Endogenous Fpr2/3 modulates vascular inflammation. Wild-type (Fpr2/3+/+) and null (Fpr2/3−/−) mice were subjected to 30 minutes’ clamping of the superior mesenteric artery, followed by a 90-minute reperfusion phase. Postcapillary venules were imaged and recorded for offline quantitation of white blood cell interaction with the endothelium. (A) Arachidonic acid metabolism into LXA4 by the concerted action of 5-lipoxygenase (LOX) and 12/15-LOX. Acetylation of cyclo-oxygenase 2 (COX) by ASA leads to 15-epi-LXA4 biosynthesis. Prostanoids produced by COX 1 or 2 isoforms are also indicated, and they include thromboxane (TX) A2 and prostaglandin (PG) of series I, E, and F. (B) Mice were given LXA4 (1, 10, or 100 ng/mouse intravenously) or vehicle (100 µL). Mean ± SEM of 6 mice; *P < .05 vs vehicle; #P < .05 vs Fpr2/3+/+. (C) Administration of Boc2 (10 µg intravenously) before (pre) or after (post) ischemia (30 minutes) affects the extent of cell emigration as measured 90 minutes after reperfusion in Fpr2/3+/+ but not Fpr2/3−/− mice. Mean ± SEM of 6 to 8 mice; *P < .05, **P < .01 vs Fpr2/3+/+ vehicle. (D) Plasma aliquots obtained at the reported phases of the IR protocol were analyzed for LXA4 content by enzyme immunoassay. Mean ± SEM of 8 mice; *P < .05 vs Fpr2/3−/− or Boc2-treated Fpr2/3+/+ mice.
