Normally, neutrophil pools are maintained by “steady-state” granulopoiesis. Inflammation, however, is thought to elicit growth factors that accelerate neutrophil production through a distinct developmental program known as “emergency” granulopoiesis. In IL-1RI-/- mice, adjuvant-induced emergency granulopoiesis is defective due to impaired progenitor proliferation. Interestingly, this hematopoietic defect is associated with impaired neutrophil mobilization from bone marrow (BM), raising the possibility that increased proliferation by hematopoietic progenitors is a response to reduced BM neutrophil density rather than pro-inflammatory signals. Consistent with this potential feedback mechanism, non-inflammatory depletions of mature BM neutrophils by passive antibody elicit emergency granulopoietic responses similar to those induced by adjuvant, and progenitor proliferation fluctuates inversely with BM neutrophil numbers. Furthermore, mice bearing a genetic defect in neutrophil survival exhibit constitutive emergency granulopoiesis. Whereas adjuvant potently induces serum G-CSF, a neutrophil growth and mobilization factor, neutrophil depletion elicits equally robust granulopoietic responses with substantially reduced levels of G-CSF. These observations suggest that other - perhaps unknown - factors mediate accelerated granulopoiesis, and we propose a common model for the feedback regulation of both steady-state and emergency granulopoiesis.