An inverse relationship between HDL concentrations and cardiovascular risk has been demonstrated in several epidemiological studies. In addition to their key role in reverse cholesterol transport, HDL particles also have antioxidative and anti-inflammatory properties. Although the anti-inflammatory effects of HDL on endothelial cells are well known, these potentially beneficial effects on monocytes have been examined less extensively. Since a critical step in the development of atherosclerotic plaques is the recruitment of monocytes, how HDL characteristics can affect the cascade of plaque formation is therefore important. The article by Murphy et al. investigated the mechanism by which HDL and apolipoprotein (apo) AI prevent and reverse leukocyte activation. A series of experiments demonstrated that HDL and apo AI decreased monocyte activation through various receptors and exerted their effects via the monocytic ATP-binding cassette transporter A1. They also reported that apo AI was equally effective as HDL in inhibiting elements of the inflammatory process. Therefore, this study suggests that the ability of HDL to prevent and reverse activation of monocytes may be of significance for the management of several inflammatory diseases. This article was accompanied by an editorial by Kerry-Anne Rye and Philip J. Barter who recognized that the study by Murphy et al. adds to a growing body of evidence that HDL and apo AI have cardioprotective effects that extend well beyond their role in reverse cholesterol transport. Because the study by Murphy demonstrated that apo AI inhibited monocyte activation while previous observations from Barter’s group reported that apo AI did not inhibit endothelial cell adhesion molecule expression, the study raised the possibility that HDL may prevent monocyte and endothelial cell activation by different mechanisms.
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