Fig. 3. DEL-1 modulates resolution of acute inflammation.

(a-c) Numbers of neutrophils in peritoneal exudates obtained from Del1^KO and their respective wild-type (WT) mice at 8 h (a, n = 11 WT and 13 Del1^KO mice), 24 h (b, n = 18 WT and 16 Del1^KO mice) and 36 h (c, n = 8 mice per group) after MSU crystal-induced inflammation. (d) Relative number of apoptotic neutrophils detected in peritoneal exudates 24 h and 36 h after MSU crystal injection in wild-type (WT) or Del1^KO mice. Number of apoptotic neutrophils was measured and expressed relative to the wild-type/24 h group, set as 1 (24 h, n = 18 WT and 16 Del1^KO mice and 36 h, n = 8 mice per group). (e-f) Concentrations of RvD1, Lipoxin A4 and RvE1 (e) and protein concentration of DEL-1 (pg/mg of total protein) (f) were measured in the supernatant of peritoneal fluid obtained from untreated (0 h) wild-type mice or wild-type mice at 8 h, 16 h, 24 h and 36 h after MSU crystal-induced inflammation (n = 6 mice per group). (g) Concentrations of RvD1, Lipoxin A4 and RvE1 were measured in the supernatant of peritoneal exudates obtained from wild-type (WT) or Del1^KO mice at 24 h and 36 h after MSU crystal-induced inflammation (n = 6 mice per group). (h) MSU crystals were injected in wild-type mice and, after 20 h, 5 μg of DEL-1-Fc or Fc control protein were administered intraperitoneally (i.p.); 4 h after the latter injection, the relative amount of apoptotic neutrophils in peritoneal exudates was assessed. Numbers of apoptotic neutrophils are expressed relative to the Fc control group, set as 1 (n = 10 mice per group). *P < 0.05, **P < 0.01, ****P < 0.0001, NS, non-significant ((a, b) two-tailed Student’s t-test; (c-d, g, h) two-tailed Mann-Whitney U-test; (f) One-way ANOVA with Tukey’s multiple comparisons test). Data are means ±SEM and are pooled from two experiments (a, c, d – 36 h time point, e-h) or three experiments (b, d – 24 h time point).