S100A9 and serum lipopolysaccharide activity: In vivo studies using S100A9-deficient mice, which fail to induce S100A8 or S100A9, were partially protected from endotoxemia and this appeared to be mediated by TLR4 [22], although, an alternate study showed S100A8 administration attenuated endotoxemia mediated inflammation and tissue injury suggesting a protective role for S100A8 [26].