ArticleMolecular medicine reports2018
Recombinant club cell protein 16 (CC16) ameliorates cigarette smoke‑induced lung inflammation in a murine disease model of COPD.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Pharmacological effect of rhCC16 on COPD: anti-senescence via the PI3K-AKT-mTOR pathway.Molecular and cellular biochemistry · 2026Article
- Impaired CC16-mediated host responses to rhinovirus in nasal epithelial cells from patients with asthma.The Journal of allergy and clinical immunology · 2026Article
- From respiratory infections to environmental exposures: CC16 is a key modulator of airway homeostasis.Frontiers in medicine · 2026Review
- Exploring the mechanism of guben kechuan granules in the treatment of COPD via network pharmacology, molecular docking and molecular dynamics simulations.Scientific reports · 2025Article
- rhCC16 Suppresses Cellular Senescence and Ameliorates COPD-Like Symptoms by Activating the AMPK/Sirt1-PGC-1-α-TFAM Pathway to Promote Mitochondrial Function.Journal of cellular and molecular medicine · 2025Article
- Controlled human exposures: a review and comparison of the health effects of diesel exhaust and wood smoke.Particle and fibre toxicology · 2024Review
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- CC16 drives VLA-2-dependent SPLUNC1 expression.Frontiers in immunology · 2023Article
- Club cell secretory protein and lung function in children with cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2022Article
- Vitamin D3 alleviates cigarette smoke extract-mediated epithelial-mesenchymal transition and fibrogenesis by upregulating CC16 expression in bronchial epithelial cells.Experimental and therapeutic medicine · 2022Article
- LKB1 deficiency upregulates RELM-α to drive airway goblet cell metaplasia.Cellular and molecular life sciences : CMLS · 2021Article
- CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells duringInternational journal of molecular sciences · 2021Article
- Very Late Antigen-4: A Novel Receptor for Club Cell Secretory Protein 16 to Control Inflammation.American journal of respiratory and critical care medicine · 2021Article
- Clara cell 16 KDa protein mitigates house dust mite-induced airway inflammation and damage via regulating airway epithelial cell apoptosis in a manner dependent on HMGB1-mediated signaling inhibition.Molecular medicine (Cambridge, Mass.) · 2021Article
- Repeated Administration of Clinically Relevant Doses of the Prescription Opioids Tramadol and Tapentadol Causes Lung, Cardiac, and Brain Toxicity in Wistar Rats.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Club Cell Protein 16 Attenuates CD16Journal of immunology research · 2021Article
- Early local neutralization of CC16 in sepsis‑induced ALI following blunt chest trauma leads to delayed mortality without benefitting overall survival.International journal of molecular medicine · 2020Article
- Renal dysfunction reduces the diagnostic and prognostic value of serum CC16 for acute respiratory distress syndrome in intensive care patients.BMC pulmonary medicine · 2020Observational
- Triterpene Acids of Loquat Leaf Improve Inflammation in Cigarette Smoking Induced COPD by Regulating AMPK/Nrf2 and NFκB Pathways.Nutrients · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Club cell protein (CC16) is expressed primarily by club cells possesses anti‑inflammatory properties and is located in the bronchiolar epithelium. Previous studies have demonstrated that CC16 deficiency is associated with the progression of chronic obstructive pulmonary disease (COPD). In the present study, the therapeutic effects of recombinant rat CC16 protein in mice with COPD were examined and the underlying mechanisms investigated. A total of 30 adult male C57/BL6 mice were randomly divided into three groups (10 mice/group). A mouse COPD model was generated by exposing 20 mice to cigarette smoke (CS) for 24 weeks. A total of 10 mice were treated intranasally with rCC16 (2.5 µg/g body weight) and control mice were exposed to normal room air. Results indicated that rCC16 treatment ameliorated pathological damage in the lungs and reduced the production of tumor necrosis factor (TNF)‑α, interleukin (IL)‑6 and IL‑8, which were induced by CS exposure. After rCC16 administration, endogenous CC16 was upregulated and the body weight of COPD mice was increased, whereas the opposite was observed in CS‑exposed mice. Additionally, rCC16 treatment inhibited the DNA binding of NF‑κB/p65 in lung tissues and reduced nuclear translocation of NF‑κB/p65 in BALF and epithelial cells. Moreover, rCC16 treatment lead to a decrease in the total number of BALF cells, including macrophages, which was elevated in COPD mice. In conclusion, the present results demonstrate that rCC16 has therapeutic effects on COPD by downregulating pro‑inflammatory factors via the NF‑κB pathway.
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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.