Evidence map›Paper›PMID 41091526›Full record

ArticleInternational forum of allergy & rhinology2026

Cadherin-26 Facilitates Transepithelial Migration of Eosinophils in Eosinophilic Chronic Rhinosinusitis.

Yeong-In Jo, Jee Won Moon, Joo-Hoo Park, Hwa Eun Yang, Subin Cho, Hyeongguk Son, Hyun-Woo Yang, Il-Ho Park

Abstract read
In one paragraph

Article in International forum of allergy & rhinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

2 citing papers in PubMed.

  1. Article
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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

8 authors.

Yeong-In JoUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.ORCID https://orcid.org/0009-0001-5344-5703
Jee Won MoonUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.ORCID https://orcid.org/0000-0003-2307-1824
Joo-Hoo ParkUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.ORCID https://orcid.org/0000-0002-3221-640X
Hwa Eun YangUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.ORCID https://orcid.org/0009-0006-4493-0690
Subin ChoUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.ORCID https://orcid.org/0009-0006-8994-1035
Hyeongguk SonUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.ORCID https://orcid.org/0000-0002-9352-9039
Hyun-Woo YangUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.ORCID https://orcid.org/0000-0002-8674-3088
Il-Ho ParkUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.ORCID https://orcid.org/0000-0002-7011-6071

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEosinophilic chronic rhinosinusitis with nasal polyps (eCRSwNP) is characterized by persistent sinonasal inflammation and marked eosinophilic infiltration. Although the relationship between eosinophils and NP formation has been extensively studied, the mechanisms governing eosinophil transepithelial migration into the nasal mucosa remain poorly understood. Cadherin-26 (CDH26), an epithelial adhesion molecule that binds to integrins α4 (ITGA4) and αE, has been implicated in eosinophilic inflammation and may play a critical role in eosinophil recruitment and tissue infiltration.

objectiveThis study aimed to investigate the role and underlying mechanism of CDH26 in facilitating eosinophil transepithelial migration in patients with eCRSwNP.

methodsSingle-cell ribonucleic acid (RNA) sequencing and immunohistochemistry (IHC) were performed on nasal tissues from patients with eCRSwNP, non-eCRSwNP, chronic rhinosinusitis without nasal polyps (CRSsNP), and healthy controls to evaluate CDH26 expression. Human primary nasal epithelial cells (hPNECs) were stimulated in vitro with interleukin-4 (IL-4) or IL-13, and CDH26 expression was assessed via reverse transcription polymerase chain reaction (RT-PCR), western blotting, and IHC. The effect of IL-4 receptor blockade using Dupilumab was evaluated in monolayer cultures. ITGA4 expression in EoL-1 eosinophil-like cells was measured by flow cytometry, and their interaction with recombinant CDH26 was evaluated using cell adhesion and Transwell migration assays.

resultsCDH26 expression was significantly upregulated in eCRSwNP tissues compared to that in other groups. IL-4 and IL-13 stimulation induced CDH26 expression in hPNECs, which was dose-dependently inhibited by Dupilumab. EoL-1 cells expressed ITGA4 and adhered to recombinant CDH26 in vitro. Th2 cytokine stimulation enhanced EoL-1 cell transepithelial migration, which was significantly reduced by CDH26 knockdown or Dupilumab treatment.

conclusionTh2 cytokine-induced upregulation of epithelial CDH26 facilitates eosinophil transepithelial migration, potentially via ITGA4 interaction. Thus, CDH26 may represent a novel therapeutic target for managing eCRSwNP.

Indexed as

CadherinsEosinophiliaEosinophilsNasal PolypsRhinitisSinusitisTransendothelial and Transepithelial MigrationAdultCell MovementCells, CulturedChronic DiseaseEpithelial CellsFemaleHumansInterleukin-4MaleCadherinsInterleukin-4cadherins | cell adhesion molecules | eosinophils | nasal polyps | rhinosinusitis | transepithelial migration

Identifiers

PMID41091526
PMCPMC12863020

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.