Sepsis is caused by the body’s overwhelming response to infection, leading to damage to organ systems and potentially death.
During sepsis, plasma levels of HDL-cholesterol drop dramatically, partly because of increased CETP (cholesteryl ester transfer protein) activity. Dr. Liam Brunham and his laboratory, including first author Mark Trinder, a MD/PhD student, found that inhibiting CETP not only preserved HDL levels during sepsis, but also improve outcomes and increased survival.
Using a mouse model of experimental sepsis, the group found that mice treated with anacetrapib (a CETP inhibitor) increased survival compared to the placebo group. Further, using data from the UK Biobank, decreased CETP function was found to be associated with significantly decreased sepsis mortality.
These results suggest that CETP may be an effective therapeutic target for sepsis treatment, and future studies will determine whether anacetrapib or other CETP inhibitors can be used to treat patients with sepsis.