Evidence map›Paper›PMID 29980278›Full record

ReviewThe Journal of allergy and clinical immunology2018

Epithelial origin of eosinophilic esophagitis.

Mark Rochman, Nurit P Azouz, Marc E Rothenberg

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 107 citations in OpenAlex.

  1. Gastrointestinal Eosinophil Responses in a Longitudinal, Randomized Trial of Peanut Oral Immunotherapy.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2021
    Trial
  2. Article
  3. Article
  4. Article
  5. Distinct oesophageal microbiota is associated with paediatric eosinophilic oesophagitis.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Immune functions of the esophagus.The Journal of allergy and clinical immunology · 2026
    Review
  11. 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
  12. Article
  13. Article
  14. The oesophagus as an immune organ.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  15. Article
  16. Update on the genetics of allergic diseases.The Journal of allergy and clinical immunology · 2025
    Review
  17. Article
  18. Article
  19. Exploring the Link Between Atopic Dermatitis and Eosinophilic Esophagitis.The Journal of clinical and aesthetic dermatology · 2025
    Review
  20. Review

8 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Mark RochmanDivision of Allergy and Immunology, Department of Pediatrics Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Nurit P AzouzDivision of Allergy and Immunology, Department of Pediatrics Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Marc E RothenbergDivision of Allergy and Immunology, Department of Pediatrics Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio. Electronic address: rothenberg@cchmc.org.
University of Cincinnati · USCincinnati Children's Hospital Medical Center · US

Funding

TSLP, IL-9-producing mucosal mast cells, and allergic inflammationU19AI070235 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI Marc E. Rothenberg · 2006 to 2026
$31.3M
TRAINING (CAREER DEVELOPMENT) COMPONENTU54AI117804 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI GLENN T FURUTA, Marc E. Rothenberg · 2014 to 2026
$18.5M
Genetic and Immunological Dissection of Eosinophilic EsophagitisR01AI124355 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI Marc E. Rothenberg · 2015 to 2026
$5.9M
Regulation of Gastrointestinal EosinophilsR37AI045898 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 2010 to 2019
$3.6M
NIAID NIH HHS R01 AI124355NIAID NIH HHS R37 AI045898NIAID NIH HHS U19 AI070235NIAID NIH HHS U54 AI117804
6 · The paper itself

Abstract

Eosinophilic esophagitis (EoE) is a chronic, allergen-driven inflammatory disease of the esophagus characterized predominantly by eosinophilic inflammation, leading to esophageal dysfunction. Converging data have placed the esophageal epithelium at the center of disease pathogenesis. In particular, the main EoE disease susceptibility loci at 2p23 and 5p22 encode for gene products that are produced by the esophageal epithelium: the intracellular protease calpain 14 and thymic stromal lymphopoietin, respectively. Furthermore, genetic and functional data establish a primary role for impaired epithelial barrier function in disease susceptibility and pathoetiology. Additionally, the EoE transcriptome, a set of genes dysregulated in the esophagi of patients with EoE, is enriched in genes that encode for proteins involved in esophageal epithelial cell differentiation. This transcriptome has a high proportion of esophagus-specific epithelial genes that are notable for the unexpected enrichment in genes encoding for proteases and protease inhibitors, as well as in IL-1 family genes, demonstrating a previously unappreciated role for innate immunity responses in the esophagus under homeostatic conditions. Among these pathways, basal production of the serine protease inhibitor, Kazal-type 7 (SPINK7) has been demonstrated to be part of the normal differentiation program of esophageal epithelium. Profound lost expression of SPINK7 occurs in patients with EoE and is sufficient for unleashing increased proteolytic activity (including urokinase plasminogen activator), impaired barrier function, and production of large quantities of proinflammatory and proallergic cytokines, including thymic stromal lymphopoietin. Collectively, we put forth a model in which the esophagus is normally equipped as an anti-inflammatory sensing organ and that defects in this pathway, mediated by epithelial protease/protease inhibitor imbalances, unleash inflammatory responses resulting in disorders, such as EoE.

Indexed as

Eosinophilic EsophagitisEpithelial CellsEpitheliumHumansPeptide HydrolasesProtease InhibitorsPeptide HydrolasesProtease InhibitorsEosinophilic esophagitiseosinophilic oesophagitisepithelial barrierepithelial differentiationesophageal epitheliumKazal typeprotease inhibitorsproteasesserine protease inhibitors

Identifiers

PMID29980278
PMCPMC8034427
OpenAlexW2811386814

What OpenQuestion holds

Textmetadata
LicenceTDM
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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.