This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Barter, P. Search for Related Content PubMed PubMed Citation Articles by Barter, P. Related Collections Lipid and lipoprotein metabolism Other Vascular biology

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1062.)
© 2002 American Heart Association, Inc.

Editorials

Effects of Inflammation on High-Density Lipoproteins

Philip Barter

From the University Department of Medicine, Royal Adelaide Hospital and the Hanson Institute, Adelaide, South Australia.

Correspondence to Philip Barter, Cardiovascular Investigation Unit, Level 6, Royal Adelaide Hospital, North Terrace, Adelaide, 5000. E-mail philip.barter@adelaide.edu.au

An extract of the first 250 words of the full text is provided, because this article has no abstract.

High-density lipoproteins (HDLs) protect against the development of atherosclerotic coronary heart disease.¹ In part, this reflects the ability of HDL to promote the efflux of cholesterol from macrophages in the artery wall² but given that atherosclerosis is an inflammatory disorder,³ it may also reflect anti-inflammatory properties of HDL.^4,5 Conversely, inflammation reduces the concentration of HDL and possibly compromises the anti-atherogenic functions of these lipoproteins.⁶ Given the pathophysiological implications of a potentially detrimental effect of inflammation on HDL function, it is clearly important to understand the mechanisms that may be involved. Such mechanisms are the subject of an article by Tietge et al⁷ in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology.

See page 1213

These authors provide compelling evidence that the effects of inflammation on HDL are the result mainly of activity of secretory phospholipase A2 (sPLA2), an acute phase reactant that is known to be present at increased concentration in plasma in a variety of inflammatory states and which has the ability to remodel HDL.⁸ Because remodeling of HDL by a variety of plasma factors is known to play a major role in regulating the concentration and subpopulation distribution of HDL, the possibility that inflammation may have an impact on this remodeling is of potentially great importance.

Remodeling of HDL in plasma plays a major part in the regulation of these lipoproteins. HDLs originate as lipid-free or lipid-poor apolipoproteins that acquire most of their lipid in the extracellular space. They accept phospholipids and cholesterol from cells in a . . . [Full Text of this Article]

This article has been cited by other articles:

				K. Okubo, K. Ikewaki, S. Sakai, N. Tada, Y. Kawaguchi, and S. Mochizuki Abnormal HDL Apolipoprotein A-I and A-II Kinetics in Hemodialysis Patients: A Stable Isotope Study J. Am. Soc. Nephrol., April 1, 2004; 15(4): 1008 - 1015. [Abstract] [Full Text] [PDF]

				W. Jin, G.-S. Sun, D. Marchadier, E. Octtaviani, J. M. Glick, and D. J. Rader Endothelial Cells Secrete Triglyceride Lipase and Phospholipase Activities in Response to Cytokines as a Result of Endothelial Lipase Circ. Res., April 4, 2003; 92(6): 644 - 650. [Abstract] [Full Text] [PDF]