(19-04-12) Resolvin D1 Limits Polymorphonuclear Leukocytes Recruitment to Inflammatory Loci: Receptor-Dependent Actions.

Norling LV, Dalli J, Flower RJ, Serhan CN, Perretti M.
Source
William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University of London, London, United Kingdom.
Abstract
OBJECTIVE:
Resolvin D1 (RvD1) limits neutrophil recruitment during acute inflammation and is derived from omega-3docosahexaenoic acid to promote catabasis. The contribution of its specific receptors, the lipoxin A(4)/Annexin-A1 receptor (FPR2/ALX) and the orphan receptor G-protein-coupled receptor 32 (GPR32) are of considerable interest.
METHODS AND RESULTS:
RvD1 reduced human polymorphonuclear leukocytes recruitment to endothelial cells under shear conditions as quantified using a flow chamber system. Receptor-specific antibodies blocked these anti-inflammatory actions of RvD1, with low (1 nmol/L) concentrations sensitive to GPR32 blockade, while the higher (10 nmol/L) concentration appeared FPR2/ALX-specific. Interestingly, polymorphonuclear leukocytes surface expression of FPR2/ALX but not GPR32 increased following activation with pro-inflammatory stimuli, corresponding with secretory vesicle mobilization. Lipid mediator metabololipidomics carried out with 24-hour exudates revealed that RvD1 in vivo gave a significant reduction in the levels of a number of pro-inflammatory mediators including prostaglandins and leukotriene B4. These actions of RvD1 were abolished in fpr2 null mice.
CONCLUSIONS:
Pro-resolving lipid mediators and their receptors, such as RvD1 and the 2 G-protein-coupled receptors, studied here regulate resolution and may provide new therapeutic strategies for diseases with a vascular inflammatory component.

Source: Arterioscler Thromb Vasc Biol. 2012 Apr 12. [Epub ahead of print]

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