Evidence map›Paper›PMID 26009788›Full record

ArticleAllergy2015

Differential activation of airway eosinophils induces IL-13-mediated allergic Th2 pulmonary responses in mice.

E A Jacobsen, A D Doyle, D C Colbert, K R Zellner, C A Protheroe, W E LeSuer, N A Lee, J J Lee

Open access · greenAbstract read
In one paragraph

Article in Allergy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

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  10. Purified Native and Recombinant MajorJournal of fungi (Basel, Switzerland) · 2021
    Article
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  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. Review
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  20. Eosinophil-derived IL-13 promotes emphysema.The European respiratory journal · 2019
    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

8 authors at 1 institution in 1 country.

E A JacobsenDivision of Pulmonary Medicine, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ, 85259, USA.
A D DoyleDivision of Pulmonary Medicine, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ, 85259, USA.
D C ColbertDivision of Hematology/Oncology, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ, 85259, USA.
K R ZellnerDivision of Pulmonary Medicine, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ, 85259, USA.
C A ProtheroeDivision of Pulmonary Medicine, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ, 85259, USA.
W E LeSuerDivision of Pulmonary Medicine, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ, 85259, USA.
N A LeeDivision of Hematology/Oncology, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ, 85259, USA.
J J LeeDivision of Pulmonary Medicine, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ, 85259, USA.
Mayo Clinic in Arizona · US

Funding

EOSINOPHIL ACTIVITIES IN MURINE MODELS OF LUNG DISEASER01HL065228 · NHLBI · MAYO CLINIC COLL OF MED, MAYO CLINIC AZ · PI JACOBSEN, ELIZABETH A · 2000 to 2017
$6.7M
MOUSE MODELS OF EOSINOPHIL ASSOCIATED LUNG DYSFUNCTIONR01HL058723 · NHLBI · MAYO CLINIC COLL OF MED, MAYO CLINIC AZ · PI LEE, NANCY A. · 1998 to 2013
$4.2M
Airway Sensory Nerves in AsthmaR01HL124165 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI JACOBSEN, ELIZABETH A, JACOBY, DAVID B · 2014 to 2017
$3.1M
Mouse Models of Eosinophil-Associated Lung DysfunctionR56HL058723 · NHLBI · MAYO CLINIC ARIZONA · PI LEE, NANCY A. · 2008 to 2008
$400k
Eosinophil-derived Tgf-beta1 in lung fibrosis and immunomodulation in asthmaF31HL124959 · NHLBI · MAYO CLINIC ARIZONA · PI DOYLE, ALFRED · 2014 to 2015
$82k
NHLBI NIH HHS F31 HL124959NHLBI NIH HHS HL 058723NHLBI NIH HHS HL 065228NHLBI NIH HHS HL 124165NHLBI NIH HHS R01 HL058723NHLBI NIH HHS R01 HL065228NHLBI NIH HHS R01 HL124165NHLBI NIH HHS R56 HL058723
6 · The paper itself

Abstract

backgroundEosinophils are hallmark cells of allergic Th2 respiratory inflammation. However, the relative importance of eosinophil activation and the induction of effector functions such as the expression of IL-13 to allergic Th2 pulmonary disease remain to be defined.

methodsWild-type or cytokine-deficient (IL-13(-/-) or IL-4(-/-) ) eosinophils treated with cytokines (GM-CSF, IL-4, IL-33) were adoptively transferred into eosinophil-deficient recipient mice subjected to allergen provocation using established models of respiratory inflammation. Allergen-induced pulmonary changes were assessed.

resultsIn contrast to the transfer of untreated blood eosinophils to the lungs of recipient eosinophil deficient mice, which induced no immune/inflammatory changes either in the lung or in the lung draining lymph nodes (LDLN), pretreatment of blood eosinophils with GM-CSF prior to transfer elicited trafficking of these eosinophils to LDLN. In turn, these LDLN eosinophils elicited the accumulation of dendritic cells and CD4(+) T cells to these same LDLNs without inducing pulmonary inflammation. However, exposure of eosinophils to GM-CSF, IL-4, and IL-33 prior to transfer induced not only immune events in the LDLN, but also allergen-mediated increases in airway Th2 cytokine/chemokine levels, the subsequent accumulation of CD4(+) T cells as well as alternatively activated (M2) macrophages, and the induction of pulmonary histopathologies. Significantly, this allergic respiratory inflammation was dependent on eosinophil-derived IL-13, whereas IL-4 expression by eosinophils had no significant role.

conclusionThe data demonstrate the differential activation of eosinophils as a function of cytokine exposure and suggest that eosinophil-specific IL-13 expression by activated cells is a necessary component of the subsequent allergic Th2 pulmonary pathologies.

Indexed as

AllergensAnimalsCells, CulturedCytokinesDisease Models, AnimalEosinophilsFemaleHypersensitivityInterleukin-13LungMacrophagesMaleMiceMice, TransgenicOvalbuminPhenotypeAllergensCytokinesInterleukin-13OvalbuminAsthmaEosinophil deficientIL-13IL-33T cells

Identifiers

PMID26009788
PMCPMC4552595
OpenAlexW1597914355

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Registered trials

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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.