ArticleThe European respiratory journal2015
Protective role for club cell secretory protein-16 (CC16) in the development of COPD.
Article in The European respiratory journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 150 citations in OpenAlex.
- Impaired CC16-mediated host responses to rhinovirus in nasal epithelial cells from patients with asthma.The Journal of allergy and clinical immunology · 2026Article
- Club Cells in Nasal Epithelial Repair: Insights From an IL-13-Induced Inflammatory Model.Allergy · 2026Article
- Maternal smoking and CC-16: implications for lung development and COPD across the lifespan.American journal of respiratory and critical care medicine · 2026Article
- The Developmental Origins of Asthma and COPD.Annual review of physiology · 2026Review
- Potential toxicity of micro- and nanoplastics in primary bronchial epithelial cells of patients with chronic obstructive pulmonary disease.Microplastics and nanoplastics · 2026Article
- From respiratory infections to environmental exposures: CC16 is a key modulator of airway homeostasis.Frontiers in medicine · 2026Review
- The role of CC16 in the associations of preterm birth with lung function and asthma in adult life.The Journal of allergy and clinical immunology · 2026Article
- A Review of Telomere Attrition in Cancer and Aging: Current Molecular Insights and Future Therapeutic Approaches.Cancers · 2025Review
- A machine learning model and identification of immune infiltration for chronic obstructive pulmonary disease based on disulfidptosis-related genes.BMC medical genomics · 2025Article
- Article
- Identification of Cuproptosis-Related Genes and Their Potential Role in COPD Pathogenesis: A Bioinformatics Analysis.International journal of chronic obstructive pulmonary disease · 2025Article
- Bi-directional regulation between inflammation and stem cells in the respiratory tract.Journal of cell science · 2024Review
- Controlled human exposures: a review and comparison of the health effects of diesel exhaust and wood smoke.Particle and fibre toxicology · 2024Review
- Enhancing peptide and PMO delivery to mouse airway epithelia by chemical conjugation with the amphiphilic peptide S10.Molecular therapy. Nucleic acids · 2024Article
- Cobalt exposure and pulmonary function reduction in chronic obstructive pulmonary disease patients: the mediating role of club cell secretory protein.Respiratory research · 2024Article
- Review
- txci-ATAC-seq: a massive-scale single-cell technique to profile chromatin accessibility.Genome biology · 2024Article
- Modelling bronchial epithelial-fibroblast cross-talk in idiopathic pulmonary fibrosis (IPF) using a human-derived in vitro air liquid interface (ALI) culture.Scientific reports · 2024Article
- Physiological and immunological barriers in the lung.Seminars in immunopathology · 2024Review
- Sputum Biomarkers in Wood and Tobacco Smoke Etiotypes of Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2024Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Club cell secretory protein-16 (CC16) is the major secreted product of airway club cells, but its role in the pathogenesis of chronic obstructive pulmonary disease (COPD) is unclear. We measured CC16 airway expression in humans with and without COPD and CC16 function in a cigarette smoke (CS)-induced COPD murine model. Airway CC16 expression was measured in COPD patients, smokers without COPD and non-smokers. We exposed wildtype (WT) and CC16(-/-)mice to CS or air for up to 6 months, and measured airway CC16 expression, pulmonary inflammation, alveolar septal cell apoptosis, airspace enlargement, airway mucin 5AC (MUC5AC) expression, small airway remodelling and pulmonary function. Smokers and COPD patients had reduced airway CC16 immunostaining that decreased with increasing COPD severity. Exposing mice to CS reduced airway CC16 expression. CC16(-/-) mice had greater CS-induced emphysema, airway remodelling, pulmonary inflammation, alveolar cell apoptosis, airway MUC5AC expression, and more compliant lungs than WT mice. These changes were associated with increased nuclear factor-κB (NF-κB) activation in CC16(-/-) lungs. CS-induced acute pulmonary changes were reversed by adenoviral-mediated over-expression of CC16. CC16 protects lungs from CS-induced injury by reducing lung NF-κB activation. CS-induced airway CC16 deficiency increases CS-induced pulmonary inflammation and injury and likely contributes to the pathogenesis of COPD.
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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.