Open Access

Recombinant club cell protein 16 (CC16) ameliorates cigarette smoke‑induced lung inflammation in a murine disease model of COPD

  • Authors:
    • Min Pang
    • Hong‑Yan Liu
    • Ting Li
    • Dan Wang
    • Xiao‑Yun Hu
    • Xin‑Ri Zhang
    • Bao‑Feng Yu
    • Rui Guo
    • Hai‑Long Wang
  • View Affiliations

  • Published online on: June 25, 2018     https://doi.org/10.3892/mmr.2018.9216
  • Pages: 2198-2206
  • Copyright: © Pang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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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August-2018
Volume 18 Issue 2

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Pang M, Liu HY, Li T, Wang D, Hu XY, Zhang XR, Yu BF, Guo R and Wang HL: Recombinant club cell protein 16 (CC16) ameliorates cigarette smoke‑induced lung inflammation in a murine disease model of COPD. Mol Med Rep 18: 2198-2206, 2018.
APA
Pang, M., Liu, H., Li, T., Wang, D., Hu, X., Zhang, X. ... Wang, H. (2018). Recombinant club cell protein 16 (CC16) ameliorates cigarette smoke‑induced lung inflammation in a murine disease model of COPD. Molecular Medicine Reports, 18, 2198-2206. https://doi.org/10.3892/mmr.2018.9216
MLA
Pang, M., Liu, H., Li, T., Wang, D., Hu, X., Zhang, X., Yu, B., Guo, R., Wang, H."Recombinant club cell protein 16 (CC16) ameliorates cigarette smoke‑induced lung inflammation in a murine disease model of COPD". Molecular Medicine Reports 18.2 (2018): 2198-2206.
Chicago
Pang, M., Liu, H., Li, T., Wang, D., Hu, X., Zhang, X., Yu, B., Guo, R., Wang, H."Recombinant club cell protein 16 (CC16) ameliorates cigarette smoke‑induced lung inflammation in a murine disease model of COPD". Molecular Medicine Reports 18, no. 2 (2018): 2198-2206. https://doi.org/10.3892/mmr.2018.9216