(Circulation. 2001;103:108.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
Elevation of Plasma High-Density Lipoprotein Concentration Reduces Interleukin-1–Induced Expression of E-Selectin in an In Vivo Model of Acute Inflammation
From the British Heart Foundation Cardiovascular Research Unit, National Heart and Lung Institute, Imperial College School of Medicine, Hammersmith Hospital Campus, London, UK (G.W.C., T.Y.H., A.W., C.S., D.O.H.); the ZLB Central Laboratory, Blood Transfusion Service SRC, Bern, Switzerland (P.G.L.); and the Department of Cardiovascular Biochemistry, St Bartholomew’s and the Royal School of Medicine and Dentistry, Queen Mary’s and Westfield College, London, UK (N.E.M.).
Correspondence to G.W. Cockerill, Department of Cardiovascular Biochemistry, St Bartholomew’s and the Royal London SMD, Queen Mary’s and Westfield College, Charterhouse Square, London EC1 M 6BQ, UK. E-mail g.w.cockerill{at}mds.qmw.ac.uk
Background—Although there is strong evidence that plasma HDL levels correlate inversely with the incidence of coronary artery disease, the precise mechanism(s) for the protective effect of HDLs remains unclear. We recently showed that HDLs inhibit endothelial cell expression of cytokine-induced leukocyte adhesion molecules in vitro. Our study therefore sought to test the hypothesis that elevating the level of circulating HDLs would inhibit endothelial cell activation in vivo.
Methods and Results—We
used a porcine model of inflammation previously established in our
laboratory, in which the level of vascular endothelial cell expression
of E-selectin in interleukin (IL)-1
–induced skin lesions was
measured by the uptake of a radiolabeled anti–E-selectin antibody
(1.2B6). Porcine plasma HDL levels were elevated by use of a bolus
injection of reconstituted discoidal HDL (recHDL). These particles
resemble nascent HDL particles in shape and contain apolipoprotein A-I
as the sole protein and soybean phosphatidylcholine as the sole
phospholipid. We found that recHDLs inhibited the expression of
IL-1–induced E-selectin by porcine aortic endothelial cells in
vitro, confirming that the inhibitory effect is conserved with
synthetic HDLs and demonstrating that the phenomenon is not restricted
to human endothelial cells. In vivo, elevating the circulating level of
HDLs 
2-fold led to significant inhibition of basal and
IL-1–induced E-selectin expression by porcine microvascular
endothelial cells.
Conclusions—These observations demonstrate the potential anti-inflammatory action of HDLs and provide support for the further investigation of the mechanisms underlying the inhibitory effects of HDLs on endothelial cell activation.
Key Words: inflammation • atherosclerosis • proteins • endothelium • apolipoproteins
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