title: G-CSF preferentially supports the generation of gut-homing Gr-1high macrophages in M-CSF-treated bone marrow cells.
abstract: The G-CSF is best known for its activity in the generation and activation of neutrophils. In addition, studies on G-CSF(-/-) or G-CSFR(-/-) mice and BMC cultures suggested a role of G-CSF in macrophage generation. However, our understanding on the role of G-CSF in macrophage development is limited. Here, using in vitro BMC models, we demonstrated that G-CSF promoted the generation of Gr-1(high)/F4/80(+) macrophage-like cells in M-BMCs, likely through suppressing cell death and enhancing generation of Gr-1(high)/F4/80(+) macrophage-like cells. These Gr-1(high) macrophage-like cells produced "M2-like" cytokines and surface markers in response to LPS and IL-4/IL-13, respectively. Adoptive transfer of EGFP-expressing (EGFP(+)) M-BMCs showed a dominant, gut-homing phenotype. The small intestinal lamina propria of G-CSFR(-/-) mice also harbored significantly reduced numbers of Gr-1(high)/F4/80(+) macrophages compared with those of WT mice, but levels of Gr-1(+)/F4/80(-) neutrophil-like cells were similar between these mice. Collectively, these results suggest a novel function of G-CSF in the generation of gut-homing, M2-like macrophages.
authors: Department of Microbiology and Immunology, Center for Human Immunology, and Schulich School of Medicine and Dentistry, and.
authors: Shahab
authors: S
authors: Meshkibaf
authors: Department of Microbiology and Immunology, Center for Human Immunology, and Schulich School of Medicine and Dentistry, and.
authors: Mark William
authors: MW
authors: Gower
authors: Department of Microbiology and Immunology, Department of Molecular Medicine, Robarts Research Institute, University of Western Ontario, London, Ontario, Canada.
authors: Gregory A
authors: GA
authors: Dekaban
authors: Department of Microbiology and Immunology, Center for Human Immunology, and Schulich School of Medicine and Dentistry, and sung.kim@schulich.uwo.ca.
authors: Sung Ouk
authors: SO
authors: Kim
mesh_terms: D000818:Animals; D000950:Antigens, Ly / Q000378:metabolism; D000954:Antigens, Surface / Q000378:metabolism; D001854:Bone Marrow Cells / Q000187:drug effects / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects / Q000276:immunology; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism; D005260:Female; D041981:Gastrointestinal Tract / Q000166:cytology* / Q000276:immunology*; D016179:Granulocyte Colony-Stimulating Factor / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D016130:Immunophenotyping; D016173:Macrophage Colony-Stimulating Factor / Q000494:pharmacology*; D008264:Macrophages / Q000166:cytology / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D010641:Phenotype; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*
chemical_list: D000950:Antigens, Ly; D000954:Antigens, Surface; D016207:Cytokines; C494192:Ly-6C antigen, mouse; D011956:Receptors, Cell Surface; C551746:granulocyte receptor 1, mouse; D016179:Granulocyte Colony-Stimulating Factor; D016173:Macrophage Colony-Stimulating Factor
keywords: GM-CSF; differentiation; myeloid cells