Effects of human apolipoprotein A-I on endotoxin-induced leukocyte adhesion on endothelial cells in vivo and on the growth of Escherichia coli in vitro.

BACKGROUND: High-density lipoprotein (HDL) has been shown to inhibit leukocyte adhesion to endothelial cells induced by endotoxin in vivo and suppress the growth of bacteria in vitro; however, the components responsible for these effects, either lipids or proteins, are not yet defined. In this study, we examined the effects of apolipoprotein (apo) A-I, the major protein of HDL, on ameliorating the effect of endotoxin and inhibiting the growth of bacteria.
MATERIALS AND METHODS: Apo A-I, purified from normal human HDL, was incubated with endotoxin. Leukocyte adhesion to endothelial cells of rat mesenteric venules was assessed using intravital fluorescence microscopy. Ability of apo A-I to inhibit the growth of Escherichia coli was assessed using a spread plate method.
RESULTS: Purified, lipid-free apo A-I could inhibit endotoxin-induced leukocyte adhesion to endothelial cells in vivo in a dose-dependent manner. In addition, apoA-I was able to suppress the growth of Escherichia coli in vitro.
CONCLUSIONS: These data suggest that apo A-I of HDL can directly interact with endotoxin, ameliorating its effect and that apo A-I may have a direct toxic effect on whole bacteria. Therefore, therapeutic use of apo A-I in septicemia and bacterial infection should be further explored.