Evidence map›Paper›PMID 25389033›Full record

ArticleMucosal immunology2015

Neurotrophic tyrosine kinase receptor 1 is a direct transcriptional and epigenetic target of IL-13 involved in allergic inflammation.

M Rochman, A V Kartashov, J M Caldwell, M H Collins, E M Stucke, K Kc, J D Sherrill, J Herren, A Barski, M E Rothenberg

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.8field-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

35 citing papers in PubMed, 52 citations in OpenAlex.

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  18. Nasal DNA methylation profiling of asthma and rhinitis.The Journal of allergy and clinical immunology · 2020
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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

10 authors at 2 institutions in 1 country.

M RochmanDivisions of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
A V KartashovDivisions of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
J M CaldwellDivisions of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
M H CollinsDivisions of Pathology and Laboratory Medicine, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
E M StuckeDivisions of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
K KcDivisions of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
J D SherrillDivisions of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
J HerrenDivisions of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
A BarskiDivisions of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
M E RothenbergDivisions of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Theresa Alenghat · 2007 to 2026
$24.4M
Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E. · 2012 to 2014
$9.9M
REGULATION OF GASTROINTESTINAL EOSINOPHILSR01AI045898 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 1999 to 2024
$4.5M
Regulation of Gastrointestinal EosinophilsR37AI045898 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 2010 to 2019
$3.6M
Short Term Medical Student Training GrantT35DK060444 · NIDDK · UNIVERSITY OF CINCINNATI · PI JASON T BLACKARD · 2002 to 2026
$2.3M
IL-13 Associated Eosinophil Lung ResponsesR01AI083450 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 2009 to 2013
$1.9M
Role of Chromatin and Gene Poising in T Cell Differentiation and ActivationK22HL098691 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI BARSKI, ARTEM · 2011 to 2013
$807k
NCATS NIH HHS UL1 TR000077NIAID NIH HHS R01 AI045898NIAID NIH HHS R01 AI083450NIAID NIH HHS R01AI083450NIAID NIH HHS R37 AI045898NIAID NIH HHS R37AI045898NIDDK NIH HHS P30 DK078392NIDDK NIH HHS T35 DK060444
6 · The paper itself

Abstract

Although interleukin (IL)-13 and neurotrophins are functionally important for the pathogenesis of immune responses, the interaction of these pathways has not been explored. Herein, by interrogating IL-13-induced responses in human epithelial cells we show that neurotrophic tyrosine kinase receptor, type 1 (NTRK1), a cognate, high-affinity receptor for nerve growth factor (NGF), is an early transcriptional IL-13 target. Induction of NTRK1 was accompanied by accumulation of activating epigenetic marks in the promoter; transcriptional and epigenetic changes were signal transducer and activator of transcription 6 dependent. Using eosinophilic esophagitis as a model for human allergic inflammation, we found that NTRK1 was increased in inflamed tissue and dynamically expressed as a function of disease activity and that the downstream mediator of NTRK1 signaling early growth response 1 protein was elevated in allergic inflammatory tissue compared with control tissue. Unlike NTRK1, its ligand NGF was constitutively expressed in control and disease states, indicating that IL-13-stimulated NTRK1 induction is a limiting factor in pathway activation. In epithelial cells, NGF and IL-13 synergistically induced several target genes, including chemokine (C-C motif) ligand 26 (eotaxin-3). In summary, we have demonstrated that IL-13 confers epithelial cell responsiveness to NGF by regulating NTRK1 levels by a transcriptional and epigenetic mechanism and that this process likely contributes to allergic inflammation.

Indexed as

Epigenesis, GeneticGene Expression RegulationTranscription, GeneticCluster AnalysisEarly Growth Response Protein 1Eosinophilic EsophagitisEpithelial CellsGene Expression ProfilingGene SilencingHumansHypersensitivityInterleukin-13Nerve Growth FactorReceptor, trkASTAT6 Transcription FactorEarly Growth Response Protein 1Interleukin-13Nerve Growth FactorReceptor, trkASTAT6 Transcription Factor

Identifiers

PMID25389033
PMCPMC4429043
OpenAlexW2000885209

What OpenQuestion holds

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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.