Evidence map›Paper›PMID 29428392›Full record

ArticleThe Journal of allergy and clinical immunology2018

Mer-mediated eosinophil efferocytosis regulates resolution of allergic airway inflammation.

Jennifer M Felton, Christopher D Lucas, David A Dorward, Rodger Duffin, Tiina Kipari, Sonja Vermeren, Calum T Robb, Kenneth G MacLeod, Bryan Serrels, Jürgen Schwarze and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Myeloid PKM2 deficiency alleviates allergic airway inflammation and promotes macrophage efferocytosis via SLC13A3.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Efferocytosis in Homeostasis.Advances in experimental medicine and biology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Efferocytosis and Respiratory Disease.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Article
  18. Pulmonary macrophages and SARS-Cov2 infection.International review of cell and molecular biology · 2022
    Article
  19. Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022
    Review
  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

13 authors at 2 institutions in 1 country.

Jennifer M FeltonMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Christopher D LucasMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom. Electronic address: christopher.lucas@ed.ac.uk.
David A DorwardMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Rodger DuffinMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Tiina KipariMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Sonja VermerenMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Calum T RobbMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Kenneth G MacLeodMRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital Campus, Edinburgh, United Kingdom.
Bryan SerrelsMRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital Campus, Edinburgh, United Kingdom.
Jürgen SchwarzeMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Christopher HaslettMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Ian DransfieldMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Adriano G RossiMRC Centre for Inflammation Research, the Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Queen's Medical Centre · GBWestern General Hospital · GB

Funding

Medical Research Council G0601481Medical Research Council G0901697Medical Research Council MR/K013386/1Wellcome TrustWellcome Trust 206566/Z/17/ZWellcome Trust WT096497
6 · The paper itself

Abstract

backgroundEosinophils play a central role in propagation of allergic diseases, including asthma. Both recruitment and retention of eosinophils regulate pulmonary eosinophilia, but the question of whether alterations in apoptotic cell clearance by phagocytes contributes directly to resolution of allergic airway inflammation remains unexplored.

objectivesIn this study we investigated the role of the receptor tyrosine kinase Mer in mediating apoptotic eosinophil clearance and allergic airway inflammation resolution in vivo to establish whether apoptotic cell clearance directly affects the resolution of allergic airway inflammation.

methodsAlveolar and bone marrow macrophages were used to study Mer-mediated phagocytosis of apoptotic eosinophils. Allergic airway inflammation resolution was modeled in mice by using ovalbumin. Fluorescently labeled apoptotic cells were administered intratracheally or eosinophil apoptosis was driven by administration of dexamethasone to determine apoptotic cell clearance in vivo.

resultsInhibition or absence of Mer impaired phagocytosis of apoptotic human and mouse eosinophils by macrophages. Mer-deficient mice showed delayed resolution of ovalbumin-induced allergic airway inflammation, together with increased airway responsiveness to aerosolized methacholine, increased bronchoalveolar lavage fluid protein levels, altered cytokine production, and an excess of uncleared dying eosinophils after dexamethasone treatment. Alveolar macrophage phagocytosis was significantly Mer dependent, with the absence of Mer attenuating apoptotic cell clearance in vivo to enhance inflammation in response to apoptotic cells.

conclusionsWe demonstrate that Mer-mediated apoptotic cell clearance by phagocytes contributes to resolution of allergic airway inflammation, suggesting that augmenting apoptotic cell clearance is a potential therapeutic strategy for treating allergic airway inflammation.

Indexed as

AllergensAnimalsApoptosisBronchoalveolar Lavage Fluidc-Mer Tyrosine KinaseCytokinesEosinophilsFemaleHumansInflammationMacrophagesMice, Inbred C57BLMice, KnockoutOvalbuminPhagocytosisRespiratory HypersensitivityAllergensc-Mer Tyrosine KinaseCytokinesMertk protein, mouseOvalbuminairway resistanceallergic airway inflammationapoptosisEosinophilinflammation resolutionMerphagocytosis

Identifiers

PMID29428392
PMCPMC6281028
OpenAlexW2786441904

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.