IntroductionThe plasma cholesteryl ester transfer protein (CETP) mediates the exchange of HDL cholesteryl esters (CE) The metabolism of HDL is regulated, in part, by the activities of lipases and lipid transfer proteins (1). Cholesteryl esters, generated in HDL by lecithin:cholesterol acyltransferase, are exchanged with triglycerides of VLDL, as a result of the activity of cholesteryl ester transfer protein (CETP)'. The subsequent activity of hepatic lipase on triglyceride-enriched HDL results in a decrease in HDL size and catabolism of the major apoliprotein of HDL, apoA-I (2). In a striking demonstration of the interaction of hypertriglyceridemia with cholesteryl ester transfer processes, hypertriglyceridemic apoC-II transgenic mice show profound reductions in HDL cholesterol and apoA-I when crossed with human CETP/apoA-I transgenic mice, to produce apoA-I/CETP/apoC-llH transgenic mice (3). In addition to plasma triglyceride concentration, effective plasma CETP activity is also influenced by changes in CETP concentration, such as those resulting from changes in dietary cholesterol or probucol therapy (4, 5).HDL is thought to mediate the reverse transport of cholesterol from peripheral tissues to the liver (6). In addition to this well-known role, Ulevitch et al. (7) have suggested another, novel function for HDL, namely to bind bacterial lipopolysaccharide (endotoxin) and thereby to modulate its biological effects. The binding of endotoxin to HDL can prevent endotoxininduced death (8). Harris et al. (9) have shown that VLDL and chylomicrons can also bind endotoxin, and protect mice against endotoxin-induced death. However, the potency of HDL appeared to be greater than that of other lipoproteins (9), and the molar concentrations of HDL in plasma are usually higher than other lipoproteins. Another role of HDL may be to provide cholesterol for adrenal corticosteroid synthesis ( 10-12), a function that could be particularly important during stress (13).The purpose of the present study was to examine the possible regulation of CETP gene expression in response to LPS administration. We suspected that CETP might be altered by LPS, since LPS has profound effects on lipoprotein metabolism and is known to regulate lipoprotein lipase and LCAT activities ( 14,15