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. 2009 Aug;205(2):442-50.
doi: 10.1016/j.atherosclerosis.2009.01.002. Epub 2009 Jan 9.

oxLDL uptake by dendritic cells induces upregulation of scavenger-receptors, maturation and differentiation

Thomas Nickel  1 , Daniel Schmauss, Henner Hanssen, Zelka Sicic, Bjarne Krebs, Sarika Jankl, Claudia Summo, Peter Fraunberger, Autar K Walli, Susanne Pfeiler, Michael Weis
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oxLDL uptake by dendritic cells induces upregulation of scavenger-receptors, maturation and differentiation

Thomas Nickel et al. Atherosclerosis. 2009 Aug.

Abstract

Background: Several studies have proposed a pathogenic role for oxidized LDL (oxLDL) in atherosclerosis. We tested the hypothesis whether oxLDL modulates dendritic cells (DCs), since these important antigen-presenting cells have been implicated in atherogenesis. We investigated the uptake of oxLDL by DCs, the scavenger-receptors involved and the resulting changes in phenotype and cytokine-spectra. In addition, we analyzed the impact of oxLDL on the nuclear transcription factor-kappa B (NF-kappaB)-pathway.

Methods and results: oxLDL (10microg/ml) increased the expression of the scavenger-receptors CD205 and CD36 and decreased the mannose-receptor expression. The lectin-like oxLDL-receptor (LOX-1)-expression was not affected. The endocytotic capacity of dextran and lucifer-yellow was moderately decreased by oxLDL. Blockage of the scavenger-receptors CD36, LOX-1 and CD205 reduced oxLDL uptake. Furthermore, oxLDL induced DC-maturation and triggered differentiation of DCs in myeloid and plasmacytoid DCs. oxLDL decreased IL-10 secretion and increased IL-6 release. Finally, oxLDL induced an activation of the NF-kappaB-pathway. Inhibition of IkappaBalpha-phosphorylation diminished the oxLDL-induced DC-maturation and -differentiation.

Conclusion: oxLDL uptake by DCs is mediated by the scavenger-receptors LOX-1, CD36, and CD205. oxLDL induces a proinflammatory cytokine profile in human DCs leading to DC-maturation and -differentiation which can, in part, be explained by an activation of the NF-kappaB-pathway. These results support the hypothesis that vascular inflammation may be aggravated by oxLDL induced DC-activation.

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