Lipocalin 2 regulates intestine bacterial survival by interplaying with siderophore in a weaned piglet model of infection.

Iron is an essential nutrient that facilitates cell proliferation and growth, which plays a pivotal role in modulating the battle for survival between mammalian hosts and their pathogens. Pathogenic bacteria secrete siderophores to acquire iron from the host. However, lipocalin 2 (Lcn2), a siderophore-binding antimicrobial protein, binds to siderophores to prevent bacterial uptake of iron, which is critical for the control of systemic infection with (). But few studies focus on the anti-infective response of Lcn2 in the intestines by inhibiting bacterial proliferation based on microbial iron metabolism. In this study, we showed that iron was sequestrated within cells in a piglet model of K88 infection. Siderophores was produced following K88 infection and siderophore-related genes expression was upregulated in iron-deficiency environment . Meanwhile, we found that Lcn2 expression was rapidly and robustly induced in jejunum by K88 infection and could be stimulated by IL-17 and IL-22. Furthermore, both Lcn2 induced in epithelial cells IPEC-1 and added exogenously as a recombinant protein could inhibit the growth of . We can conclude that Lcn2 is a crucial component of mucosal immune defense against intestinal infection with K88.