Evidence map›Paper›PMID 25700973›Full record

ArticleImmunobiology2015

The adult murine heart has a sparse, phagocytically active macrophage population that expands through monocyte recruitment and adopts an 'M2' phenotype in response to Th2 immunologic challenge.

Katie J Mylonas, Stephen J Jenkins, Raphael F P Castellan, Dominik Ruckerl, Kieran McGregor, Alexander T Phythian-Adams, James P Hewitson, Sharon M Campbell, Andrew S MacDonald, Judith E Allen and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Immunobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
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  7. Macrophages in myocardial infarction.American journal of physiology. Cell physiology · 2022
    Review
  8. Coronavirus Disease 2019 and Takotsubo Syndrome.Reviews in cardiovascular medicine · 2022
    Review
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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

11 authors at 3 institutions in 1 country.

Katie J MylonasBHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute (QMRI), University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, Scotland, United Kingdom. Electronic address: kmylonas@staffmail.ed.ac.uk.
Stephen J JenkinsCentre for Inflammation Research, QMRI, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, Scotland, United Kingdom.
Raphael F P CastellanBHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute (QMRI), University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, Scotland, United Kingdom.
Dominik RuckerlInstitute of Immunology and Infection Research (IIIR), The King's Buildings, University of Edinburgh, Charlotte Auerbach Road, Edinburgh EH9 3FL, Scotland, United Kingdom.
Kieran McGregorBHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute (QMRI), University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, Scotland, United Kingdom.
Alexander T Phythian-AdamsInstitute of Immunology and Infection Research (IIIR), The King's Buildings, University of Edinburgh, Charlotte Auerbach Road, Edinburgh EH9 3FL, Scotland, United Kingdom; Manchester Collaborative Centre for Inflammation Research (MCCIR), University of Manchester, Grafton Street, Manchester M13 9NT, England, United Kingdom.
James P HewitsonInstitute of Immunology and Infection Research (IIIR), The King's Buildings, University of Edinburgh, Charlotte Auerbach Road, Edinburgh EH9 3FL, Scotland, United Kingdom.
Sharon M CampbellInstitute of Immunology and Infection Research (IIIR), The King's Buildings, University of Edinburgh, Charlotte Auerbach Road, Edinburgh EH9 3FL, Scotland, United Kingdom.
Andrew S MacDonaldInstitute of Immunology and Infection Research (IIIR), The King's Buildings, University of Edinburgh, Charlotte Auerbach Road, Edinburgh EH9 3FL, Scotland, United Kingdom; Manchester Collaborative Centre for Inflammation Research (MCCIR), University of Manchester, Grafton Street, Manchester M13 9NT, England, United Kingdom.
Judith E AllenInstitute of Immunology and Infection Research (IIIR), The King's Buildings, University of Edinburgh, Charlotte Auerbach Road, Edinburgh EH9 3FL, Scotland, United Kingdom.
Gillian A GrayBHF/University Centre for Cardiovascular Science, Queen's Medical Research Institute (QMRI), University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, Scotland, United Kingdom.
University of Edinburgh · GBThe Queen's Medical Research Institute · GBUniversity of Manchester · GB

Funding

Medical Research Council G0701437Medical Research Council MR/K01207X/1Medical Research Council MR/L008076/1Wellcome TrustWellcome Trust WT091720MA
6 · The paper itself

Abstract

Tissue resident macrophages have vital homeostatic roles in many tissues but their roles are less well defined in the heart. The present study aimed to identify the density, polarisation status and distribution of macrophages in the healthy murine heart and to investigate their ability to respond to immune challenge. Histological analysis of hearts from CSF-1 receptor (csf1-GFP; MacGreen) and CX3CR1 (Cx3cr1(GFP/+)) reporter mice revealed a sparse population of GFP positive macrophages that were evenly distributed throughout the left and right ventricular free walls and septum. F4/80+CD11b+ cardiac macrophages, sorted from myocardial homogenates, were able to phagocytose fluorescent beads in vitro and expressed markers typical of both 'M1' (IL-1β, TNF and CCR2) and 'M2' activation (Ym1, Arg 1, RELMα and IL-10), suggesting no specific polarisation in healthy myocardium. Exposure to Th2 challenge by infection of mice with helminth parasites Schistosoma mansoni, or Heligmosomoides polygyrus, resulted in an increase in cardiac macrophage density, adoption of a stellate morphology and increased expression of Ym1, RELMα and CD206 (mannose receptor), indicative of 'M2' polarisation. This was dependent on recruitment of Ly6ChighCCR2+ monocytes and was accompanied by an increase in collagen content. In conclusion, in the healthy heart resident macrophages are relatively sparse and have a phagocytic role. Following Th2 challenge this population expands due to monocyte recruitment and adopts an 'M2' phenotype associated with increased tissue fibrosis.

Indexed as

AnimalsAntigens, Differentiationbeta-N-AcetylhexosaminidasesCD11b AntigenCX3C Chemokine Receptor 1Green Fluorescent ProteinsHeartIntercellular Signaling Peptides and ProteinsLectinsLectins, C-TypeMacrophagesMannose-Binding LectinsMannose ReceptorMiceMice, KnockoutMyocardiumAntigens, Differentiationbeta-N-AcetylhexosaminidasesCD11b AntigenChil3 protein, mouseCX3C Chemokine Receptor 1Cx3cr1 protein, mouseGreen Fluorescent ProteinsIntercellular Signaling Peptides and ProteinsLectinsLectins, C-TypeMannose-Binding LectinsMannose Receptormonocyte-macrophage differentiation antigenReceptor, Macrophage Colony-Stimulating FactorReceptors, Cell SurfaceReceptors, ChemokineRetnla protein, mouseHeartHelminth infectionMacrophage

Identifiers

PMID25700973
PMCPMC4451497
OpenAlexW2159622082

What OpenQuestion holds

Textmetadata
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.