LCN2 and escherichia coli infection: Lcn2-deficient mice in which exons 1–5 or exons 2–5 were replaced are viable but exhibit increased sensitivity to E. coli infections and lipopolysaccharides showing that LCN2 is an important component of the innate immune systems and the acute phase response. It limits bacterial growth by sequestering iron-laden siderophores. Respective mice show alterations in intracellular lipid droplet formation.