Evidence map›Paper›PMID 40567585›Full record

ArticleJournal of inflammation research2025

IL-17A as a Key Mediator of Pulmonary-Intestinal Immune Interactions in a Mouse Model of Asthma and Colitis.

Chengyong Wu, Xuxu Hu, Zhongyuan Mo, Yan Meng, Yingying Du, Yunyu Duan, Zaopin Zeng, Jiahui Shan, Juan Li, Nali Zhang and 8 more

Abstract read
In one paragraph

Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Advances in Research onMolecules (Basel, Switzerland) · 2026
    Review
  2. Review
  3. Article
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

18 authors.

Chengyong WuDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Xuxu HuDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Zhongyuan MoDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Yan MengDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Yingying DuDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Yunyu DuanDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Zaopin ZengDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Jiahui ShanDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Juan LiDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Nali ZhangDepartment of Respiratory and Critical Care Medicine, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, Henan Province, 471009, People's Republic of China.
Youfeng MaDepartment of Respiratory and Critical Care Medicine, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, Henan Province, 471009, People's Republic of China.
Huaqi WangDepartment of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, 450052, People's Republic of China.
Chi LiuDepartment of Physiology, School of Basic Medicine Science, Central South University, Changsha, Hunan Province, 410083, People's Republic of China.
Guojun ZhangDepartment of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, 450052, People's Republic of China.
Paul S FosterWoolcock Institute of Medical Research, Macquarie University, Sydney, New South Wales, 2109, Australia.
Huisha XuDepartment of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Fuguang Li *Department of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.
Ming Yang *Department of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, 450001, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The immunological interaction between the lung and gut remains underexplored, particularly in the context of coexisting mucosal inflammation. While IL-17A has been implicated in both asthma and colitis independently, its role in coordinating systemic immune responses across tissue compartments is not well defined. Methods: In this study, we developed a combined house dust mite-induced asthma model and dextran sulfate sodium-induced colitis model to investigate the role of IL-17A in driving inflammation in both the lungs and the intestines. Results: Our findings demonstrate that IL-17A neutralization markedly reduced airway and intestinal inflammation, attenuated mucus hypersecretion, downregulated pro-inflammatory cytokine expression, and alleviated colitis severity. Histopathological analysis revealed decreased infiltration of immune cells, including eosinophils, lymphocytes, and macrophages, in both the lungs and colonic tissues following IL-17A blockade. Additionally, we observed a reduction in mucus production, particularly in the airways, highlighting IL-17A's direct role in mucin regulation. Transcriptomic analysis confirmed that IL-17A blockade downregulated several immune-related pathways in colon tissues, further supporting its central role in mediating multi-organ inflammation. Conclusion: These findings indicate that IL-17A represents a systemic immunomodulator, which orchestrates compartmentalized immune responses along the lung-gut axis. The observed tissue-specific redistribution of IL-17A and the therapeutic benefit of its neutralization suggest that IL-17A may serve as a clinically actionable target in patients with overlapping asthma and colitis. The study also shows that IL-17A plays a reciprocal role in influencing immune responses in both lung and gut.

Indexed as

asthmacolitisIL-17Ainflammationlung-gut axis

Identifiers

PMID40567585
PMCPMC12191152

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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.