S100A8 and serum lipopolysaccharide activity: Consistent with this result, our findings showed that myeloid cell-specific deletion of the Mrp8 gene attenuated the inflammatory response and lung injury in endotoxemic mice, and this effect could be reversed by exogenous recombinant MRP8/14, indicating that MRP8/14 is involved in the inflammatory response and contributes to lung injury in endotoxemia.