ArticleRespiratory research2013
IL-17A is essential to the development of elastase-induced pulmonary inflammation and emphysema in mice.
Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 88 citations in OpenAlex.
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- Interleukin-17A Orchestrates Lung Injury and Remodeling Through p53 and uPA System Crosstalk.International journal of molecular sciences · 2026Article
- IL-17-secreting γδ T-cell-driven Siglec-FCellular & molecular immunology · 2025Article
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- Modulating asthma-COPD overlap responses with IL-17 inhibition.Frontiers in immunology · 2023Article
- IL-17 Cytokines and Chronic Lung Diseases.Cells · 2022Review
- IL-17A Promotes Epithelial ADAM9 Expression in Cigarette Smoke-Related COPD.International journal of chronic obstructive pulmonary disease · 2022Article
- Reactive Oxygen Species and Antioxidative Defense in Chronic Obstructive Pulmonary Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Dual interleukin-17A/F deficiency protects against acute and chronic response to cigarette smoke exposure in mice.Scientific reports · 2021Article
- Tumor-associated macrophages promote the metastasis and growth of non-small-cell lung cancer cells through NF-κB/PP2Ac-positive feedback loop.Cancer science · 2021Article
- Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice.Respiratory research · 2021Article
- Monocyte-derived dendritic cells link localized secretory IgA deficiency to adaptive immune activation in COPD.Mucosal immunology · 2021Article
- The Induction of Alpha-1 Antitrypsin by Vitamin D in Human T Cells Is TGF-β Dependent: A Proposed Anti-inflammatory Role in Airway Disease.Frontiers in nutrition · 2021Article
- Multiomics of World Trade Center Particulate Matter-induced Persistent Airway Hyperreactivity. Role of Receptor for Advanced Glycation End Products.American journal of respiratory cell and molecular biology · 2020Article
- Herbal Combinational Medication ofNutrients · 2020Article
- Relationship of Serum Levels of IL-17, IL-18, TNF-Mediators of inflammation · 2020Article
- Th1/Th17 Cytokine Profiles are Associated with Disease Severity and Exacerbation Frequency in COPD Patients.International journal of chronic obstructive pulmonary disease · 2020Article
- Quantitative lung morphology: semi-automated measurement of mean linear intercept.BMC pulmonary medicine · 2019Article
- Therapeutic effect of carbon monoxide-releasing molecule-3 on acute lung injury after hemorrhagic shock and resuscitation.Experimental and therapeutic medicine · 2019Article
- Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model.PloS one · 2019Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulmonary emphysema is characterized by alveolar destruction and persistent inflammation of the airways. Although IL-17A contributes to many chronic inflammatory diseases, it's role in the inflammatory response of elastase-induced emphysema remains unclear.
methodsIn a model of elastase-induced pulmonary emphysema we examined the response of IL-17A-deficient mice, monitoring airway inflammation, static compliance, lung histology and levels of neutrophil-related chemokine and pro-inflammatory cytokines in bronchoalveolar lavage (BAL) fluid.
resultsWild-type mice developed emphysematous changes in the lung tissue on day 21 after elastase treatment, whereas emphysematous changes were decreased in IL-17A-deficient mice compared to wild-type mice. Neutrophilia in BAL fluid, seen in elastase-treated wild-type mice, was reduced in elastase-treated IL-17A-deficient mice on day 4, associated with decreased levels of KC, MIP-2 and IL-1 beta. Elastase-treated wild-type mice showed increased IL-17A levels as well as increased numbers of IL-17A+ CD4 T cells in the lung in the initial period following elastase treatment.
conclusionsThese data identify the important contribution of IL-17A in the development of elastase-induced pulmonary inflammation and emphysema. Targeting IL-17A in emphysema may be a potential therapeutic strategy for delaying disease progression.
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