Emergency granulopoiesis refers to the increased production of neutrophils in 
bone marrow and their release into circulation induced by severe infection. 
Several studies point to a critical role for G-CSF as the main mediator of 
emergency granulopoiesis. However, the consequences of G-CSF stimulation on the 
transcriptome of neutrophils and their precursors have not yet been investigated 
in humans. In this work, we examine the changes in mRNA expression induced by 
administration of G-CSF in vivo, as a model of emergency granulopoiesis in 
humans. Blood samples were collected from healthy individuals after 5 d of G-CSF 
administration. Neutrophil precursors were sorted into discrete stages of 
maturation by flow cytometry, and RNA was subjected to microarray analysis. mRNA 
levels were compared with previously published expression levels in 
corresponding populations of neutrophil precursors isolated from bone marrow of 
untreated, healthy individuals. One thousand one hundred and ten mRNAs were 
differentially expressed >2-fold throughout terminal granulopoiesis. Major 
changes were seen in pathways involved in apoptosis, cytokine signaling, and TLR 
pathways. In addition, G-CSF treatment reduced the levels of four of five 
measured granule proteins in mature neutrophils, including the proantibacterial 
protein hCAP-18, which was completely deficient in neutrophils from 
G-CSF-treated donors. These results indicate that multiple biological processes 
are altered to satisfy the increased demand for neutrophils during G-CSF-induced 
emergency granulopoiesis in humans.