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1
Faculty of Biology, Department of Cell Biology, University of Kaiserslautern, Kaiserslautern, Germany
Activation and deactivation of macrophages are of considerable
importance during the development of various disease states,
atherosclerosis among others. Macrophage activation is achieved by
oxidized lipoproteins (oxLDL) and is determined by oxygen radical (ROS)
formation. The oxidative burst was measured by flow cytometry and
quantitated by oxidation of the redox-sensitive dye
dichlorodihydrofluorescein diacetate. Short-time stimulation
dose-dependently elicited ROS formation. Diphenylene iodonium prevented
ROS formation, thus pointing to the involvement of a NAD(P)H oxidase in
producing reduced oxygen species. In contrast, preincubation of
macrophages with oxLDL for 16 h showed an attenuated oxidative
burst upon a second contact with oxLDL. Taking into account that oxLDL
is an established peroxisome proliferator-activated receptor-
(PPAR) agonist and considering the anti-inflammatory properties
of PPAR, we went on and showed that a PPAR agonist such as
ciglitazone attenuated ROS formation. Along that line, major lipid
peroxidation products of oxLDL, such as 9- and
13-hydroxyoctadecadienoic acid, shared that performance. Supporting
evidence that PPAR activation accounted for reduced ROS generation
came from studies in which proliferator-activated receptor response
element decoy oligonucleotides, but not a mutated oligonucleotide,
supplied in front of oxLDL delivery regained a complete oxidative burst
upon cell activation. We conclude that oxLDL not only elicits an
oxidative burst upon first contact, but also promotes desensitization
of macrophages via activation of PPAR. Desensitization of
macrophages may have important consequences for the behavior of
macrophages/foam cells in atherosclerotic
lesions.
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