Using a murine model of LPS-induced endotoxemia, we further confirmed the presence of Lcn2 in the intestinal crypt cells under physiological conditions and demonstrated the existence of correlations between the severity of illness in critically ill individuals and the accumulation of Lcn2 in the crypt lamina of the ileum and colon and its discharge into the intestinal lumen, the first scene of gut-origin sepsis [25]. This evidence concerns the gene LCN2 and serum lipopolysaccharide activity.