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The mechanisms that drive programmed resolution of inflammation remain elusive. Here, we report the temporal regulation of soluble (s) and transmembrane (m) fibrinogen-like protein 2 (Fgl2) during inflammation and show that both sFgl2 and mFgl2 correlate with the outcome. The expression and ectodomain shedding of Fgl2 are respectively promoted by miR-466l and metalloproteinases (ADAM10 and ADAM17) during inflammation resolution. Deficiency of Fgl2 enhances polymorphonuclear neutrophil (PMN) infiltration but impairs macrophage (MΦ) maturation and phagocytosis and inhibits the production of n-3 docosapentaenoic acid-derived resolvin 5 (RvDp5). In contrast, administration of sFgl2 blunts PMN infiltration as well as promotes PMN apoptosis and RvDp5 biosynthesis. By activating ALX/FPR2, RvDp5 enhances sFgl2 secretion via ADAM17 and synergistically accelerates resolution of inflammation. These results uncover a previously unknown endogenous programmed mechanism by which Fgl2 regulates resolution of inflammation and shed new light on clinical sepsis treatments.

Fibrinogen-like protein 2 controls sepsis catabasis by interacting with resolvin Dp5