevated CETP activity was associated with a gain-of-function CETP variant, leading to an exacerbated decline in HDL-C and lower survival rates in sepsis patients. These findings may form the basis for future studies to examine the feasibility of inhibiting CETP to increase HDL-C levels and improve outcomes for sepsis.