Iron recycling is important in preventing anemia, and its role in preventing anemia during infection is unclear. In severe Plasmodium falciparum malaria, acute kidney injury (AKI) is associated with life-threatening anemia. A study using a rodent model shows that renal proximal tubule epithelial cells (RPTECs) have the ability to store and recycle iron during P. chabaudi chabaudi (Pcc) infection, preventing the onset of life-threatening malarial anemia.
Iron recycling prevents the development of anemia under homeostatic conditions. Whether iron recycling was co-opted as a defense strategy to prevent the development of anemia in response to infection is unclear. We find that in severe Plasmodium falciparum malaria, the onset of life-threatening anemia is associated with acute kid-ney injury (AKI), irrespective of parasite load. Using a well-established experimental rodent model of malaria anemia, we identify a transcriptional response that endows renal proximal tubule epithelial cells (RPTECs) with the capacity to store and recycle iron during P. chabaudi chabaudi (Pcc) infection. This response encom-passes the induction of ferroportin 1/SLC40A1, which exports iron from RPTECs and counteracts AKI while supporting compensatory erythropoiesis and preventing the onset of life-threatening malarial anemia. Iron recycling by myeloid cells is dispensable to this protective response, suggesting that RPTECs provide an iron-recycling salvage pathway that prevents the pathogenesis of life-threatening malarial anemia.
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