ArticleClinical science (London, England : 1979)2015
Innate cellular sources of interleukin-17A regulate macrophage accumulation in cigarette- smoke-induced lung inflammation in mice.
Article in Clinical science (London, England : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 76 citations in OpenAlex.
- Molecular and Cellular Mechanisms Responsible for Beneficial Effects of Mesenchymal Stem Cell-Derived Product "Exo-d-MAPPS" in Attenuation of Chronic Airway Inflammation.Analytical cellular pathology (Amsterdam) · 2020Trial
- Ferroptosis-related genes MDM2 and CDKN1A as potential biomarkers for COPD.Journal of inflammation (London, England) · 2025Article
- Impact of Curcumin on the IL-17A-Mediated p53-Fibrinolytic System: Mouse Proteomics and Integrated Human Fibrosis scRNAseq Insights.Inflammation · 2025Article
- An unconventional T cell nexus drives HCK-mediated chronic obstructive pulmonary disease in mice.EBioMedicine · 2025Article
- Parental Smoking and Risk of Allergic Conjunctivitis in Chinese Pediatric Population: A Cross-Sectional Study.Journal of asthma and allergy · 2025Article
- The Lung-Brain Axis in Chronic Obstructive Pulmonary Disease-Associated Neurocognitive Dysfunction: Mechanistic Insights and Potential Therapeutic Options.International journal of biological sciences · 2025Review
- Assessing Progression of Biologic Therapies Based on Smoking Status in Patients With Crohn's Disease.Inflammatory bowel diseases · 2024Article
- Article
- Type V collagen-induced nasal tolerance prevents lung damage in an experimental model: new evidence of autoimmunity to collagen V in COPD.Frontiers in immunology · 2024Article
- Aminopeptidase N/CD13 Crosslinking Promotes the Activation and Membrane Expression of Integrin CD11b/CD18.Biomolecules · 2023Article
- Periodontitis contributes to COPD progression via affecting ferroptosis.BMC oral health · 2023Article
- Cigarette smoke depletes alveolar macrophages and delays clearance ofAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
- Blocking CD40 Alleviates Th1 and Th17 Cell Responses in Elastin Peptide-Induced Murine Emphysema.International journal of chronic obstructive pulmonary disease · 2023Article
- The Role of Inflammation and Oxidative Stress in Rheumatic Heart Disease.International journal of molecular sciences · 2022Review
- Targeting the human βRespirology (Carlton, Vic.) · 2022Article
- Ebselen prevents cigarette smoke-induced cognitive dysfunction in mice by preserving hippocampal synaptophysin expression.Journal of neuroinflammation · 2022Article
- IL-17A Promotes Epithelial ADAM9 Expression in Cigarette Smoke-Related COPD.International journal of chronic obstructive pulmonary disease · 2022Article
- Exposure to second-hand smoke is an independent risk factor of small airway dysfunction in non-smokers with chronic cough: A retrospective case-control study.Frontiers in public health · 2022Article
- Emerging and multifaceted role of neutrophils in lung cancer.Translational lung cancer research · 2021Review
- NK Cells in the Pathogenesis of Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoke (CS) is the major cause of chronic obstructive pulmonary disease (COPD). Interleukin-17A (IL-17A) is a pivotal cytokine that regulates lung immunity and inflammation. The aim of the present study was to investigate how IL-17A regulates CS-induced lung inflammation in vivo. IL-17A knockout (KO) mice and neutralization of IL-17A in wild-type (WT) mice reduced macrophage and neutrophil recruitment and chemokine (C-C motif) ligand 2 (CCL2), CCL3 and matrix metalloproteinase (MMP)-12 mRNA expression in response to acute CS exposure. IL-17A expression was increased in non-obese diabetic (NOD) severe combined immunodeficiency SCID) mice with non-functional B- and T-cells over a 4-week CS exposure period, where macrophages accumulated to the same extent as in WT mice. Gene expression analysis by QPCR (quantitative real-time PCR) of isolated immune cell subsets detected increased levels of IL-17A transcript in macrophages, neutrophils and NK/NKT cells in the lungs of CS-exposed mice. In order to further explore the relative contribution of innate immune cellular sources, intracellular IL-17A staining was performed. In the present study, we demonstrate that CS exposure primes natural killer (NK), natural killer T (NKT) and γδ T-cells to produce more IL-17A protein and CS alone increased the frequency of IL17+ γδ T-cells in the lung, whereas IL-17A protein was not detected in macrophages and neutrophils. Our data suggest that activation of innate cellular sources of IL-17A is an essential mediator of macrophage accumulation in CS-exposed lungs. Targeting non-conventional T-cell sources of IL-17A may offer an alternative strategy to reduce pathogenic macrophages in COPD.
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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.