ArticleFrontiers in immunology2025
IL-17-neutralizing antibody mitigates functional and structural changes in cigarette smoke-induced COPD model.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Review
- Unfolding Immune Dysregulation in COPD: Identification of a Three-Gene Signature and Functional Validation ofInternational journal of molecular sciences · 2026Article
- The role of IL-17 in orchestrating macrophage polarization via NF-κB, mTOR/HIF-1α and pyroptosis in diabetes.Scientific reports · 2026Article
- Interleukin-23 in lung and airway diseases: from pathogenesis to precision-guided therapeutic targeting.Frontiers in pharmacology · 2026Review
- Time-series transcriptomic analysis of cigarette smoke-associated lung responses reveals COPD-related inflammatory and epithelial remodeling modules in murine models.Frontiers in medicine · 2026Article
- IL-17RA Promotes Cigarette Smoke-Induced Alveolar Epithelial Cell Pyroptosis in COPD via Dual Activation of the NLRP3/Caspase1/GSDMD and NF-κB/GSDME Pathways.Journal of inflammation research · 2026Article
- Dual role of IL-17A in COPD: amplifier of inflammatory cascades and mediator of airway remodeling and alveolar destruction.Frontiers in immunology · 2026Review
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14 authors.
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Abstract
Smoking remains the main risk factor for the development of chronic obstructive pulmonary disease (COPD). The inflammatory response mediated by innate and adaptive immune cells has been described in the development and progression of the disease, and the importance of Th17 cytokines has been observed. Studies have shown that blocking interleukin (IL)-17 can reduce inflammation in experimental models of lung injury. This study evaluated the effect of an IL-17 inhibitor in a cigarette smoke-induced COPD model in C57BL/6 mice. The effects of treatment with an IL-17 inhibitor were evaluated in an experimental model of COPD. Mice were exposed to cigarette smoke for 6 months, and treatment with IL-17 inhibitor was initiated in the fifth month. Four experimental groups were constituted: Control group-animals housed in a vivarium, receiving filtered room air; Control anti-IL-17 group-animals housed in a vivarium, receiving filtered room air and treatment with an anti-IL-17-neutralizing antibody; COPD group-animals exposed to cigarette smoke; and COPD anti-IL-17 group-animals exposed to cigarette smoke and treated with an anti-IL-17-neutralizing antibody. In the COPD groups, an increase in mean linear intercept was observed, along with a decrease in tissue elastance and tissue damping, confirming the COPD development. Administration of the IL-17-neutralizing antibody reversed these structural and functional alterations. Additionally, the COPD group exhibited an inflammatory response characterized by increased infiltration of polymorphonuclear and mononuclear cells and elevated numbers of IL-17- and IL-6-positive cells. These findings were consistent with the increased expression of IL-17 and IL-6 in lung homogenates, as assessed by ELISA. Treatment with the IL-17-neutralizing antibody effectively reversed this inflammatory response by reducing the expression of these inflammatory markers. These results were further supported by the evaluation of
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