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.