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Stress erythropoiesis during inflammation
Whereas steady-state erythropoiesis occurs in the bone marrow, stress erythropoiesis occurs in the spleen and liver. Hypoxia and acute anemia induce stress erythropoiesis to restore adequate numbers of red blood cells. Bennett et al. found that sterile inflammation mediated by Toll-like receptors (TLRs) induced stress erythropoiesis in mice by stimulating erythrocyte phagocytosis by splenic macrophages. This resulted in production of the transcription factor SPI-C, which cooperated with TLR signaling to induce the production of cytokines that increased the number of stress erythroid progenitors in the spleen. This work reveals a mechanism that compensates for the inhibition of steady-state erythropoiesis by proinflammatory cytokines.
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