Evidence map›Paper›PMID 20214667›Full record

ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2010

Transforming growth factor-β stimulates the expression of eotaxin/CC chemokine ligand 11 and its promoter activity through binding site for nuclear factor-κβ in airway smooth muscle cells.

S Matsukura, M Odaka, M Kurokawa, H Kuga, T Homma, H Takeuchi, K Notomi, F Kokubu, M Kawaguchi, R P Schleimer and 2 more

Abstract read
In one paragraph

Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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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

12 authors at 5 institutions in 3 countries.

S MatsukuraFirst Department of Internal Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan. smatsuku@med.showa-u.ac.jp
M Odaka
M Kurokawa
H Kuga
T Homma
H Takeuchi
K Notomi
F Kokubu
M Kawaguchi
R P Schleimer
M W Johnson
M Adachi
Showa University · JPGlaxoSmithKline (United Kingdom) · GBNorthwestern University · USShowa University Fujigaoka Hospital · JPUniversity of Tsukuba · JP

Funding

Glucocorticosteroid Action In Inflammatory DiseaseR37HL068546 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2009 to 2018
$3.5M
Role of Epithelium in Immunity, Inflammation and DiseaseR01HL078860 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2006 to 2013
$3.0M
GLUCOCORTICOSTEROID ACTION IN INFLAMMATORY DISEASER01HL068546 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2001 to 2008
$2.9M
Epithelial BAFF and APRIL in Airway Inflammation, Immunity and DiseaseR01AI072570 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2007 to 2011
$2.3M
NHLBI NIH HHS R01 HL068546NHLBI NIH HHS R01 HL078860NHLBI NIH HHS R37 HL068546NIAID NIH HHS R01 AI072570
6 · The paper itself

Abstract

backgroundChemokines ligands of CCR3 including eotaxin/CC chemokine ligand 11 (CCL11) may contribute to the pathogenesis of asthma. These chemokines and a growth factor (TGF-beta) may be involved in the process of airway remodelling.

objectiveWe analysed the effects of TGF-beta on the expression of CCR3 ligands in human airway smooth muscle (HASM) cells and investigated the mechanisms.

methodsHASM cells were cultured and treated with TGF-beta and Th2 cytokines IL-4 or IL-13. Expression of mRNA was analysed by real-time PCR. Secretion of CCL11 into the culture medium was analysed by ELISA. Transcriptional regulation of CCL11 was analysed by luciferase assay using CCL11 promoter-luciferase reporter plasmids.

resultsIL-4 or IL-13 significantly up-regulated the expression of mRNAs for CCL11 and CCL26. TGF-beta alone did not increase the expression of chemokine mRNAs, but enhanced the induction of only CCL11 by IL-4 or IL-13 among CCR3 ligands. Activity of the CCL11 promoter was stimulated by IL-4, and this activity was enhanced by TGF-beta. Activation by IL-4 or IL-4 plus TGF-beta was lost by mutation of the binding site for signal transducers and activators of transcription-6 (STAT6) in the promoter. Cooperative activation by IL-4 and TGF-beta was inhibited by mutation of the binding site for nuclear factor-kappaB (NF-kappaB) in the promoter. Pretreatment with an inhibitor of NF-kappaB and glucocorticoid fluticasone propionate significantly inhibited the expression of CCL11 mRNA induced by IL-4 plus TGF-beta, indicating the importance of NF-kappaB in the cooperative activation of CCL11 transcription by TGF-beta and IL-4.

conclusionThese results indicate that Th2 cytokines and TGF-beta may contribute to the pathogenesis of asthma by stimulating expression of CCL11. The transcription factors STAT6 and NF-kappaB may play pivotal roles in this process.

Indexed as

AsthmaBinding SitesCell LineChemokine CCL11Gene Expression RegulationHumansInterleukin-13Interleukin-4Muscle, SmoothNF-kappa BPromoter Regions, GeneticProtein BindingRecombinant ProteinsTh2 CellsTranscription, GeneticTransforming Growth Factor betaChemokine CCL11Interleukin-13Interleukin-4NF-kappa BRecombinant ProteinsTransforming Growth Factor beta

Identifiers

PMID20214667
PMCPMC3712283
OpenAlexW2112094575

What OpenQuestion holds

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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.