Fig. 6.

Pharmacological blockade of ALX/FPR2 attenuates the proresolving actions of IFN-β. Acute lung inflammation was induced in female C57BL/6 mice by intratracheal instillation of 5 × 10⁶ live E. coli plus CpG DNA (1 μg/g b.w., i.p.). At 6 h post E. coli, mice were first injected intraperitoneally with WRW4 (1 μg/g b.w.) or cyclosporin H (5 μg/g b.w.) and 10 min later were treated with IFN-β (2.5 ng/g b.w., i.p.) (A). Mice were killed at 24 h post E. coli, and bronchoalveolar lavage was performed or lungs were processed for analysis without lavage. (B) Lung tissue sections from naïve mice (control) and vehicle or IFN-β ± WRW4 or cyclosporin H–treated mice. Hematoxylin and eosin stain was used. (Scale bars: 100 μm.) (C) Lung tissue of E. coli content, (D) lung tissue of MPO content, (E) lavage fluid neutrophil number, (F) lavage fluid monocyte/macrophage number, (G) the percentage of annexin-V positive neutrophils (identified as Ly6G-positive cells) in lavage fluid, (H) the percentage of macrophages with apoptotic bodies, (I) lavage fluid protein concentration, (J) lavage fluid 15-epi-LXA₄, and (K) RvD1 levels. Results are means ± SEM (n = 5 to 7 mice per group). *P < 0.05, **P < 0.01 (Dunn’s multiple contrast hypothesis test).