No abstract

JapanBoth iron-deficient anemia (IDA) and malaria remain a threat to children in developing countries. Children with IDA are resistant to malaria, but the reasons for this are unknown. In this study, we addressed the mechanisms underlying the protection against malaria observed in IDA individuals using a rodent malaria parasite, Plasmodium yoelii (Py). We showed that the intra-erythrocytic proliferation and amplification of Py parasites were not suppressed in IDA erythrocytes and immune responses specific for Py parasites were not enhanced in IDA mice. We also found that parasitized IDA cells were more susceptible to engulfment by phagocytes in vitro than control cells, resulting in rapid clearance of parasitized cells and that protection of IDA mice from malaria was abrogated by inhibiting phagocytosis. One possible reason for this rapid clearance might be increased exposure of phosphatidylserine at the outer leaflet of parasitized IDA erythrocytes. The results of this study suggest that parasitized IDA erythrocytes are eliminated by phagocytic cells, which sense alterations in the membrane structure of parasitized IDA erythrocytes.

An error was introduced in Fig. 3E in this article. The correct Fig. 3E is shown below.(E) To assess the effects of IDA on susceptibility of T-cell-deficient nude mice, we infected the indicated mice with PyL and monitored parasitemia and survival rate. Values for parasitemia are arithmetic mean7SD from six mice in each group. Ã po0.05, in parasitemia between iron-sufficient and IDA WT mice and between iron-sufficient and IDA nude mice 7 and 9 days after infection, respectively (left panel). Two repeated experiments showed similar results. Figure 3. Effects of IDA on acquired immunity in mice infected with Py. Correction