Acute trauma and critical illness cause increases in G-CSF that correlate with post-injury outcomes and are associated with changes in bone marrow progenitor populations.

Trauma induces a rapid increase in plasma G-CSF levels that is strongly correlated with plasma IL-1β, suggesting that as in murine models, IL-1 may be driving G-CSF production. As in mice, NSCI induced EH, characterized by expansion of the HSC cohort and a shift toward myelopoiesis. In critically ill humans these data suggest that sterile injury induces IL-1 and G-CSF mediated EH, recapitulating the murine finding.