Infections and inflammation trigger neutrophilias that are supported by a 
hematopoietic program of accelerated granulopoiesis known as emergency 
granulopoiesis. The intrinsic factors that drive reactive neutrophilias and 
emergency granulopoiesis have been inferred but not demonstrated. Here, we show 
that alum cannot elicit reactive neutrophilias in IL-1R type I (IL-1RI)(-/-) 
mice, whereas other inflammatory responses, including eosinophilia and Ab 
production, remain intact. Analysis of this specific impairment revealed an 
unanticipated role for IL-1RI in supporting increased proliferation by 
granulocyte/macrophage progenitors and, surprisingly, multipotent progenitors 
and hematopoietic stem cells (HSC). Indeed, HSC and multipotent progenitor 
proliferative responses were most suppressed in IL-1RI(-/-) mice, suggesting a 
critical role for their proliferation in inflammatory granulopoiesis. Whereas 
IL-1 drives increased HSC proliferation directly in vitro, IL-1RI expression by 
radiation-resistant host cells was both necessary and sufficient for 
alum-induced HSC, multipotent progenitor, and granulocyte/macrophage progenitor 
proliferation and reactive neutrophilias in radiation chimeric mice. Thus, IL-1 
plays a necessary, but indirect, role in the support of alum-induced 
neutrophilias by expanding both pluripotent and myeloid progenitor compartments 
to accelerate granulopoiesis.