Evidence map›Paper›PMID 35309360›Full record

ArticleFrontiers in immunology2022

Eosinophil-Derived Osteopontin Induces the Expression of Pro-Inflammatory Mediators and Stimulates Extracellular Matrix Production in Nasal Fibroblasts: The Role of Osteopontin in Eosinophilic Chronic Rhinosinusitis.

Hyun-Woo Yang, Joo-Hoo Park, Min-Sik Jo, Jae-Min Shin, Dae Woo Kim, Il-Ho Park

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Roles of Exosomes in Chronic Rhinosinusitis: A Systematic Review.International journal of molecular sciences · 2022
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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

6 authors at 2 institutions in 1 country.

Hyun-Woo YangUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.
Joo-Hoo ParkUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.
Min-Sik JoUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.
Jae-Min ShinUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.
Dae Woo KimDepartment of Otorhinolaryngology-Head & Neck Surgery, Boramae Medical Center, Seoul National University College of Medicine, Seoul, South Korea.
Il-Ho ParkUpper Airway Chronic Inflammatory Diseases Laboratory, Korea University College of Medicine, Seoul, South Korea.
Korea University · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Eosinophilic chronic rhinosinusitis (ECRS) is a subtype of chronic rhinosinusitis (CRS) and is a refractory or intractable disease. However, a reliable clinical marker or an effective treatment strategy has not yet been established. ECRS is accompanied by excessive eosinophil infiltration and Th2 inflammatory response, which is closely related to tissue remodeling in the upper airways. Objectives: We sought to investigate the effect of eosinophils on tissue remodeling in ECRS. The purpose of this study was to identify the effects of eosinophils on the expression of pro-inflammatory mediators and extracellular matrix (ECM) in nasal fibroblasts and the key mediators that stimulate them. Methods: Butyric acid was used to differentiate EOL-1 cells into eosinophils. We co-cultured differentiated EOL-1 cells and fibroblasts to measure the expression of pro-inflammatory mediators and ECM in fibroblasts. Among the cytokines secreted from the differentiated EOL-1 cells, factors that induced tissue remodeling of fibroblasts were identified. Results: Treatment with butyric acid (BA) differentiated EOL-1 cells into eosinophils. Differentiated EOL-1 cells induced fibroblasts to produce pro-inflammatory mediators, IL-6 and IL-8, and tissue remodeling factor, VEGF. It also induced myofibroblast differentiation and overexpression of ECM components. Differentiated EOL-1 cells overexpressed osteopontin (OPN), and recombinant OPN increased the expression of IL-6, IL-8, VEGF, and ECM components in nasal fibroblast. OPN was overexpressed in the nasal tissue of patients with ECRS and was associated with the severity of CRS. Conclusions: Eosinophil-derived OPN stimulated nasal fibroblasts and contributed to inflammation and tissue remodeling in ECRS. Moreover, the expression level of OPN was proportional to the severity of ECRS. Therefore, OPN regulation is a potential treatment for ECRS.

Indexed as

Nasal PolypsSinusitisButyric AcidChronic DiseaseEosinophilsExtracellular MatrixFibroblastsHumansInflammation MediatorsInterleukin-6Interleukin-8OsteopontinVascular Endothelial Growth Factor AButyric AcidInflammation MediatorsInterleukin-6Interleukin-8OsteopontinSPP1 protein, humanVascular Endothelial Growth Factor Aeosinophileosinophilic chronic rhinosinusitisfibroblastosteopontintissue remodeling

Identifiers

PMID35309360
PMCPMC8924074
OpenAlexW4214821674

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.