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The Oxidation State of Phospholipids Controls the Oxidative Burst in Neutrophil Granulocytes¹

Stephan Blüml^2,*, Berit Rosc^*, Akos Lorincz, Maria Seyerl^*, Stefanie Kirchberger^*, Olga Oskolkova, Valery N. Bochkov, Otto Majdic^*, Erzsebet Ligeti and Johannes Stöckl^*

^* Institute of Immunology and Department of Vascular Biology and Thrombosis Research, Medical University Vienna, Vienna, Austria; and Department of Physiology, Semmelweis University, Puskin, Budapest, Hungary

The activation of neutrophil granulocytes has to be carefully controlled to balance desired activity against invading pathogens while avoiding overwhelming activation leading to host tissue damage. We now show that phospholipids are potential key players in this process by either enhancing or dampening the production of reactive oxygen species (ROS) during the oxidative burst. Unoxidized phospholipids induce the production of ROS, and they also work synergistically with FMLP in potentiating the oxidative burst in neutrophil granulocytes. Oxidation of these phospholipids, however, turns them into potent inhibitors of the oxidative burst. OxPls specifically inhibit ROS production by inhibiting the assembly of the phagocyte oxidase complex but do not alter neutrophil viability, nor do they interfere with MAPK activation. Furthermore, up-regulation of the activation marker Mac-1 and phagocytosis of bacteria is not affected. Therefore, phospholipids may act as sensors of oxidative stress in tissues and either positively or negatively regulate neutrophil ROS production according to their oxidation state.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by the Wiener Wissenschafts-, Forschungs-, und Technologiefond (WWTF) and a grant from the Austrian Science Fund (SFB005.2).

² Address correspondence and reprint requests to Dr. Stephan Blüml at the current address: Institute of Immunology and Department of Rheumatology, Medical University of Vienna, Borschkegasse 8a, A-1090 Vienna, Austria. E-mail address: stephan.blueml{at}meduniwien.ac.at

³ Abbreviations used in this paper: ROS, reactive oxygen species; phox, phagocyte oxidase; Ox, oxidized; OxPl, Ox phospholipid; PAPC, 1-palmitoyl-2-arachidoyl-sn-glycero-3-phosphorylcholine; PLPC, 1-palmitoyl-2-linoyl-sn-glycero-3-phosphorylcholine; PAPS, 1-palmitoyl-2-arachidoyl-sn-glycero-3-[phospho-L-serine]; PAPG, 1-palmitoyl-2-arachidonoyl-sn-glycero-3-[phospho-rac-(1-glycerol)]; PAPE, 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphoethanolamine; DMPC, 1,2-dimyristoyl-sn-glycero-3-phosphocholine; PAF, platelet-activating factor; PGN, peptidoglycan; DCF-DA, 2'7'-dichlorodihydrofluorescein diacetate; AA, arachidonic acid.

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