biostudies-literatureBajrami BFAMRINatural Science Foundation of Tianjin CityNIAID NIH HHSNHLBI NIH HHSNational Institutes of HealthNational Natural Sciences Foundation of China1999-2018https://www.ebi.ac.uk/biostudies/studies/S-EPMC5030805biostudies-literatureUnknown213(10)Cytokine-induced neutrophil mobilization from the bone marrow to circulation is a critical event in acute inflammation, but how it is accurately controlled remains poorly understood. In this study, we report that CXCR2 ligands are responsible for rapid neutrophil mobilization during early-stage acute inflammation. Nevertheless, although serum CXCR2 ligand concentrations increased during inflammation, neutrophil mobilization slowed after an initial acute fast phase, suggesting a suppression of neutrophil response to CXCR2 ligands after the acute phase. We demonstrate that granulocyte colony-stimulating factor (G-CSF), usually considered a prototypical neutrophil-mobilizing cytokine, was expressed later in the acute inflammatory response and unexpectedly impeded CXCR2-induced neutrophil mobiThe Journal of experimental medicineG-CSF maintains controlled neutrophil mobilization during acute inflammation by negatively regulating CXCR2 signaling.PMC5030805R01 HL09202031471116R01 AI10314212JCZDJC24600P01 HL095489R01AI103142CIA 123008R01HL09202031271484Kwak HJNombela-Arrieta CMondal SBajrami BZhu HZhang YCPark SYSilberstein LELoison FLuo HRSakai JGeng GHou QKaratepe KXu YfalseG-CSF maintains controlled neutrophil mobilization during acute inflammation by negatively regulating CXCR2 signaling.Cytokine-induced neutrophil mobilization from the bone marrow to circulation is a critical event in acute inflammation, but how it is accurately controlled remains poorly understood. In this study, we report that CXCR2 ligands are responsible for rapid neutrophil mobilization during early-stage acute inflammation. Nevertheless, although serum CXCR2 ligand concentrations increased during inflammation, neutrophil mobilization slowed after an initial acute fast phase, suggesting a suppression of neutrophil response to CXCR2 ligands after the acute phase. We demonstrate that granulocyte colony-stimulating factor (G-CSF), usually considered a prototypical neutrophil-mobilizing cytokine, was expressed later in the acute inflammatory response and unexpectedly impeded CXCR2-induced neutrophil mobi2016-01-01T00:00:00Z2016 Sep2025-04-22T06:33:49.51Z2019-10-18T07:00:57ZS-EPMC50308052755115310.1084/jem.20160393