Background Atherosclerosis is a chronic metabolic disease of inflammatory processes. Immune cells including monocytes are recruited to the subintimal lesion of the vascular wall and store lipids to transform themselves to the foam cells. The cholesterol crystal formed inside of the foam cells stimulates NLRP3 inflammaosme to secrete IL-1 and further inflammation. The lipid profiles in the serum are shown to be risk factors for developing atherosclerosis, such as high LDL (low density lipoprotein) or low HDL (high density lipoprotein) concentration. In addition to deliver cholesterol from vascular wall to liver, HDL is supposed to exert antiinflammatory properties which are not well characterized.

Objectives To investigate the antiinflammatory function of reconstituted HDL (rHDL) in the Kawasaki arteritis murine model in vivo.

Methods Coronary arteritis mimicking Kawasaki disease was induced by administrating 20 microgram of lipopolysaccharide followed by weekly injection of 500 microgram of the nucleotide-binding oligomerization domain 1 (NOD1) ligand FK-565 for 4 times. 2 mg of rHDL or control PBS was injected 4 times along with FK-565 administration. After a week of the last injection of FK-565 or control PBS, the severity of coronary arteritis was quantified by measuring the inflammation area surrounding the coronary arteries.

Results The rHDL treatment reduced the inflammatory area of coronary arteries compared with the control PBS treated groups, showing statistically significance (P<0.05 with Student t-test, 0.31±0.29 mm² (PBS control group) and 0.14±0.08 mm² (rHDL group)).

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Conclusions The data indicate that rHDL exerts an antiinflammatory activity in the NOD1 ligand induced Kawasaki arteritis model in vivo.

1. Nishio H et al. Arterioscler Thromb Vasc Biol. 2011, 31: 1093-9

2. Duewell P, Kono H, et al. Nature 2010, 464: 1357-61.

Disclosure of Interest None Declared