G-CSF is an essential regulator of neutrophil trafficking from the bone marrow to the blood
Open accessAbstract
Neutrophils are released from the bone marrow in a regulated fashion to maintain homeostatic levels in the blood and to respond to physiological stresses, including infection. We show that under basal conditions granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil release from the bone marrow. Nonredundant signals generated by the membrane-proximal 87 amino acids of the G-CSF receptor (G-CSFR) are sufficient to mediate this response. Surprisingly, G-CSFR expression on neutrophils is neither necessary nor sufficient for their mobilization from the bone marrow, suggesting that G-CSF induces neutrophil mobilization indirectly through the generation of trans-acting signals. Evidence is provided suggesting that downregulation of stromal cell-derived factor 1 expression in the bone marrow may represent such a signal.
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Lower levels of GCSF are observed in THS-exposed mouse wounds.
“However, we observed lower levels of GCSF, which not only is a key regulator of neutrophil production [60] but also plays an essential role in neutrophil trafficking [61].”
From Tobacco toxins deposited on surfaces (third hand smoke) impair wound healing (2016) · cites this paper as [61]
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References 47 · Cited by 450
- Authors
- Semerad, C. L., Liu, F., Gregory, A. D., Stumpf, K., & Link, D. C.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Link, Daniel C
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2002-10
- Volume
- 17
- Issue
- 4
- Pages
- 413-423
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2038796948
- Cited by
- 450
- References
- 47
- Citations by year
- 2026: 16 · 2025: 16 · 2024: 20 · 2023: 29 · 2022: 21 · 2021: 36 · 2020: 19 · 2019: 33 · 2018: 18 · 2017: 21 · 2016: 26 · 2015: 17 · 2014: 26 · 2013: 24 · 2012: 18
- FWCI
- 3.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 3942 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01 HL60772-01A1, R01HL060772, T32 HL07088-23, T32HL007088)
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Keywords
- granulocyte colony-stimulating factor, G-CSF receptor, neutrophil mobilization, neutrophil trafficking, bone marrow, CXCL12, hematopoietic homeostasis
- MeSH terms
- Animals, Blood Cells, Bone Marrow Cells, Cell Movement, Mice, Inbred C57BL, Mice, Transgenic, Neutrophils, Recombinant Proteins, Signal Transduction, Granulocyte Colony-Stimulating Factor, Receptors, Granulocyte Colony-Stimulating Factor, Interleukin-8, Mutagenesis, Chemokines, CXC, Mice, Chemokine CXCL12
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