Infection and inflammation-induced proatherogenic changes of lipoproteins

Epidemiologic studies suggest a link between infection/inflammation and ath erosclerosis. During the acute-phase response to infection and inflammation , cytokines induce tissue and plasma events that lead to changes in lipopro tein. Many of these changes are similar to those proposed to promote athero genesis. The changes of lipoproteins during infection and inflammation are reviewed with a focus on those that are potentially proatherogenic. Hypertr iglyceridemia, elevated triglyceride-rich lipoproteins, the appearance of s mall dense low-density lipoproteins, increased platelet-activating factor a cetylhydrolase activity, and secretory phospholipase A(2), sphingolipid-enr iched lipoproteins, and decreased high-density lipoprotein (HDL) cholestero l are changes that could promote atherogenesis. Moreover, alterations of pr oteins associated with HDL metabolism (e.g., paraoxonase, apolipoprotein A- T, lecithin:cholesterol acyltransferase, cholesterol. ester transfer protei n, hepatic lipase, phospholipid transfer protein, and serum amyloid A) coul d decrease the ability of HDL to protect against atherogenesis through anti oxidation and reverse cholesterol transport mechanisms. These proatherogeni c changes of Lipoproteins may contribute to the link between infection/infl ammation and atherosclerosis.