Friend Turns Foe: Transformation of Anti-Inflammatory HDL to Proinflammatory HDL during Acute-Phase Response

Figure 2

Model of bidirectional conversion of HDL from anti-inflammatory to proinflammatory. Normal anti-inflammatory HDLs are rich in apolipoproteins (ovals) and antioxidant enzymes (squares). After exposure to pro-oxidants, oxidized lipids, and proteases, proinflammatory HDLs have less lipoprotein and the major transporter apolipoprotein A-I are disabled by the addition of chlorine, nitrogen, and oxygen to protein moieties. PON1 cannot exert its antioxidant enzyme activity as Apo A-I can no longer stabilize it. In addition, pro-oxidant acute-phase proteins are added to the particle (serum amyloid A (SAA) and ceruloplasmin). “Apo A-I ↑”, “PON1 ↑” indicates that the number of respective molecules present in anti-inflammatory HDL is more when compared to that of proinflammatory HDL. Apo J: apolipoprotein J; CE: cholesterol ester; PON1: paraoxonase-1; GSH: glutathione; SAA: serum amyloid A; Apo A-I: apolipoprotein A-I; Apo-AII: apolipoprotein A-II; LCAT: lecithin cholesterol acyltransferase; PAF-AH: platelet-activating acyl hydrolase.