Fig. 7
IFN-β favors macrophage reprogramming during the resolution of inflammation. a–d Macrophages were recovered from peritoneal exudates of male Ifnb+/+ or Ifnb−/− mice at 48–66 h PPI and cultured with LPS (1 μg/ml) for 24 h. Culture supernatants were then collected and levels of IL-10 (a), IL-6 (b), IL-12 (c) and CCL3 (d) were determined by selective ELISAs. Results are means ± SEM from four independent experiments. *P < 0.05, ***P < 0.005 (Tukey’s HSD). e–f Macrophages were recovered from peritoneal exudates of Ifnb+/+ mice at 48–66 h PPI and cultured with mouse IFN-β or IFN-α (20 ng/ml each) for 48 h. Then, culture supernatants were collected and levels of IL-10 (e) and IL-12 (f) were determined by ELISA. Results are means ± SEM (n = 4). ***P < 0.005 (Tukey’s HSD). g Macrophages were recovered from peritoneal exudates of Ifnb+/+ mice 48–66 h PPI and incubated with IFN-β (20 ng/ml) for 48 h. The cells were then immunostained for F4/80 and CD11b and the percentage of CD11blow macrophages was determined by flow cytometry. Results are means ± SEM from three independent experiments. ***P < 0.005 (Tukey’s HSD). h–i Mice undergoing peritonitis were treated with IFN-β (20 ng/mouse, i.p.) or vehicle at 24 h PPI. Peritoneal macrophages were collected at 48 h PPI, lysed and immunoblotted for 12/15-LO, arginase 1, ISG15 and GAPDH. Representative blots (h) and densitometry analysis (means ± SEM) (i) for three independent experiments. *P < 0.05 (Student’s t test). Source data are provided as a Source Data file
