{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bajrami B"],"funding":["FAMRI","Natural Science Foundation of Tianjin City","NIAID NIH HHS","NHLBI NIH HHS","National Institutes of Health","National Natural Sciences Foundation of China"],"pagination":["1999-2018"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5030805"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["213(10)"],"pubmed_abstract":["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 mobi"],"journal":["The Journal of experimental medicine"],"pubmed_title":["G-CSF maintains controlled neutrophil mobilization during acute inflammation by negatively regulating CXCR2 signaling."],"pmcid":["PMC5030805"],"funding_grant_id":["R01 HL092020","31471116","R01 AI103142","12JCZDJC24600","P01 HL095489","R01AI103142","CIA 123008","R01HL092020","31271484"],"pubmed_authors":["Kwak HJ","Nombela-Arrieta C","Mondal S","Bajrami B","Zhu H","Zhang YC","Park SY","Silberstein LE","Loison F","Luo HR","Sakai J","Geng G","Hou Q","Karatepe K","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"G-CSF maintains controlled neutrophil mobilization during acute inflammation by negatively regulating CXCR2 signaling.","description":"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 mobi","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Sep","modification":"2025-04-22T06:33:49.51Z","creation":"2019-10-18T07:00:57Z"},"accession":"S-EPMC5030805","cross_references":{"pubmed":["27551153"],"doi":["10.1084/jem.20160393"]}}