LCN2 and Sepsis: On the bench side, Lcn2-null mice manifested greater susceptibility to sepsis with a significantly accelerated mortality rate, higher bacterial load in organs, and more severe organ damages [27, 28, 31, 54, 64, 67], and Lcn2-null immune cells exhibited reduced local bactericidal activities and excessive systemic inflammatory responses [32, 38, 41, 47, 51–54]; in both of the above cases, the conditions could be rescued by exogenous administration of recombinant Lcn2.