Evidence map›Paper›PMID 36174993›Full record

ArticleAllergy, asthma & immunology research2022

IL-24 Contributes to Neutrophilic Asthma in an IL-17A-Dependent Manner and Is Suppressed by IL-37.

Kang-Ni Feng, Ping Meng, Min Zhang, Xiao-Ling Zou, Shuang Li, Chu-Qin Huang, Ke-Fang Lai, Hong-Tao Li, Tian-Tuo Zhang

Open access · diamondAbstract read
In one paragraph

Article in Allergy, asthma & immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Gngt2 promotes inflammatory dendritic cell programming through an ATG5-NF-κB signaling axis in neutrophilic asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  15. Interleukin-24: A Multidimensional Therapeutic for Treatment of Human Diseases.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology
    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 at 2 institutions in 1 country.

Kang-Ni Feng *Department of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Institute of Respiratory Disease of Sun Yat-sen University, Guangzhou, China.ORCID https://orcid.org/0000-0002-9706-8428
Ping Meng *Department of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Institute of Respiratory Disease of Sun Yat-sen University, Guangzhou, China.ORCID https://orcid.org/0000-0002-3393-6628
Min ZhangDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Institute of Respiratory Disease of Sun Yat-sen University, Guangzhou, China.ORCID https://orcid.org/0000-0001-7886-3875
Xiao-Ling ZouDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Institute of Respiratory Disease of Sun Yat-sen University, Guangzhou, China.ORCID https://orcid.org/0000-0002-4455-8087
Shuang LiDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Institute of Respiratory Disease of Sun Yat-sen University, Guangzhou, China.ORCID https://orcid.org/0000-0001-7819-0404
Chu-Qin HuangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Ke-Fang LaiState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Hong-Tao LiDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Institute of Respiratory Disease of Sun Yat-sen University, Guangzhou, China. lht791@163.com.ORCID https://orcid.org/0000-0002-3337-483X
Tian-Tuo ZhangDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Institute of Respiratory Disease of Sun Yat-sen University, Guangzhou, China. zhtituli@163.com.ORCID https://orcid.org/0000-0002-9239-0434
Sun Yat-sen University · CNFirst Affiliated Hospital of Guangzhou Medical University · CN

Funding

National Natural Science Foundation of China 81970017National Natural Science Foundation of China 81973984
6 · The paper itself

Abstract

purposeNeutrophilic asthma is associated with asthma exacerbation, steroid insensitivity, and severe asthma. Interleukin (IL)-24 is overexpressed in asthma and is involved in the pathogenesis of several allergic inflammatory diseases. However, the role and specific mechanism of IL-24 in neutrophilic asthma are unclear. We aimed to elucidate the roles of IL-24 and IL-37 in neutrophilic asthma, the relationships with IL-17A and the mechanisms regulating neutrophilic asthma progression.

methodsPurified human neutrophils were isolated from healthy volunteers, and a cell coculture system was used to evaluate the function of IL-24 in epithelium-derived IL-17A-dependent neutrophil migration. IL-37 or a small interfering RNA (siRNA) targeting IL-24 was delivered intranasally to verify the effect in a murine model of house dust mite (HDM)/lipopolysaccharide (LPS)-induced neutrophilic asthma.

resultsIL-24 enhanced IL-17A production in bronchial epithelial cells via the STAT3 and ERK1/2 signaling pathways; this effect was reversed by exogenous IL-37. Anti-IL-17A monoclonal antibodies reduced neutrophil chemotaxis induced by IL-24-treated epithelial cells

conclusionsIL-24 aggravated neutrophilic airway inflammation by increasing epithelium-derived IL-17A production, which could be suppressed by IL-37. Targeting the IL-24/IL-17A signaling axis is a potential strategy, and IL-37 is a potential candidate agent for alleviating neutrophilic airway inflammation in asthma.

Indexed as

Asthmaepithelial cellsinflammationinterleukin-17Ainterleukin-24neutrophils

Identifiers

PMID36174993
PMCPMC9523421
OpenAlexW4298087933

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.