The involvement of both oxidative stress and hyperlipaemia in atherosclerosis development is well established.
Oxidative burst is an innate immune response to infection, the latter being associated also with marked changes in lipid
and lipoprotein metabolism, aimed to neutralize endotoxin toxic effects. On the other hand, lipid overload may increase
lipopolysaccharide circulating levels and oxidative stress. Whilst these changes may be beneficial from the perspective of
host defense, if they become chronic, they likely increase the risk of atherosclerosis. In particular, oxidation of
lipoproteins, resulting from an imbalance of the pro- and antioxidant equilibrium, is involved in the pathologic process of
atherosclerosis, changing cellular functions. Lipid oxidation, induced by leukocytes derived reactive oxygen species, can
amplify foam cell formation through oxidized low density lipoproteins LDL (oxLDL) formation and uptake. The main
enzymes, operating during oxidative burst, involved in LDL oxidation are NADPH oxidase and myeloperoxidase. In vitro
studies have shown that oxLDL are able to induce many proatherogenic processes, including modulation of oxidative
burst. OxLDL may also induce maturation of dendritic cells and regulate the shift from classical (M1) to alternative (M2)
macrophage activation and from T helper 1 to T helper 2 response, suggesting that these could act as a bridge between
innate and adaptative immunity, both involved in plaque development. Understanding the relationship between oxLDL
and leukocyte oxidative burst helps to explain the involvement of innate immune responses in the early phases of
atherosclerosis. The present review focuses on this interplay.
Keywords: Atherosclerosis, immunity, lipoproteins, low density, oxidative burst, hyperlipaemia, lipopolysaccharide circulating levels, oxidized low density lipoproteins LDL (oxLDL), Atherogenesis, endothelial injury, plasma antioxidants, cardiovascular diseases (CVD).
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