Evidence map›Paper›PMID 41298412›Full record

ArticleNature communications2025

GPR43 in eosinophils suppresses the emergence of pathogenic Siglec-F

Jihyun Yu, Seongryong Kim, Hyun-Sup Song, Jieun Kim, Woojung Shin, Jong-Eun Park, Ikuo Kimura, Hye-Young Kim, You-Me Kim

Abstract read
In one paragraph

Article in Nature communications, 2025. 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

9 authors.

Jihyun YuGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0003-3522-6846
Seongryong KimGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.
Hyun-Sup SongGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.
Jieun KimDepartment of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.ORCID http://orcid.org/0009-0002-0394-2987
Woojung ShinDepartment of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0002-1780-0317
Jong-Eun ParkGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0002-1687-2423
Ikuo KimuraGraduate School of Biostudies, Kyoto University, Kyoto, Japan.ORCID http://orcid.org/0000-0001-8778-145X
Hye-Young KimDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0001-5978-512X
You-Me KimGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea. youmekim@kaist.ac.kr.ORCID http://orcid.org/0000-0001-8780-704X

Funding

National Research Foundation of Korea (NRF) 2022R1A6A3A1306363412, RS-2024-00439160, RS-2025-02232977
6 · The paper itself

Abstract

Eosinophils are major effector cells in type 2 immune responses, contributing to host defense and allergic diseases. They also contribute to maintaining tissue homeostasis by regulating various immune cell types, including neutrophils. Here we show that eosinophils directly associate with neutrophils in the lungs of asthma-induced mice. Eosinophil-specific deficiency of the short-chain fatty acid receptor, GPR43, results in hyperactivation of eosinophils and increases the expression of neutrophil chemoattractants and PECAM-1, thereby enhancing the interaction between eosinophils and neutrophils. This interaction exposes neutrophils to eosinophil-derived IL-4 and GM-CSF, which induce the conversion of conventional neutrophils into more pathogenic, Siglec-F

Indexed as

AsthmaEosinophilsNeutrophilsReceptors, G-Protein-CoupledAnimalsCell DifferentiationDisease Models, AnimalFemaleGranulocyte-Macrophage Colony-Stimulating FactorInflammationInterleukin-4LungMiceMice, Inbred C57BLMice, KnockoutSialic Acid Binding Immunoglobulin-like LectinsFfar2 protein, mouseGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-4Receptors, G-Protein-CoupledSialic Acid Binding Immunoglobulin-like LectinsSiglecf protein, mouse

Identifiers

PMID41298412
PMCPMC12657986

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.