Evidence map›Paper›PMID 34975898›Full record

ArticleFrontiers in immunology2021

The Expression of ephrinA1/ephA2 Receptor Increases in Chronic Rhinosinusitis and ephrinA1/ephA2 Signaling Affects Rhinovirus-Induced Innate Immunity in Human Sinonasal Epithelial Cells.

Sang Hag Lee, Sung Hoon Kang, Mun Soo Han, Ji Won Kwak, Hyeon Geun Kim, Tae Hoon Lee, Da Bin Lee, Tae Hoon Kim

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Unveiling the prevalence and impact of silent rhinovirus infection in chronic rhinosinusitis with nasal polyps.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Sang Hag LeeDepartment of Otorhinolaryngology-Head & Neck Surgery, College of Medicine, Korea University, Seoul, South Korea.
Sung Hoon KangDepartment of Otorhinolaryngology-Head & Neck Surgery, College of Medicine, Korea University, Seoul, South Korea.
Mun Soo HanDepartment of Otorhinolaryngology-Head & Neck Surgery, College of Medicine, Korea University, Seoul, South Korea.
Ji Won KwakDepartment of Otorhinolaryngology-Head & Neck Surgery, College of Medicine, Korea University, Seoul, South Korea.
Hyeon Geun KimDepartment of Otorhinolaryngology-Head & Neck Surgery, College of Medicine, Korea University, Seoul, South Korea.
Tae Hoon LeeDepartment of Otorhinolaryngology-Head & Neck Surgery, College of Medicine, Korea University, Seoul, South Korea.
Da Bin LeeDepartment of Otorhinolaryngology-Head & Neck Surgery, College of Medicine, Korea University, Seoul, South Korea.
Tae Hoon KimDepartment of Otorhinolaryngology-Head & Neck Surgery, College of Medicine, Korea University, Seoul, South Korea.
Korea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EphA2 receptor and its ephrin ligands are involved in virus infection, epithelial permeability, and chemokine secretion. We hypothesized that ephrinA1/ephA2 signaling participates in rhinovirus (RV)-induced antiviral immune response in sinonasal mucosa of patients with chronic rhinosinusitis (CRS). Therefore, we investigated the expression of ephrinA1/ephA2 in normal and inflamed sinonasal mucosa and evaluated whether they regulate chemokine secretion and the production of antiviral immune mediators including interferons (IFNs) in RV-infected human primary sinonasal epithelial cells. For this purpose, the expression and distribution of ephrinA1/ephA2 in sinonasal mucosa were evaluated with RT-qPCR, immunofluorescence, and western blot. Their roles in chemokine secretion and the production of antiviral immune mediators such as type I and III IFNs, and interferon stimulated genes were evaluated by stimulating ephA2 with ephrinA1 and inactivating ephA2 with ephA2 siRNA or inhibitor in cells exposed to RV and poly(I:C). We found that ephrinA1/ephA2 were expressed in normal mucosa and their levels increased in inflamed sinonasal mucosa of CRS patients. RV infection or poly(I:C) treatment induced chemokine secretion which were attenuated by blocking the action of ephA2 with ephA2 siRNA or inhibitor. The production of antiviral immune mediators enhanced by rhinovirus or poly (I:C) is increased by blocking ephA2 compared with that of cells stimulated by either rhinovirus or poly(I:C) alone. In addition, blocking ephA2 attenuated RV replication in cultured cells. Taken together, these results describe a novel role of ephrinA1/ephA2 signaling in antiviral innate immune response in sinonasal epithelium, suggesting their participation in RV-induced development and exacerbations of CRS.

Indexed as

Case-Control StudiesCells, CulturedChronic DiseaseCommon ColdCytokinesEphrin-A1Ephrin-A2Epithelial CellsHost-Pathogen InteractionsHumansImmunity, InnateNasal MucosaPoly I-CReceptor, EphA2RhinitisRhinovirusCytokinesEFNA1 protein, humanEPHA2 protein, humanEphrin-A1Ephrin-A2Poly I-CReceptor, EphA2chronic rhinosinusitis with nasal polypschronic rhinosinusitis without nasal polypsephrinA1/ephA2 signalinginnate immune responseinterferon stimulated genesrhinovirustype III interferontype I interferon

Identifiers

PMID34975898
PMCPMC8716742
OpenAlexW4200107649

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.