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. 2020 May 18;117(22):12281–12287. doi: 10.1073/pnas.1918508117

Fig. 4.

Fig. 4.

Gdf15−/− mice demonstrate better control of local infection due to CXCL5-mediated neutrophil influx into the peritoneum. (A and B) Percentage (A) and total number of neutrophils (B) in the peritoneal lavage of WT (n = 4) and Gdf15−/− (n = 5) mice at 8 h after CLP. (C) ELISA quantification of CXCL5 in the peritoneal lavage of WT and Gdf15−/− mice at 8 h after CLP or control (noninfected; NI) . (D) Number of neutrophils in peritoneal lavage after CLP in WT vehicle-treated mice (WT; n = 7) and Gdf15−/− mice treated with CXCR2 inhibitor SB225002 (Gdf15−/−; n = 6). (E) Survival to CLP in WT vehicle-treated mice (WT; n = 4) and Gdf15−/− mice treated with CXCR2 inhibitor SB225002 (Gdf15−/−; n = 4). (F) Number of neutrophils in peritoneal lavage after CLP in WT isotype control-treated mice (n = 3) and WT mice treated with anti-GR1 antibody (n = 3). (G) Survival to CLP in WT isotype control-treated mice (n = 6) and WT anti-GR1–treated mice (n = 6) and Gdf15−/− mice treated anti-GR1 antibody (n = 6).