In many disorders resulting from a lack of iron, hemoglobin synthesis is deeply suppressed, resulting Mitomycin C order in iron-deficient anemia (IDA). IDA is characterized by small erythrocytes (microcytic) that contain less hemoglobin (hypochromic). IDA is mainly caused by a low dietary intake of iron, but can also be caused by chronic intestinal hemorrhage associated with hookworm infestation or by vitamin A deficiency, which is critical for iron metabolism. Both are common in

developing countries 1. Nearly half of the children living in developing countries are estimated to suffer from IDA; twice the number in industrialized countries. Iron deficiency adversely affects cognitive performance, behavior and physical growth, and IDA patients experience impaired gastrointestinal function and altered patterns of hormone production and metabolism 1. Moreover, morbidity

due to infectious diseases is increased in iron-deficient populations because of its adverse effects on the immune system HM781-36B 1, 2. Based on this, the World Health Organization recommends iron supplementation for children and pregnant women to treat IDA. Malaria is still a major health problem, resulting in more than 200 million infections and around a million deaths annually 3. Almost all victims of malaria are children under 5 years of age living in sub-Saharan Africa 3, whose geographical and age distribution completely overlap those of IDA. Thus, the coexistence of IDA and malaria seems common, and IDA may modulate the course of malaria. In Kenya, however, clinical malaria is significantly less frequent among iron-deficient children 4. In infants from Papua New Guinea, iron supplementation increased the prevalence of parasitemia 5. In the largest study, involving Zanzibari children, routine supplementation with iron and folate was found to increase the risk of severe malaria and death 6. Taken together, these findings suggest that routine supplementation with iron, or iron plus folate, increases childhood morbidity and mortality from malaria. Recently, one study assessed the effect of iron supplementation on the intermittent preventive treatment of malaria 7;

however, the mechanisms involved are still not fully understood. Here, we addressed the mechanisms underlying decreased susceptibility to malaria in IDA individuals crotamiton using a mouse malaria model. We found that macrophages preferentially sensed and engulfed parasitized erythrocytes from IDA mice, resulting in rapid clearance of the parasite from the circulation. One possible reason for this rapid clearance may be increased phosphatidylserine (PS) exposure at the outer leaflet of parasitized IDA erythrocytes. C57BL/6 mice were fed with a chemically defined iron-deficient diet to mimic IDA, the most prevalent form of anemia observed in endemic areas of malaria. The effect of this diet on hematopoiesis was assessed by measuring a number of hematological variables (Table 1).