Based on this finding, we examined the function and mechanism of MRP8/14-induced late-phase IP-10 production in the context of endotoxemia and showed that MRP8/14 promoted inflammation and lung injury in the context of endotoxemia through the IFNβ-JAK1/TYK2-STAT1-IRF7-IP-10-CXCR3 signaling pathway. Here, IFNB1 is linked to serum lipopolysaccharide activity.