ArticlePloS one2017
IL-25-induced activation of nasal fibroblast and its association with the remodeling of chronic rhinosinusitis with nasal polyposis.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 36 citations in OpenAlex.
- SM17, an anti-interleukin-17 receptor B antibody, ameliorates pathogenesis of chronic rhinosinusitis with nasal polyps and idiopathic pulmonary fibrosisERJ open research · 2026Article
- Intranasal Application of Foxp3 Introduced with Poly(d,l-lactic-Pharmaceutics · 2025Article
- A Combination of Anatolian Propolis and Curcumin Protects Fibroblasts Against Beclomethasone (Nazal Steroid)-Induced Oxidative Stress by Modulating IL-25, MMP-2, VEGF, and FGF-2 Expressions.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The Inhibition Effect and Mechanism of Staurosporine Isolated fromMarine drugs · 2024Article
- Role of Fibroblasts in Chronic Inflammatory Signalling in Chronic Rhinosinusitis with Nasal Polyps-A Systematic Review.Journal of clinical medicine · 2023Review
- Pathogenesis of Nasal Polyposis: Current Trends.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2023Article
- Role of Nasal Fibroblasts in Airway Remodeling of Chronic Rhinosinusitis: The Modulating Functions Reexamined.International journal of molecular sciences · 2023Review
- Immunological Aspects of Chronic Rhinosinusitis.Diagnostics (Basel, Switzerland) · 2022Review
- ILCs and Allergy.Advances in experimental medicine and biology · 2022Article
- Therapeutic candidates for keloid scars identified by qualitative review of scratch assay research for wound healing.PloS one · 2021Review
- The Epithelial-Immune Crosstalk in Pulmonary Fibrosis.Frontiers in immunology · 2021Review
- Aspirin Actions in Treatment of NSAID-Exacerbated Respiratory Disease.Frontiers in immunology · 2021Review
- Formation of nasal polyps: The roles of innate type 2 inflammation and deposition of fibrin.The Journal of allergy and clinical immunology · 2020Review
- Level of sex hormones and their association with acetylsalicylic acid intolerance and nasal polyposis.PloS one · 2020Article
- Contribution of Epithelial Cell Dysfunction to the Pathogenesis of Chronic Rhinosinusitis with Nasal Polyps.American journal of rhinology & allergy · 2019Review
- Article
- Aberrant expression of miR-663 and transforming growth factor-β1 in nasal polyposis in children.Experimental and therapeutic medicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectiveInterleukin (IL)-25 has been shown to play an important role in the pathogenesis of chronic rhinosinusitis with nasal polyps. Nasal polyps are associated with chronic inflammation of the mucous membranes in the paranasal sinuses and are involved in extracellular matrix (ECM) accumulation. The aim of this study is to evaluate the effects of IL-25 on myofibroblast differentiation, ECM production and the expression of matrix metalloproteinases in nasal polyp derived fibroblasts (NPDFs) and to determine the molecular mechanism underlying these processes. MATERIALS AND
methodsA total of 40 patients were enrolled in this study for Immunofluorescence studies. Expression of IL17 receptor B was evaluated by real time reverse transcription polymerase chain reaction (PCR) in NPDFs. NPDFs were stimulated with IL-25 for 48 h in the presence or absence of mitogen-activated protein kinase (MAPK) and NF-κB inhibitors or small interfering RNAs (siRNA). The protein levels of fibrosis active mediators were examined using western blotting. Fibroblast migration was evaluated with a scratch assay. The total collagen amount was analyzed with the Sircol collagen assay.
resultsIL-25 induced α-SMA, fibronectin, and MMP-1 and -13, which were dependent on IL-17RB. IL-25 also induced activation of NF-κB and mitogen-activated protein kinase (MAPKs). By using the specific inhibitor of ERK, p38, JNK and NF-κB (U, SB, SP and Bay), we found that IL-25-induced expressions of α-SMA, fibronectin, and MMPs was regulated by the signaling pathways of MAPKs and NF-κB. IL-25 also induces α-SMA, fibronectin, and MMPs expression through IL-17RB-dependent pathways in NPDFs. The increased migration ability induced by IL-25 was suppressed by the specific inhibitors of MAPKs and NF-κB.
conclusionOur data indicate that IL-25 induced myofibroblast differentiation, fibronectin production, and MMP-1 and -13 expressions through the signaling pathways of MAPKs and NF-κB. in NPDFs and increased expression of IL-25 were also involved in the pathogenesis of nasal polyposis by affecting nasal fibroblasts in chronic rhinosinusitis with nasal polyps.
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Registered trials
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.