Evidence map›Paper›PMID 21106848›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Chemoattractant-induced signaling via the Ras-ERK and PI3K-Akt networks, along with leukotriene C4 release, is dependent on the tyrosine kinase Lyn in IL-5- and IL-3-primed human blood eosinophils.

Yiming Zhu, Paul J Bertics

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  14. IL-5 induces suspended eosinophils to undergo unique global reorganization associated with priming.American journal of respiratory cell and molecular biology · 2014
    Article
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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

2 authors at 1 institution in 1 country.

Yiming ZhuMolecular and Cellular Pharmacology Program, University of Wisconsin, Madison, WI 53706, USA.
Paul J Bertics
University of Wisconsin–Madison · US

Funding

Thr Role of Pin1 in AirwayP01HL088594 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI JARJOUR, NIZAR N · 2008 to 2017
$21.0M
SCOR--CELLULAR AND MOLECULAR MECHANISMS OF ASTHMAP50HL056396 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MALTER, JAMES S · 1997 to 2006
$13.8M
Severe Asthma From Respiratory InfectionsR01HL069116 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI BUSSE, WILLIAM W. · 2001 to 2010
$7.6M
RV-Mediated Mechanisms of Neutrophil Motility /InflammatU19AI070503 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI GERN, JAMES E. · 2006 to 2010
$6.8M
NHLBI NIH HHS HL069116NHLBI NIH HHS HL0885940NHLBI NIH HHS HL56396NHLBI NIH HHS P01 HL088594NHLBI NIH HHS P50 HL056396NHLBI NIH HHS R01 HL069116NIAID NIH HHS AI070503NIAID NIH HHS U19 AI070503
6 · The paper itself

Abstract

Human blood eosinophils exhibit a hyperactive phenotype in response to chemotactic factors after cell "priming" with IL-5 family cytokines. Earlier work has identified ERK1/2 as molecular markers for IL-5 priming, and in this article, we show that IL-3, a member of the IL-5 family, also augments fMLP-stimulated ERK1/2 phosphorylation in primary eosinophils. Besides ERK1/2, we also observed an enhancement of chemotactic factor-induced Akt phosphorylation after IL-5 priming of human blood eosinophils. Administration of a peptide antagonist that targets the Src family member Lyn before cytokine (IL-5/IL-3) priming of blood eosinophils inhibited the synergistic increase of fMLP-induced activation of Ras, ERK1/2 and Akt, as well as the release of the proinflammatory factor leukotriene C(4). In this study, we also examined a human eosinophil-like cell line HL-60 clone-15 and observed that these cells exhibited significant surface expression of IL-3Rs and GM-CSFRs, as well as ERK1/2 phosphorylation in response to the addition of IL-5 family cytokines or the chemotactic factors fMLP, CCL5, and CCL11. Consistent with the surface profile of IL-5 family receptors, HL-60 clone-15 recapitulated the enhanced fMLP-induced ERK1/2 phosphorylation observed in primary blood eosinophils after priming with IL-3/GM-CSF, and small interfering RNA-mediated knockdown of Lyn expression completely abolished the synergistic effects of IL-3 priming on fMLP-induced ERK1/2 phosphorylation. Altogether, our data demonstrate a central role for Lyn in the mechanisms of IL-5 family priming and suggest that Lyn contributes to the upregulation of the Ras-ERK1/2 and PI3K-Akt cascades, as well as the increased leukotriene C(4) release observed in response to fMLP in "primed" eosinophils.

Indexed as

AdolescentAdultAmino Acid SequenceAsthmaEosinophilsHL-60 CellsHumansInterleukin-3Interleukin-5Leukotriene C4Middle AgedMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Molecular Sequence DataN-Formylmethionine Leucyl-PhenylalaninePhosphatidylinositol 3-KinasesIL3 protein, humanIL5 protein, humanInterleukin-3Interleukin-5Leukotriene C4lyn protein-tyrosine kinaseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3N-Formylmethionine Leucyl-PhenylalaninePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktras Proteinssrc-Family Kinases

Identifiers

PMID21106848
PMCPMC3156584
OpenAlexW2123613151

What OpenQuestion holds

Textmetadata
LicenceTDM
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.