Evidence map›Paper›PMID 37652141›Full record

ArticleThe Journal of allergy and clinical immunology2023

IL-13-induced STAT3-dependent signaling networks regulate esophageal epithelial proliferation in eosinophilic esophagitis.

Sahiti Marella, Ankit Sharma, Varsha Ganesan, Daysha Ferrer-Torres, James W Krempski, Gila Idelman, Sydney Clark, Zena Nasiri, Simone Vanoni, Chang Zeng and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
9.5field-weighted citation impact, top 1% 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, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Oesophageal Epithelial Cell-Intrinsic MHCII Regulates Food Antigen-Dependent Eosinophilic Esophagitis in an IFNγ-Dependent Manner.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026
    Article
  4. Immune functions of the esophagus.The Journal of allergy and clinical immunology · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Mouse models of eosinophilic esophagitis: molecular and translational insights.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Review
  15. Article
  16. Article
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  18. Review
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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

18 authors at 4 institutions in 1 country.

Sahiti MarellaDepartment of Pathology, University of Michigan, Ann Arbor, Mich.
Ankit SharmaDepartment of Pathology, University of Michigan, Ann Arbor, Mich; Mary H. Weiser Food Allergy Center, University of Michigan, Ann Arbor, Mich.
Varsha GanesanDepartment of Pathology, University of Michigan, Ann Arbor, Mich; Mary H. Weiser Food Allergy Center, University of Michigan, Ann Arbor, Mich.
Daysha Ferrer-TorresInternal Medicine, University of Michigan, Ann Arbor, Mich.
James W KrempskiDepartment of Pathology, University of Michigan, Ann Arbor, Mich; Mary H. Weiser Food Allergy Center, University of Michigan, Ann Arbor, Mich.
Gila IdelmanDepartment of Pathology, University of Michigan, Ann Arbor, Mich; Mary H. Weiser Food Allergy Center, University of Michigan, Ann Arbor, Mich.
Sydney ClarkDepartment of Pathology, University of Michigan, Ann Arbor, Mich.
Zena NasiriCollege of Literature, Science, and the Arts, University of Michigan, Ann Arbor, Mich.
Simone VanoniDivision of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Chang ZengDivision of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Andrej A DlugoszDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
Haibin ZhouPharmacology and Medicinal Chemistry, University of Michigan, Ann Arbor, Mich.
Shaomeng WangPharmacology and Medicinal Chemistry, University of Michigan, Ann Arbor, Mich.
Alfred D DoyleDivision of Allergy, Asthma and Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Benjamin L WrightDivision of Allergy, Asthma and Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz; Section of Allergy and Immunology, Division of Pulmonology, Phoenix Children's Hospital, Phoenix, Ariz.
Jason R SpenceInternal Medicine, University of Michigan, Ann Arbor, Mich.
Mirna ChehadeMount Sinai Center for Eosinophilic Disorders, Jaffe Food Allergy Institute, Icahn School of Medicine at Mount Sinai, New York, NY.
Simon P HoganDepartment of Pathology, University of Michigan, Ann Arbor, Mich; Mary H. Weiser Food Allergy Center, University of Michigan, Ann Arbor, Mich. Electronic address: sihogan@med.umich.edu.
University of Michigan · USCincinnati Children's Hospital Medical Center · USWinnMed · USIcahn School of Medicine at Mount Sinai · US

Funding

University of Michigan Skin Biology and Diseases Resource-based CenterP30AR075043 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Johann Eli Gudjonsson · 2019 to 2026
$6.6M
SLC9A3 regulation of esophageal dilated intercellular spaces in EoE SubtypesR01AI140133 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOGAN, SIMON PATRICK · 2019 to 2022
$2.5M
Food Allergy and Goblet Cell Antigen PassagesR01AI112626 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOGAN, SIMON PATRICK, NEWBERRY, RODNEY D · 2015 to 2019
$2.4M
Pro-Type 2 Goblet Cell Antigen Passages in Food Sensitization and ReactivityR37AI112626 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SIMON Patrick HOGAN, Rodney D Newberry · 2023 to 2026
$2.2M
Intestinal epithelial immunological responses and food allergen samplingR21AI138177 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOGAN, SIMON PATRICK · 2019 to 2020
$429k
IL-9-producing MC precursor ancestry and function in Food AllergyR56AI175165 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOGAN, SIMON PATRICK · 2023 to 2023
$330k
NIAID NIH HHS R01 AI112626NIAID NIH HHS R01 AI140133NIAID NIH HHS R21 AI138177NIAID NIH HHS R37 AI112626NIAID NIH HHS R56 AI175165NIAMS NIH HHS P30 AR075043
6 · The paper itself

Abstract

backgroundBasal zone hyperplasia (BZH) and dilated intercellular spaces (DISs) are thought to contribute to the clinical manifestations of eosinophilic esophagitis (EoE); however, the molecular pathways that drive BZH remain largely unexplored.

objectiveWe sought to define the role of IL-13-induced transcriptional programs in esophageal epithelial proliferation in EoE.

methodsWe performed RNA sequencing, bioinformatics, Western blot, reverse transcriptase quantitative PCR, and histologic analyses on esophageal biopsies from healthy control and patients with EoE, primary esophageal cells derived from patients with EoE, and IL-13-stimulated esophageal epithelial keratinocytes grown at the air-liquid interface (EPC2-ALI). Genetic (shRNA) and pharmacologic (proteolysis-targeting chimera degrader) approaches and in vivo model of IL-13-induced esophageal epithelial remodeling (Krt5-rtTA x tetO-IL-13Tg) were used to define the role of signal transducer and activator of transcription 3 (STAT3) and STAT6 and secreted frizzled-related protein 1 (SFRP1) in esophageal epithelial proliferation.

resultsRNA-sequencing analysis of esophageal biopsies (healthy control vs EoE) and EPC2-ALI revealed 82 common differentially expressed genes that were enriched for putative STAT3 target genes. In vitro and in vivo analyses revealed a link between IL-13-induced STAT3 and STAT6 phosphorylation, SFRP1 mRNA expression, and esophageal epithelial proliferation. In vitro studies showed that IL-13-induced esophageal epithelial proliferation was STAT3-dependent and regulated by the STAT3 target SFRP1. SFRP1 mRNA is increased in esophageal biopsies from patients with active EoE compared with healthy controls or patients in remission and identifies an esophageal suprabasal epithelial cell subpopulation that uniquely expressed the core EoE proinflammatory transcriptome genes (CCL26, ALOX15, CAPN14, ANO1, and TNFAIP6).

conclusionsThese studies identify SFRP1 as a key regulator of IL-13-induced and STAT3-dependent esophageal proliferation and BZH in EoE and link SFRP1

Indexed as

Eosinophilic EsophagitisCell ProliferationEpithelial CellsHumansInterleukin-13RNA, MessengerSTAT3 Transcription FactorInterleukin-13RNA, MessengerSTAT3 protein, humanSTAT3 Transcription FactorEosinophilic esophagitis, epithelium, proliferation, basal zone hyperplasia, STAT3, SFRP1, bioinformatics

Identifiers

PMID37652141
PMCPMC11102758
OpenAlexW4386248584

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.