Evidence map›Paper›PMID 20516641›Full record

ArticleThe Journal of clinical investigation2010

CXCR2 and CXCR4 antagonistically regulate neutrophil trafficking from murine bone marrow.

Kyle J Eash, Adam M Greenbaum, Priya K Gopalan, Daniel C Link

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 479 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
479citing papers in PubMed, 1 pooled it
11.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

479 citing papers in PubMed, 1 synthesis or guideline pooled it, 765 citations in OpenAlex.

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  16. Immature neutrophils are elevated in human PGD and linked to G-CSF-driven injury in a murine model of lung ischemia-reperfusion.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026
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419 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Kyle J EashDivision of Oncology, Department of Medicine, Washington University School of Medicine, Saint Louis, Missouri 63110, USA.
Adam M Greenbaum
Priya K Gopalan
Daniel C Link
Washington University in St. Louis · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
ROLE OF THE G-CSF RECEPTOR IN PROGENITOR MOBILIZATIONR01HL060772 · NHLBI · WASHINGTON UNIVERSITY · PI LINK, DANIEL C · 1999 to 2014
$3.9M
NCI NIH HHS P30 CA091842NCI NIH HHS P30 CA91842NHLBI NIH HHS R01 HL060772NHLBI NIH HHS R01 HL60772
6 · The paper itself

Abstract

Neutrophils are a major component of the innate immune response. Their homeostasis is maintained, in part, by the regulated release of neutrophils from the bone marrow. Constitutive expression of the chemokine CXCL12 by bone marrow stromal cells provides a key retention signal for neutrophils in the bone marrow through activation of its receptor, CXCR4. Attenuation of CXCR4 signaling leads to entry of neutrophils into the circulation through unknown mechanisms. We investigated the role of CXCR2-binding ELR+ chemokines in neutrophil trafficking using mouse mixed bone marrow chimeras reconstituted with Cxcr2(-/-) and WT cells. In this context, neutrophils lacking CXCR2 were preferentially retained in the bone marrow, a phenotype resembling the congenital disorder myelokathexis, which is characterized by chronic neutropenia. Additionally, transient disruption of CXCR4 failed to mobilize Cxcr2(-/-) neutrophils. However, neutrophils lacking both CXCR2 and CXCR4 displayed constitutive mobilization, showing that CXCR4 plays a dominant role in neutrophil trafficking. With regard to CXCR2 ligands, bone marrow endothelial cells and osteoblasts constitutively expressed the ELR+ chemokines CXCL1 and CXCL2, and CXCL2 expression was induced in endothelial cells during G-CSF-induced neutrophil mobilization. Collectively, these data suggest that CXCR2 signaling is a second chemokine axis that interacts antagonistically with CXCR4 to regulate neutrophil release from the bone marrow.

Indexed as

AnimalsBone MarrowBone Marrow CellsCell MovementChemokine CXCL1Chemokine CXCL12Chemokine CXCL2ChemokinesGranulocyte Colony-Stimulating FactorHomeostasisMiceMice, CongenicMice, Inbred C57BLMice, KnockoutMice, TransgenicNeutrophilsChemokine CXCL1Chemokine CXCL12Chemokine CXCL2ChemokinesCXCL2 protein, humanGranulocyte Colony-Stimulating FactorReceptors, CXCR4

Identifiers

PMID20516641
PMCPMC2898597
OpenAlexW1991562400

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.