Our study showed that Mrp8 gene deficiency significantly blocked LPS-induced IP-10 expression and that the administration of exogenous MRP8/14 restored IP-10 induction in BALF; blocking IP-10 restrained lung injury in endotoxemic mice, indicating that MRP8/14 was a key inducer of IP-10, which is crucial for the inflammatory response and lung injury during endotoxemia. This evidence concerns the gene S100A8 and serum lipopolysaccharide activity.