ArticleFrontiers in immunology2023
Modulating asthma-COPD overlap responses with IL-17 inhibition.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- From Susceptibility to Disease Severity: Re-Discovering the Clinical Role ofLife (Basel, Switzerland) · 2026Article
- Breaking the bottleneck of asthma treatment: the future of omni-targeted therapy.Journal of advanced research · 2026Review
- Article
- Serum OX40 ligand as a biochemical regulator of Th2-dominant immune activation in asthma: An integrated cytokine network analysis.Journal of medical biochemistry · 2026Article
- Inflammatory memory: the core mechanism driving allergic asthma recurrence and chronicity.Journal of thoracic disease · 2026Review
- N4BP1 acts as a potent negative regulator of IL-17 signaling by blocking the translation of Act1 mRNA.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Dual role of IL-17A in COPD: amplifier of inflammatory cascades and mediator of airway remodeling and alveolar destruction.Frontiers in immunology · 2026Review
- Ironing out COPD: ferroptosis-driven immune dysregulation, metabolic rewiring, and precision therapeutic opportunities.Frontiers in immunology · 2026Review
- Targeting IL-17/NF-κB/VAChT/Rho-kinase signaling and oxidative stress in exacerbated chronic allergic inflammation: functional and therapeutic implications of IL-17 blockade.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
- Multiomics Approach Identifies Novel Genetic Determinants and Therapeutic Targets for Asthma.Canadian respiratory journal · 2026Article
- From clinical phenotypes to cellular mechanisms: a precision medicine framework for COPD.Frontiers in immunology · 2026Review
- Analysis of the effects of perfluorooctane sulfonate on COPD using network toxicology and molecular docking.iScience · 2025Article
- Mechanism by which porcine transmissible gastroenteritis virus disrupts host innate immunity.Frontiers in immunology · 2025Review
- Immune cell regulatory networks in chronic obstructive pulmonary disease: mechanistic analysis from innate to adaptive immunity.Frontiers in immunology · 2025Review
- Established and Emerging Biological Therapies for the Treatment of Comorbid Asthma and Chronic Obstructive Pulmonary Disease.Journal of inflammation research · 2025Review
- Identification of potential diagnostic markers and molecular mechanisms of asthma and ulcerative colitis based on bioinformatics and machine learning.Frontiers in molecular biosciences · 2025Article
- Editorial: The current state of knowledge on asthma-COPD overlap (ACO) in clinical and experimental research: what do we know so far?Frontiers in immunology · 2025Article
- Silencing SMAD4 inhibits inflammation and ferroptosis in asthma by blocking the IL-17A signaling pathway.Respiratory research · 2024Article
- Anti-inflammatory effects and related mechanisms of naringenin in human periodontal ligament stem cells under lipopolysaccharide stimulation based on RNA sequencing.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2024Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: IL-17 is a modulator of the inflammatory response and is implicated in lung remodeling in both asthma and chronic obstructive pulmonary disease (COPD). Well as and probably in patients with asthma-COPD overlap (ACO). Methods: In this study, we evaluated the response of the airways and alveolar septa to anti-IL-17 treatment in an ACO model. Fifty-six male BALB/c mice were sensitized with ovalbumin (OVA group), received porcine pancreatic elastase (PPE group), or both (ACO group). Mice were then treated with either anti-IL-17 monoclonal antibody or saline. We evaluated hyperresponsiveness, bronchoalveolar lavage fluid (BALF) cell counts, and mean alveolar diameter. We quantified inflammatory, response, extracellular matrix remodeling, oxidative stress markers, and signaling pathway markers. Results: Anti-IL-17 treatment in the ACO anti-IL-17 group reduced the maximum response of respiratory system Rrs, Ers, Raw, Gtis, this when compared to the ACO group (p<0.05). There was a reduction in the total number of inflammatory cells, neutrophils, and macrophages in the BALF in the ACO anti-IL-17 group compared to the ACO group (p<0.05). There was attenuated dendritic cells, CD4+, CD8+, FOXP3, IL-1β, IL-2, IL-6, IL-13, IL-17, IL-33 in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p<0.05). We observed a reduction of MMP-9, MMP-12, TIMP-1, TGF-β, collagen type I in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p < 0.05). We also observed a reduction of iNOS and 8-iso-PGF2α in the airways and in the alveolar septum was reduced in the ACO anti-IL-17group compared to the ACO group (p < 0.05). Regarding the signaling pathways, NF-kB, ROCK-1, and ROCK-2 in the airway and alveolar septum were attenuated in the ACO anti-IL-17 group when compared to the ACO group (p<0.05). Conclusions: Our results suggest that inhibiting IL-17 modulates cell-associated cytokine production in lung tissue, extracellular matrix remodeling, and oxidative stress in ACO through the modulation of NF-kB and FOXP3.
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