caa a22 4500 463256433 CHVBK 20180405153357.0 cr unu---uuuuu 170326e20070401xx s 000 0 eng 10.1007/s00277-006-0246-6 doi (NATIONALLICENCE)springer-10.1007/s00277-006-0246-6 Leukocyte numbers correlate with plasma levels of granulocyte-macrophage colony-stimulating factor in sickle cell disease [Elektronische Daten] [Nicola Conran, Sara Saad, Fernando Costa, Tohru Ikuta] Despite a clear role for leukocytes in modulating the pathophysiology of sickle cell disease (SCD), the mechanism by which leukocyte numbers are increased in this disorder remains unclear. Hypothesizing that the chronic inflammatory state, elicited by adhesive interactions involving various cell types, might underlie leukocytosis, we measured plasma levels of proinflammatory or myeloid cytokines that play a role in leukocytosis and examined their correlations with leukocyte numbers in patients with SCD. Our studies found that, although plasma levels of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin 3, and macrophage colony-stimulating factor are elevated in steady-state patients with SCD, only plasma GM-CSF levels are positively correlated with the numbers of total leukocytes, neutrophils, monocytes, and eosinophils, regardless of whether they received hydroxyurea. GM-CSF levels were significantly decreased in patients on hydroxyurea therapy. These data suggest a role of GM-CSF in leukocytosis of SCD. In contrast, plasma levels of granulocyte colony-stimulating factor, a major cytokine that induces leukocytosis due to bacterial infection, were lower than those of control subjects. These results indicate that elevated GM-CSF levels may contribute, at least in part, to high leukocyte numbers in SCD. As plasma GM-CSF levels were decreased in patients on hydroxyurea therapy, hydroxyurea may decrease leukocyte numbers by reducing circulating GM-CSF levels. Springer-Verlag, 2007 Sickle cell disease nationallicence Leukocytosis nationallicence Cytokines nationallicence Hydroxyurea nationallicence Inflammation nationallicence Conran Nicola Hematology and Hemotherapy Center, University of Campinas, UNICAMP-SP, Campinas, Brazil aut Saad Sara Hematology and Hemotherapy Center, University of Campinas, UNICAMP-SP, Campinas, Brazil aut Costa Fernando Hematology and Hemotherapy Center, University of Campinas, UNICAMP-SP, Campinas, Brazil aut Ikuta Tohru Department of Medicine, Institute of Molecular Medicine and Genetics, Medical College of Georgia, 1120 15th Street CB-2803, 30912, Augusta, GA, USA aut Annals of Hematology Springer-Verlag 86/4(2007-04-01), 255-261 0939-5555 86:4<255 2007 86 277 https://doi.org/10.1007/s00277-006-0246-6 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00277-006-0246-6 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Conran Nicola Hematology and Hemotherapy Center, University of Campinas, UNICAMP-SP, Campinas, Brazil aut NATIONALLICENCE 700 1- Saad Sara Hematology and Hemotherapy Center, University of Campinas, UNICAMP-SP, Campinas, Brazil aut NATIONALLICENCE 700 1- Costa Fernando Hematology and Hemotherapy Center, University of Campinas, UNICAMP-SP, Campinas, Brazil aut NATIONALLICENCE 700 1- Ikuta Tohru Department of Medicine, Institute of Molecular Medicine and Genetics, Medical College of Georgia, 1120 15th Street CB-2803, 30912, Augusta, GA, USA aut NATIONALLICENCE 773 0- Annals of Hematology Springer-Verlag 86/4(2007-04-01), 255-261 0939-5555 86:4<255 2007 86 277 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer