
-   LCN2 protects against infection and sepsis and shapes intestinal microbial community structures by binding enterobactin type siderophores, thereby preventing bacterial iron acquisition and the growth of siderophore-dependent strains [PMID: 28214071].
-   The role of LCN-2 in protecting again infection was demonstrated in LCN-2 deficient mice - when challenged with sub lethal dose of E.Coli, mice demonstrated markedly increased bacteraemia and bacterial burden compared to normal controls. The bacteriostatic effect of LCN-2 was absolutely specific for bacteria that acquire iron through LCN-2-binding siderophores (for example enterochelin and mycobactin) [PMID: 15531878].
-   In mouse CKD model Lcn2 expression was elevated following EGFR activation and mediated EGFR's mitogenic effects during renal deterioration. Hif-1alpha was essential for EGFR-induced Lcn2 overexpression [PMID: 20921623].
-   In psoriasis model Lcn2 stimulated human neutrophils to produce proinflammatory mediators via 24p3R and activated the ERK1/2 and p38 MAPK signaling pathways, which also mediated Lcn2-induced neutrophil chemotaxis in vitro [PMID: 26979478].

## Summary

Lcn2 codes for Lipocalin-2, a protein involved in innate immunity by binding bacterial siderophores, thereby sequestering iron to limit bacterial growth [CS: 10]. In kidney diseases or toxicity, the kidney is vulnerable to infections and iron dysregulation [CS: 9]. Increased expression of Lcn2 would result in more Lipocalin-2 capable of binding siderophores like enterobactin from bacteria, which prevents bacterial use of iron, potentially limiting infection and bacterial proliferation secondary to the renal injury [CS: 8].

In acute and chronic kidney damage, the overexpression of Lcn2 indicates renal injury and functions in response to cellular stress [CS: 9]. Higher levels of Lipocalin-2 in kidney tissue have implications for iron homeostasis; it can help modulate iron availability by binding to siderophores and regulate its cellular distribution [CS: 8]. In conditions leading to oxidative stress where iron might be deleterious, Lipocalin-2 aids in chelating and exporting iron from cells, lowering the risk of further oxidative damage during renal injury [CS: 7]. Conversely, the iron-bound form can facilitate iron uptake into cells where it may be needed for cellular repair processes [CS: 6]. Thus, the upregulation of Lcn2 in response to renal toxicity serves to balance iron dynamics in favor of injury mitigation and cellular recovery [CS: 7].
