Abstract
Sepsis is a life-threatening condition resulting from a dysregulated host response to infection. Currently, there is no effective therapy for sepsis due to an incomplete understanding of its pathogenesis. Scavenger receptor BI (SR-BI) is a high-density lipoprotein (HDL) receptor that plays a key role in HDL metabolism by modulating the selective uptake of cholesteryl ester from HDL. Recent studies, including those from our laboratory, indicate that SR-BI protects against sepsis through multiple mechanisms: (1) preventing nitric oxide-induced cytotoxicity; (2) promoting hepatic lipopolysaccharide (LPS) clearance and regulating cholesterol metabolism in the liver; (3) inhibiting LPS-induced inflammatory signaling in macrophages; and (4) mediating the uptake of cholesterol from HDL for inducible glucocorticoid (iGC) synthesis in the adrenal gland, which controls systemic inflammatory response. In this article, we review the roles of SR-BI in sepsis.