Secondary Logo

Institutional members access full text with Ovid®

Share this article on:

Effect of inflammation on HDL structure and function

Feingold, Kenneth R.; Grunfeld, Carl

doi: 10.1097/MOL.0000000000000333
ATHEROSCLEROSIS: CELL BIOLOGY AND LIPOPROTEINS Edited by Andrew Newby and Mohamad Navab

Purpose of review Studies have shown that chronic inflammatory disorders, such as rheumatoid arthritis, systemic lupus erythematosus, and psoriasis are associated with an increased risk of atherosclerotic cardiovascular disease. The mechanism by which inflammation increases cardiovascular disease is likely multifactorial but changes in HDL structure and function that occur during inflammation could play a role.

Recent findings HDL levels decrease with inflammation and there are marked changes in HDL-associated proteins. Serum amyloid A markedly increases whereas apolipoprotein A-I, lecithin:cholesterol acyltransferase, cholesterol ester transfer protein, paraoxonase 1, and apolipoprotein M decrease. The exact mechanism by which inflammation decreases HDL levels is not defined but decreases in apolipoprotein A-I production, increases in serum amyloid A, increases in endothelial lipase and secretory phospholipase A2 activity, and decreases in lecithin:cholesterol acyltransferase activity could all contribute. The changes in HDL induced by inflammation reduce the ability of HDL to participate in reverse cholesterol transport and protect LDL from oxidation.

Summary During inflammation multiple changes in HDL structure occur leading to alterations in HDL function. In the short term, these changes may be beneficial resulting in an increase in cholesterol in peripheral cells to improve host defense and repair but over the long term these changes may increase the risk of atherosclerosis.

Metabolism Section, Department of Veterans Affairs Medical Center, University of California San Francisco, San Francisco, California, USA

Correspondence to Dr Kenneth R. Feingold, MD, Metabolism Section (111F), Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA. Tel: +1 415 750 2005; fax: +1 415 750 6927; e-mail: kenneth.feingold@ucsf.edu

Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.