High Density Lipoprotein-Lipopolysaccharide Binding Lowers HDL’s Basal Antioxidant Capacity

Clinically, high density lipoprotein (HDL) is known to be a potent negative risk factor of cardiovascular disease due to its ability to stimulate anti-atherosclerotic, anti-inflammation and antioxidant pathways. It has been established that HDL has a role in the innate immune system through its ability to sequester lipopolysaccharide (LPS) or lipoteichoic acid (LTA) in the blood. This sequestering prevents the endotoxins from binding to their respective toll-like receptors and subsequently stimulating the transcription of pro-inflammatory cytokines. Elevated HDL levels are seen to attenuate sepsis by rapidly removing LPS molecules from the blood. LPS molecules appear to bind to the apoproteins contained on the periphery of the HDL particles. The binding of LPS to apoproteins, specifically ApoA1, causes a conformational change to the apoproteins. These conformational changes may inhibit the apoprotein’s abilities to interact with cell surface receptors. It is not known how the binding of LPS affects HDL’s ...