Evidence map›Paper›PMID 27922744›Full record

ArticleAmerican journal of respiratory and critical care medicine2017

Lung Pathologies in a Chronic Inflammation Mouse Model Are Independent of Eosinophil Degranulation.

Elizabeth A Jacobsen, Sergei I Ochkur, Alfred D Doyle, William E LeSuer, Wen Li, Cheryl A Protheroe, Dana Colbert, Katie R Zellner, HuaHao H Shen, Charles G Irvin and 2 more

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Eosinophils and eosinophil-associated diseases: An update.The Journal of allergy and clinical immunology · 2018
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Eosinophil extracellular traps in respiratory ailment: Pathogenic mechanisms and clinical translation.World journal of otorhinolaryngology - head and neck surgery · 2024
    Review
  6. Article
  7. Article
  8. The Enigma of Eosinophil Degranulation.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Assessment of Lung Eosinophils In Situ Using Immunohistological Staining.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  14. Review
  15. Deciphering the role of eosinophils in solid organ transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Eosinophil-derived IL-13 promotes emphysema.The European respiratory journal · 2019
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Elizabeth A Jacobsen1 Division of Pulmonary Medicine and.
Sergei I Ochkur1 Division of Pulmonary Medicine and.
Alfred D Doyle1 Division of Pulmonary Medicine and.
William E LeSuer1 Division of Pulmonary Medicine and.
Wen Li2 Department of Medicine, Guizhou Provincial People's Hospital, Guizhou, China; and.
Cheryl A Protheroe3 Division of Hematology/Oncology, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, Scottsdale, Arizona.
Dana Colbert3 Division of Hematology/Oncology, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, Scottsdale, Arizona.
Katie R Zellner1 Division of Pulmonary Medicine and.
HuaHao H Shen2 Department of Medicine, Guizhou Provincial People's Hospital, Guizhou, China; and.
Charles G Irvin4 Vermont Lung Center, Department of Medicine, University of Vermont, Burlington, Vermont.
James J Lee1 Division of Pulmonary Medicine and.
Nancy A Lee3 Division of Hematology/Oncology, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, Scottsdale, Arizona.
Pulmonary Associates · USMayo Clinic in Arizona · USGuizhou Provincial People's Hospital · CNUniversity of Vermont · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleThe release of eosinophil granule proteins in the lungs of patients with asthma has been dogmatically linked with lung remodeling and airway hyperresponsiveness. However, the demonstrated inability of established mouse models to display the eosinophil degranulation occurring in human subjects has prevented a definitive in vivo test of this hypothesis.

objectivesTo demonstrate in vivo causative links between induced pulmonary histopathologies/lung dysfunction and eosinophil degranulation.

methodsA transgenic mouse model of chronic T-helper cell type 2-driven inflammation overexpressing IL-5 from T cells and human eotaxin 2 in the lung (I5/hE2) was used to test the hypothesis that chronic histopathologies and the development of airway hyperresponsiveness occur as a consequence of extensive eosinophil degranulation in the lung parenchyma. MEASUREMENT AND MAIN

resultsStudies targeting specific inflammatory pathways in I5/hE2 mice surprisingly showed that eosinophil-dependent immunoregulative events and not the release of individual secondary granule proteins are the central contributors to T-helper cell type 2-induced pulmonary remodeling and lung dysfunction. Specifically, our studies highlighted a significant role for eosinophil-dependent IL-13 expression. In contrast, extensive degranulation leading to the release of major basic protein-1 or eosinophil peroxidase was not causatively linked to many of the induced pulmonary histopathologies. However, these studies did define a previously unappreciated link between the release of eosinophil peroxidase (but not major basic protein-1) and observed levels of induced airway mucin.

conclusionsThese data suggest that improvements observed in patients with asthma responding to therapeutic strategies ablating eosinophils may occur as a consequence of targeting immunoregulatory mechanisms and not by simply eliminating the destructive activities of these purportedly end-stage effector cells.

Indexed as

AnimalsChemokine CCL24Chronic DiseaseDisease Models, AnimalEosinophilsFlow CytometryInflammationInterleukin-5LungMiceMice, Inbred C57BLMice, TransgenicTh2 CellsChemokine CCL24Interleukin-5asthmachronic inflammationeosinophil peroxidaselungmajor basic protein

Identifiers

PMID27922744
PMCPMC5443899
OpenAlexW2572023575

What OpenQuestion holds

Textmetadata
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.