Evidence map›Paper›PMID 39568050›Full record

ArticleCell communication and signaling : CCS2024

Contribution of IL-17C-mediated macrophage polarization to Type 17 inflammation in neutrophilic asthma.

Yuhuan Wen, Qile Chen, Hao Wang, Shiyun Xie, Honglv Chen, Wenruo Yao, Le Zhang, Weimin Sun, Junjie Wen, Xiaojing Yang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 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

14 authors.

Yuhuan WenThe State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, Sino-French Hoffmann Institute, Guangzhou Medical University, Guangzhou, 510260, China.
Qile ChenThe State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, Sino-French Hoffmann Institute, Guangzhou Medical University, Guangzhou, 510260, China.
Hao WangDepartment of Hematology, Guangzhou First People's HospitalInstitute of Blood Transfusion and Hematology, Guangzhou Medical University, Guangzhou, Guangdong, China.
Shiyun XieThe State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, Sino-French Hoffmann Institute, Guangzhou Medical University, Guangzhou, 510260, China.
Honglv ChenThe State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, Sino-French Hoffmann Institute, Guangzhou Medical University, Guangzhou, 510260, China.
Wenruo YaoThe State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, Sino-French Hoffmann Institute, Guangzhou Medical University, Guangzhou, 510260, China.
Le ZhangThe State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, Sino-French Hoffmann Institute, Guangzhou Medical University, Guangzhou, 510260, China.
Weimin SunDepartment of Laboratory Medicine, The Seventh Affiliated Hospital of Southern Medical University, Foshan, China.
Junjie WenPulmonary and Critical Care Medicine, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Xiaojing YangPulmonary and Critical Care Medicine, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Kian Fan ChungNational Heart and Lung Institute, Imperial College & Biomedical Research Unit, Royal Brompton & Harefield NHS Trust, London, UK.
Qingling ZhangPulmonary and Critical Care Medicine, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China. zqling68@hotmail.com.
Ailin TaoThe State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, Sino-French Hoffmann Institute, Guangzhou Medical University, Guangzhou, 510260, China. taoailin@gzhmu.edu.cn.
Jie YanThe State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, The Second Affiliated Hospital, Sino-French Hoffmann Institute, Guangzhou Medical University, Guangzhou, 510260, China. jieyan@gzhmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIL-17C has been described in a variety of inflammatory diseases driven by neutrophils. However, the role of IL-17C in neutrophilic asthma has not been completely characterized.

methodsThe level of IL-17C in asthmatic patients and mice was assessed. Il-17c-deficient mice or mice treated with exogenous rmIL-17C were performed for OVA/CFA-induced asthmatic mice model. Pulmonary inflammation was evaluated by histological analysis, flow cytometry and cytokine analysis. Il-17re-overexpressed Raw264.7 were used in vitro to investigate the role of IL-17C in macrophage polarization.

resultsHere, we show IL-17C were increased in serum or plasma from asthmatic patients and OVA/CFA-induced asthma mice. In the OVA/CFA-induced model, exogenous rmIL-17C aggravated neutrophil- and Type 17-dominated inflammation and promoted M1 macrophage differentiation, whereas deficiency of Il-17c reversed the pro-inflammatory phenotypes and inhibited the expansion of M1 macrophages. In vitro, IL-17C in synergy with IFN-γ induced STAT1 activation in Il-17re overexpressed Raw264.7 to upregulate M1-related genes expression, and promoted pro-inflammatory M1 polymerization, whereas IL-17C in contrast to the effect of IL-4 inhibited STAT6 activation, to reduce Raw264.7 differentiation to M2 macrophage and functional M2-related genes expression.

conclusionsIL-17C promotes allergic inflammation via M1 polarization of pulmonary macrophages in neutrophilic asthma. Modulation of the IL-17C/IL-17RE axis represents a novel therapeutic target in neutrophilic asthma.

Indexed as

AsthmaCell PolarityInterleukin-17MacrophagesNeutrophilsAnimalsDisease Models, AnimalFemaleHumansInflammationMaleMiceMice, Inbred C57BLRAW 264.7 CellsSTAT1 Transcription FactorInterleukin-17STAT1 Transcription FactorAsthmaIL-17CIL-17REMacrophages

Identifiers

PMID39568050
PMCPMC11580697

What Socratic 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 Socratic graph.