A neo cassette replaces exons 2-5 of the lipocalin 2 (Lcn2) gene, abolishing gene expression. LCN2 is an iron-trafficking protein involved in apoptosis and the regulation of the innate immune systems response to bacterial growth and infection. Toll-like receptors on innate immune cells stimulate the production and secretion of LCN2 upon bacterial infection. LCN2 limits bacterial growth by iron sequestration, which is required by bacteria in order to replicate. 


Homozygous LCN2-deficient mice are viable and fertile and should be housed in a specific pathogen free (SPF) facility. Escherichia coli challenge causes an increase in bacterial burden in the liver and spleen along with physical signs of sepsis such as lethargy, hunched posture, and ruffled fur. E Coli infection caused no difference in leukocyte numbers, neutrophil infiltration, or tissue iron distribution. Also, after induction of accelerated nephrotoxic serum nephritis (NTS), LCN2 KO mice exhibit more glomerular damage with increased proteinuria and interstitial leukocyte accumulation than wildtype mice. 

Other mutations of Lcn2 show this gene to be a bone-derived hormone with metabolic regulatory effects. In these mutants, LCN2 suppresses appetite in a MC4R-dependent manner, and show that the control of appetite is an endocrine function of bone intake.

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Lcn2 deficient mice may be useful for studying the role of iron trafficking in the regulation of innate immunity.

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B6.129P2-Lcn2<tm1Aade>/AkiJ Frozen Embryo