Evidence map›Paper›PMID 25071763›Full record

ReviewFrontiers in immunology2014

Eosinophils in the lung - modulating apoptosis and efferocytosis in airway inflammation.

Jennifer M Felton, Christopher D Lucas, Adriano G Rossi, Ian Dransfield

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.8field-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

42 citing papers in PubMed, 79 citations in OpenAlex.

  1. 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
  2. Article
  3. Review
  4. Review
  5. Cell Death and Infection: Implications for Host and Microbe.Advances in experimental medicine and biology · 2025
    Review
  6. Article
  7. EndothelialResearch square · 2024
    Article
  8. Review
  9. Article
  10. CXAmerican journal of respiratory and critical care medicine · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Leukocyte Function in COPD: Clinical Relevance and Potential for Drug Therapy.International journal of chronic obstructive pulmonary disease · 2021
    Review
  17. Article
  18. Review
  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

4 authors at 2 institutions in 1 country.

Jennifer M FeltonMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh , Edinburgh , UK.
Christopher D LucasMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh , Edinburgh , UK.
Adriano G RossiMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh , Edinburgh , UK.
Ian DransfieldMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh , Edinburgh , UK.
University of Edinburgh · GBQueen's Medical Centre · GB

Funding

Medical Research Council G0601481Medical Research Council G0901697Medical Research Council MR/K013386/1
6 · The paper itself

Abstract

Due to the key role of the lung in efficient transfer of oxygen in exchange for carbon dioxide, a controlled inflammatory response is essential for restoration of tissue homeostasis following airway exposure to bacterial pathogens or environmental toxins. Unregulated or prolonged inflammatory responses in the lungs can lead to tissue damage, disrupting normal tissue architecture, and consequently compromising efficient gaseous exchange. Failure to resolve inflammation underlies the development and/or progression of a number of inflammatory lung diseases including asthma. Eosinophils, granulocytic cells of the innate immune system, are primarily involved in defense against parasitic infections. However, the propagation of the allergic inflammatory response in chronic asthma is thought to involve excessive recruitment and impaired apoptosis of eosinophils together with defective phagocytic clearance of apoptotic cells (efferocytosis). In terms of therapeutic approaches for the treatment of asthma, the widespread use of glucocorticoids is associated with a number of adverse health consequences after long-term use, while some patients suffer from steroid-resistant disease. A new approach for therapeutic intervention would be to promote the resolution of inflammation via modulation of eosinophil apoptosis and the phagocytic clearance of apoptotic cells. This review focuses on the mechanisms underpinning eosinophil-mediated lung damage, currently available treatments and therapeutic targets that might in future be harnessed to facilitate inflammation resolution by the manipulation of cell survival and clearance pathways.

Indexed as

airwayallergyapoptosiseosinophilinflammationlungphagocytosisresolution

Identifiers

PMID25071763
PMCPMC4076794
OpenAlexW2097903090

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.