Evidence map›Paper›PMID 23121982›Full record

ArticleCellular immunology

In vivo imaging implicates CCR2(+) monocytes as regulators of neutrophil recruitment during arthritis.

Baomei Wang, Bernd H Zinselmeyer, Herbert A Runnels, Timothy P LaBranche, Phillip A Morton, Daniel Kreisel, Matthias Mack, Cheryl Nickerson-Nutter, Paul M Allen, Mark J Miller

Open access · bronzeAbstract read
In one paragraph

Article in Cellular immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  3. Review
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  11. Noninvasive Imaging of CCR2American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2016
    Article
  12. Patrolling monocytes promote intravascular neutrophil activation and glomerular injury in the acutely inflamed glomerulus.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  13. Review
  14. Article
  15. Article
  16. Cellular imaging in rheumatic diseases.Nature reviews. Rheumatology · 2015
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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

10 authors at 3 institutions in 2 countries.

Baomei WangDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Bernd H Zinselmeyer
Herbert A Runnels
Timothy P LaBranche
Phillip A Morton
Daniel Kreisel
Matthias Mack
Cheryl Nickerson-Nutter
Paul M Allen
Mark J Miller
Washington University in St. Louis · USPfizer (United States) · USUniversity of Regensburg · DE

Funding

Epithelial Responses to Bacterial InvasionR01AI077600 · NIAID · WASHINGTON UNIVERSITY · PI MILLER, MARK JAMES · 2009 to 2021
$3.8M
RECOGNITION AND SIGNALING IN POSITIVE SELECTION OF CD4+ T CELLSR01AI024157 · NIAID · WASHINGTON UNIVERSITY · PI ALLEN, PAUL M · 1987 to 2016
$2.5M
NIAID NIH HHS R01 AI024157NIAID NIH HHS R01 AI077600NIAID NIH HHS R01 AI0776003
6 · The paper itself

Abstract

The infiltration of neutrophils and monocytes is a prominent feature of inflammatory diseases including human rheumatoid arthritis. Understanding how neutrophil recruitment is regulated during pathogenesis is crucial for developing anti-inflammatory therapies. We optimized the K/B×N serum-induced mouse arthritis model to study neutrophil trafficking dynamics in vivo using two-photon microscopy. Arthritogenic serum was injected subcutaneously into one hind footpad to induce a local arthritis with robust neutrophil recruitment. Using this approach, we showed that the depletion of monocytes with clodronate liposomes impaired neutrophil recruitment specifically at the transendothelial migration step. The depletion of CCR2(+) monocytes with the monoclonal antibody MC-21 reproduced these effects, implicating CCR2(+) monocytes as key regulators of neutrophil extravasation during arthritis initiation. However, monocyte depletion did not prevent neutrophil extravasation in response to bacterial challenge. These findings suggest that anti-inflammatory therapies targeting monocytes may act in part through antagonizing neutrophil extravasation at sites of aseptic inflammation.

Indexed as

AnimalsAntibodies, MonoclonalArthritis, ExperimentalArthritis, RheumatoidClodronic AcidFemaleHumansInjections, SubcutaneousLiposomesMiceMice, Inbred C57BLMicroscopy, Fluorescence, MultiphotonMonocytesNeutrophil InfiltrationNeutrophilsReceptors, CCR2Antibodies, MonoclonalCcr2 protein, mouseClodronic AcidLiposomesReceptors, CCR2

Identifiers

PMID23121982
PMCPMC3760198
OpenAlexW2014637340

What OpenQuestion holds

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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.