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, 2007b), we hypothesized that it may regulate the interactions between iron homeostasis and the immune system during malaria infection. Our results reveal that Lcn2 has a pivotal role in controlling parasite levels as well as host innate and adaptive responses during Plasmodium blood-stage malaria infections and that this role may involve host iron status. To investigate the role of Lcn2 during malaria infection, we measured the serum Lcn2 levels of P.?vivax patients from Anti-cancer Compound Library concentration southeastern Turkey, where persistent focal P.?vivax malaria occurs. Study participants (detailed patient information is published elsewhere [ Yildiz Zeyrek et?al., 2011; Zeyrek et?al., 2008] [ Table S1]) were divided into two groups according to the parasite load in the blood, as determined by microscopy: patients with fewer than 1,000 parasites/��l of blood (n?= 15) and with more than 1,000 parasites/��l of blood (n?= 54). We observed significantly higher Lcn2 levels with increasing parasite density ( Figure?1A), which suggests that P.?vivax infection stimulates Lcn2 production. Plasmodium yoelii nonlethal (PyNL) infection in mice has many features in common with P.?vivax infection in Ceramidase humans ( Vig��rio et?al., 2001). To evaluate whether an increase in parasitemia also correlated with higher Lcn2 levels in PyNL-infected mice, mice were injected with 105PyNL-infected erythrocytes and followed for up to 40?days for parasitemia (expressed as the percentage of infected red blood cells [iRBCs] and serum Lcn2 protein levels). As in the P.?vivax malaria patients, Lcn2 sera levels were found to increase with parasitemia during blood-stage PyNL infection AZD8055 clinical trial ( Figure?1B). Next, Lcn2?/? mice were infected and followed throughout the blood-stage course of infection. Infected Lcn2?/? mice had significantly higher parasitemia ( Figure?1C) with reduced survival ( Figure?1D, ?? p?