ArticleRespiratory research2023
IL-25 induces airway remodeling in asthma by orchestrating the phenotypic changes of epithelial cell and fibrocyte.
Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Fibrocytes with different phenotypes are recruited in chronic obstructive pulmonary disease.Scientific reports · 2026Article
- Review
- Epithelial alarmins TSLP, IL-33, and IL-25 in asthma pathogenesis: mechanistic roles and therapeutic implications.Molecular biology reports · 2026Review
- Obesity, Air Pollution, and Epigenetic Modifications as Risk Factors for Asthma Phenotypes.International journal of molecular sciences · 2026Review
- The Major Role of Type 2 Inflammation in Asthma: From the Perspective of Immunological Mechanism.BioMed research international · 2026Review
- The Role of Alarmins in the Pathogenesis of Asthma.Biomolecules · 2025Review
- Epithelial-derived cytokines in the pathogenesis of severe asthma.Frontiers in allergy · 2025Review
- Immunological factors, important players in the development of asthma.BMC immunology · 2024Review
- Upper Airway Alarmin Cytokine Expression in Asthma of Different Severities.Journal of clinical medicine · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPrevious studies have shown that IL-25 levels are increased in patients with asthma with fixed airflow limitation (FAL). However, the mechanism by which IL-25 contributes to airway remodeling and FAL remains unclear. Here, we hypothesized that IL-25 facilitates pro-fibrotic phenotypic changes in bronchial epithelial cells (BECs) and circulating fibrocytes (CFs), orchestrates pathological crosstalk from BECs to CFs, and thereby contributes to airway remodeling and FAL.
methodsFibrocytes from asthmatic patients with FAL and chronic asthma murine models were detected using flow cytometry, multiplex staining and multispectral imaging analysis. The effect of IL-25 on BECs and CFs and on the crosstalk between BECs and CFs was determined using cell culture and co-culture systems.
resultsWe found that asthmatic patients with FAL had higher numbers of IL-25 receptor (i.e., IL-17RB)
conclusionThese results suggest that IL-25 may serve as a potential therapeutic target for asthmatic patients with FAL.
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Registered trials
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