Neutrophils are short-lived, terminally differentiated cells produced in the bone marrow through granulopoiesis. In severe infection or tissue injury, neutrophil production is augmented in a process known as emergency granulopoiesis (EG). Emergency granulopoiesis has been shown to generate phenotypically unique neutrophils, but their involvement in inflammation and the resolution of infection is not clear. Therefore, we established an experimental peritonitis model injecting 1x105 CFUs of E. coli into the peritoneal space and characterized immune cells mobilizing and entering the peritoneal space via flow cytometry. We utilized a self-resolving dosage of E. coli where infection was fully resolved within 48 hours. Neutrophils were rapidly mobilized from the bone marrow and entered the peripheral blood and peritoneum within 12 hours (p < 0.05, n = 4-5, Student’s T-test). This neutrophil population expressed significantly lower levels of CD101, a canonical maturity marker of neutrophils, indicating “left-shift,” a release of immature neutrophils in response to stress (p < 0.05, n = 4-5, Student’s T-test). Determination of neutrophil production was measured with EdU incorporation, where we found neutrophil production surged within the bone marrow and spleen in the first 24 hours displaying activation of emergency and extramedullary granulopoiesis even within the low dose of E. coli (p < 0.05, n = 4-5, Student’s T-test). Collectively, these findings demonstrate that emergency granulopoiesis is robustly activated during self-resolving peritonitis and promotes recruitment of phenotypically heterogeneous neutrophil populations to sites of infection. Ongoing studies are defining how EG drives metabolic and functional reprogramming of recruited neutrophils to support antimicrobial activity and inflammation resolution. Future studies employing genetic models targeting key transcriptional regulators will further elucidate the molecular mechanisms governing EG-driven neutrophil remodeling and host defense. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Jobe et al. (Fri,) studied this question.