Serum from patients with chronic obstructive pulmonary disease induces senescence-related phenotype in bronchial epithelial cells

Sci Rep. 2018 Aug 28;8(1):12940. doi: 10.1038/s41598-018-31037-w.


Chronic obstructive pulmonary disease (COPD) is a risk factor for the development of lung cancer (LC). The mechanism of interplay between both diseases remains poorly recognized. This report examines whether COPD may cause a senescence response in human bronchial epithelial cells (HBECs), leading to the progression of LC in a senescence-dependent manner. The results show that HBECs exposed to serum from COPD patients manifest increased expression of markers of cellular senescence, including senescence-associated β-galactosidase (SA-β-Gal), histone γ-H2A.X, and p21, as compared to the serum of healthy donors. This effect coincides with an increased generation of reactive oxygen species by these cells. The clinical analysis demonstrated that COPD may cause the senescence, independently on smoking status and disease severity. The concentrations of CXCL5, CXCL8/IL-8 and VEGF were higher in conditioned medium (CM) harvested from HBECs after exposure to COPD serum as compared to controls. In addition, CM treated with serum from COPD patients stimulated adhesion of A549 cancer cells to HBECs, as well as accelerating cancer cell proliferation and migration in vitro. Collectively, these findings indicate that COPD may induce senescence-like changes in HBECs and thus enhance some processes associated with the progression of lung cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Antigens, Differentiation / metabolism
  • Bronchi / metabolism*
  • Bronchi / pathology
  • Cells, Cultured
  • Cellular Senescence*
  • Cytokines / metabolism
  • Epithelial Cells / metabolism*
  • Epithelial Cells / pathology
  • Female
  • Humans
  • Male
  • Middle Aged
  • Pulmonary Disease, Chronic Obstructive / blood*
  • Pulmonary Disease, Chronic Obstructive / pathology
  • Serum*


  • Antigens, Differentiation
  • Cytokines