Evidence map›Paper›PMID 22761864›Full record

ArticlePloS one2012

IL-4 engagement of the type I IL-4 receptor complex enhances mouse eosinophil migration to eotaxin-1 in vitro.

Nicola M Heller, William M Gwinn, Raymond P Donnelly, Stephanie L Constant, Achsah D Keegan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Association of the interleukin-4Rα rs1801275 and rs1805015 polymorphisms with glioma risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Breaking down the complex pathophysiology of eosinophilic esophagitis.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2023
    Review
  8. Eosinophilic esophagitis: Immune mechanisms and therapeutic targets.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Eosinophil persistence in vivo and sustained viability ex vivo in response to respiratory challenge with fungal allergens.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2018
    Article
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  16. Observational
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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

5 authors at 3 institutions in 1 country.

Nicola M HellerDepartment of Microbiology and Immunology and the Center for Vascular and Inflammatory Diseases, The University of Maryland School of Medicine, Baltimore, Maryland, United States of America.
William M Gwinn
Raymond P Donnelly
Stephanie L Constant
Achsah D Keegan
George Washington University · USUniversity of Maryland, Baltimore · USCenter for Drug Evaluation and Research · US

Funding

Molecular Mechanisms of IL-4 and IL-13 SignalingR01AI038985 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI KEEGAN, ACHSAH D. · 2001 to 2010
$3.7M
MOLECULAR MECHANISM OF IL4 SIGNALINGR29AI038985 · NIAID · AMERICAN NATIONAL RED CROSS · PI KEEGAN, ACHSAH D. · 1996 to 2000
$96k
NIAID NIH HHS AI038985NIAID NIH HHS R01 AI038985NIAID NIH HHS R29 AI038985
6 · The paper itself

Abstract

backgroundPrevious work from our laboratory demonstrated that IL-4Rα expression on a myeloid cell type was responsible for enhancement of Th2-driven eosinophilic inflammation in a mouse model of allergic lung inflammation. Subsequently, we have shown that IL-4 signaling through type I IL-4 receptors on monocytes/macrophages strongly induced activation of the IRS-2 pathway and a subset of genes characteristic of alternatively activated macrophages. The direct effect(s) of IL-4 and IL-13 on mouse eosinophils are not clear. The goal of this study was determine the effect of IL-4 and IL-13 on mouse eosinophil function.

methodsStandard Transwell chemotaxis assay was used to assay migration of mouse eosinophils and signal transduction was assessed by Western blotting.

resultsHere we determined that (i) mouse eosinophils express both type I and type II IL-4 receptors, (ii) in contrast to human eosinophils, mouse eosinophils do not chemotax to IL-4 or IL-13 although (iii) pre-treatment with IL-4 but not IL-13 enhanced migration to eotaxin-1. This IL-4-mediated enhancement was dependent on type I IL-4 receptor expression: γC-deficient eosinophils did not show enhancement of migratory capacity when pre-treated with IL-4. In addition, mouse eosinophils responded to IL-4 with the robust tyrosine phosphorylation of STAT6 and IRS-2, while IL-13-induced responses were considerably weaker.

conclusionsThe presence of IL-4 in combination with eotaxin-1 in the allergic inflammatory milieu could potentiate infiltration of eosinophils into the lungs. Therapies that block IL-4 and chemokine receptors on eosinophils might be more effective clinically in reducing eosinophilic lung inflammation.

Indexed as

AnimalsBase SequenceBlotting, WesternChemokine CCL11DNA PrimersEosinophilsInterleukin-4In Vitro TechniquesMiceReal-Time Polymerase Chain ReactionReceptors, Interleukin-4Signal TransductionChemokine CCL11DNA PrimersInterleukin-4Receptors, Interleukin-4

Identifiers

PMID22761864
PMCPMC3386270
OpenAlexW2012893538

What OpenQuestion holds

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LicenceCC BY
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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.