Open Access

Nicotine promotes chronic obstructive pulmonary disease via inducing pyroptosis activation in bronchial epithelial cells

  • Authors:
    • Rubing Mo
    • Jun Zhang
    • Yongxing Chen
    • Yipeng Ding
  • View Affiliations

  • Published online on: January 18, 2022     https://doi.org/10.3892/mmr.2022.12608
  • Article Number: 92
  • Copyright: © Mo et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Nicotine is one of the primary components in cigarettes, which is responsible for addiction. Numerous studies have investigated the effects of nicotine on pulmonary disease. The health of epithelial cells is important in the development of chronic obstructive pulmonary disease (COPD). Accumulating evidence has suggested that epithelial cell death may initiate or contribute to the progression of a number of lung diseases via airway remodeling. Pyroptosis is a unique form of inflammatory cell death mediated by the activation of caspase‑1 and the NOD‑like receptor protein‑3 (NLRP3) inflammasome. The present study aimed to evaluate whether pyroptosis of epithelial cells was involved in the progression of COPD. The normal human bronchial epithelial cell line 16HBE was treated with 0.1 or 1 µM nicotine. Then the proliferation ability of 16HBE cells was detected by CCK‑8. Cell death was detected by flow cytometry analysis and TUNEL assay. Subsequently, the levels of pro‑caspase 1, caspase 1, IL‑1β, IL‑18, NLRP3, ASC and cleaved GSDMD were examined by western blotting. It was revealed that nicotine treatment significantly induced cell death and suppressed proliferation of 16HBE cells. Furthermore, nicotine exposure increased the expression levels of caspase‑1, IL‑1β, IL‑18, NLRP3, apoptosis‑associated speck‑like protein and gasdermin D in 16HBE cells. Therefore, the present study concluded that nicotine treatment induced pyroptosis in 16HBE cells, which may be associated with the progression of COPD.
View Figures
View References

Related Articles

Journal Cover

March-2022
Volume 25 Issue 3

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

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Mo R, Zhang J, Chen Y and Ding Y: Nicotine promotes chronic obstructive pulmonary disease via inducing pyroptosis activation in bronchial epithelial cells. Mol Med Rep 25: 92, 2022.
APA
Mo, R., Zhang, J., Chen, Y., & Ding, Y. (2022). Nicotine promotes chronic obstructive pulmonary disease via inducing pyroptosis activation in bronchial epithelial cells. Molecular Medicine Reports, 25, 92. https://doi.org/10.3892/mmr.2022.12608
MLA
Mo, R., Zhang, J., Chen, Y., Ding, Y."Nicotine promotes chronic obstructive pulmonary disease via inducing pyroptosis activation in bronchial epithelial cells". Molecular Medicine Reports 25.3 (2022): 92.
Chicago
Mo, R., Zhang, J., Chen, Y., Ding, Y."Nicotine promotes chronic obstructive pulmonary disease via inducing pyroptosis activation in bronchial epithelial cells". Molecular Medicine Reports 25, no. 3 (2022): 92. https://doi.org/10.3892/mmr.2022.12608