Evidence map›Paper›PMID 34033752›Full record

ArticleImmunity2021

Age-related changes in the local milieu of inflamed tissues cause aberrant neutrophil trafficking and subsequent remote organ damage.

Anna Barkaway, Loïc Rolas, Régis Joulia, Jennifer Bodkin, Tchern Lenn, Charlotte Owen-Woods, Natalia Reglero-Real, Monja Stein, Laura Vázquez-Martínez, Tamara Girbl and 13 more

Open access · hybridAbstract read
In one paragraph

Article in Immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
8.8field-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

104 citing papers in PubMed, 153 citations in OpenAlex.

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  10. Malignant cell-secreted chemokines drive colorectal cancer progression through endothelial cell activation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  20. Review

44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 7 institutions in 3 countries.

Anna BarkawayCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Loïc RolasCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Régis JouliaCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Jennifer BodkinCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Tchern LennCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Charlotte Owen-WoodsCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Natalia Reglero-RealCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Monja SteinCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Laura Vázquez-MartínezCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Tamara GirblCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Robin N PostonCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Matthew GoldingCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Rebecca S SaleebCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Aude ThiriotDepartment of Immunology and HMS Center for Immune Imaging, Harvard Medical School, Boston, MA, MA 02115, USA; The Ragon Institute of MGH, MIT and Harvard, Cambridge MA 02139, USA.
Ulrich H von AndrianDepartment of Immunology and HMS Center for Immune Imaging, Harvard Medical School, Boston, MA, MA 02115, USA; The Ragon Institute of MGH, MIT and Harvard, Cambridge MA 02139, USA.
Johan DucheneInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximillians-Universität (LMU) München, Munich 80336, Germany.
Mathieu-Benoit VoisinCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Cleo L BishopCentre for Cell Biology and Cutaneous Research, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
David VoehringerDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg (FAU), Erlangen 91054, Germany.
Axel RoersInstitute for Immunology, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, Dresden 01069, Germany.
Antal RotCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK; Centre for Inflammation and Therapeutic Innovation, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Tim LämmermannMax Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Sussan NoursharghCentre for Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK; Centre for Inflammation and Therapeutic Innovation, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK. Electronic address: s.nourshargh@qmul.ac.uk.
William Harvey Research Institute · GBQueen Mary University of London · GBRagon Institute of MGH, MIT and Harvard · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DELudwig-Maximilians-Universität München · DEMax Planck Institute of Immunobiology and Epigenetics · DEUniversity Hospital Carl Gustav Carus · DE

Funding

British Heart Foundation FS/14/3/30518British Heart Foundation PG/17/85/33395Wellcome Trust 098291/Z/12/ZWellcome Trust 200817/Z/16/Z
6 · The paper itself

Abstract

Aging is associated with dysregulated immune functions. Here, we investigated the impact of age on neutrophil diapedesis. Using confocal intravital microscopy, we found that in aged mice, neutrophils adhered to vascular endothelium in inflamed tissues but exhibited a high frequency of reverse transendothelial migration (rTEM). This retrograde breaching of the endothelium by neutrophils was governed by enhanced production of the chemokine CXCL1 from mast cells that localized at endothelial cell (EC) junctions. Increased EC expression of the atypical chemokine receptor 1 (ACKR1) supported this pro-inflammatory milieu in aged venules. Accumulation of CXCL1 caused desensitization of the chemokine receptor CXCR2 on neutrophils and loss of neutrophil directional motility within EC junctions. Fluorescent tracking revealed that in aged mice, neutrophils undergoing rTEM re-entered the circulation and disseminated to the lungs where they caused vascular leakage. Thus, neutrophils stemming from a local inflammatory site contribute to remote organ damage, with implication to the dysregulated systemic inflammation associated with aging.

Indexed as

AgingAnimalsBiological TransportChemokine CXCL1Endothelial CellsEndothelium, VascularFemaleInflammationIntercellular JunctionsLungMaleMiceMice, Inbred C57BLNeutrophilsReceptors, Interleukin-8BVenulesChemokine CXCL1Receptors, Interleukin-8BACKR1agingchemokinesCXCR2diapedesisendotheliumextravasationinflammationmast cellsNeutrophils

Identifiers

PMID34033752
PMCPMC8284598
OpenAlexW3165676370

What OpenQuestion holds

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LicenceCC BY
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.