We observed that the CXCR2-selective antagonist inhibited the excess neutrophil recruitment observed in Gdf15−/− (Fig. 4D), and that in these conditions the survival advantage of Gdf15−/− mice to CLP was lost (Fig. 4E), suggesting that increased local levels of CXCL5 in Gdf15−/− mice is a necessary component of their increased survival of a peritoneal polymicrobial infection. Here, CXCR2 is linked to infection.