Evidence map›Paper›PMID 42439675›Full record

ReviewCells2026

The Evolving Role of Eosinophils in Eosinophilic Esophagitis: Mechanisms, Crosstalk, and Therapeutic Perspectives.

Federico Caldart, Luisa Bertin, Annalisa Tortora, Alberto Barchi, Niccolò Seregni, Pierfrancesco Visaggi, Nicola De Bortoli, Marco Caminati, Marco Zurlo, Luca Frulloni and 1 more

Abstract readReview
In one paragraph

Review in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

11 authors.

Federico CaldartGastroenterology Unit, Department of Medicine, Verona University Hospital, Piazzale L.A. Scuro 9, 37134 Verona, Italy.ORCID 0000-0002-2798-552X
Luisa BertinDepartment of Surgery, Oncology and Gastroenterology, University of Padua, Via Giustiniani 2, 35128 Padua, Italy.ORCID 0009-0001-9816-4171
Annalisa TortoraGastroenterology Unit, Department of Medicine, Verona University Hospital, Piazzale L.A. Scuro 9, 37134 Verona, Italy.ORCID 0000-0003-0406-4290
Alberto BarchiDivision of Gastroenterology and Gastrointestinal Endoscopy, IRCCS Ospedale San Raffaele, Via Olgettina 58, 20132 Milan, Italy.ORCID 0000-0002-0179-8929
Niccolò SeregniDivision of Gastroenterology and Gastrointestinal Endoscopy, IRCCS Ospedale San Raffaele, Via Olgettina 58, 20132 Milan, Italy.
Pierfrancesco VisaggiGastroenterology Unit, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Lungarno Pacinotti 43, 56126 Pisa, Italy.ORCID 0000-0002-6985-5301
Nicola De BortoliGastroenterology Unit, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Lungarno Pacinotti 43, 56126 Pisa, Italy.ORCID 0000-0003-1995-1060
Marco CaminatiAllergy Unit and Asthma Center, Department of Medicine, Verona Integrated University Hospital, Piazzale L.A. Scuro 9, 37134 Verona, Italy.ORCID 0000-0001-7383-1487
Marco ZurloAllergy Unit and Asthma Center, Department of Medicine, Verona Integrated University Hospital, Piazzale L.A. Scuro 9, 37134 Verona, Italy.ORCID 0000-0003-4064-070X
Luca FrulloniGastroenterology Unit, Department of Medicine, Verona University Hospital, Piazzale L.A. Scuro 9, 37134 Verona, Italy.ORCID 0000-0001-7417-2655
Edoardo Vincenzo SavarinoDepartment of Surgery, Oncology and Gastroenterology, University of Padua, Via Giustiniani 2, 35128 Padua, Italy.ORCID 0000-0002-3187-2894

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionEosinophilic esophagitis (EoE) is a chronic immune-mediated esophageal disease characterized by eosinophilic infiltration, epithelial barrier dysfunction, and progressive tissue remodeling. Increasing evidence identifies eosinophils as central drivers of inflammation and fibrosis, linking EoE to type 2 immune responses and allergic disorders. However, the molecular mechanisms underlying eosinophil-mediated esophageal damage and their interaction with gastroesophageal reflux disease (GERD) remain incompletely understood. MATERIAL AND

methodsA comprehensive narrative review of the current literature was conducted, focusing on studies investigating eosinophil biology, inflammatory signaling pathways, epithelial remodeling, fibrosis, and therapeutic targets in EoE. Clinical, translational, and experimental studies evaluating the association between EoE, GERD, and allergic comorbidities were critically analyzed.

resultsAvailable evidence demonstrates that eosinophils actively contribute to EoE pathogenesis through the release of cytotoxic granule proteins, cytokines, chemokines, and lipid mediators, leading to chronic inflammation and fibrostenotic remodeling. Dysregulation of type 2 cytokines, particularly IL-4, IL-5, and IL-13, plays a pivotal role in disease progression and immune cell recruitment. Significant overlap between EoE and GERD suggests shared inflammatory mechanisms and diagnostic challenges. Furthermore, EoE frequently coexists with systemic allergic diseases, supporting the concept of a broader atopic inflammatory phenotype. Emerging biologic therapies targeting eosinophilic and type 2 inflammatory pathways have shown promising efficacy in reducing symptoms and histologic activity.

conclusionsEosinophils represent key regulators of EoE pathobiology and constitute promising biomarkers and therapeutic targets. A deeper understanding of eosinophil-driven inflammatory networks may improve diagnostic accuracy, patient stratification, and the development of personalized therapeutic strategies for EoE and related esophageal inflammatory disorders.

Indexed as

Eosinophilic EsophagitisEosinophilsAnimalsCytokinesGastroesophageal RefluxHumansInflammationSignal TransductionCytokineseosinophilic esophagitiseosinophilsGERD

Identifiers

PMID42439675
PMCPMC13359447

What OpenQuestion holds

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Registered trials

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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.