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<p>Cigarette smoke (CS) is a major driver of chronic obstructive pulmonary disease (COPD), however also exposure to polystyrene nanoparticles (PS-NPs) may contribute to COPD development. This study investigated how cigarette smoke extract (CSE) influences epithelial responses to PS-NPs in vitro using BEAS-2B cells and human bronchial epithelial cells (16HBE). Cytotoxicity was evaluated through metabolic activity and lactate dehydrogenase (LDH) release. The proportion of PS-NP-positive cells after CSE exposure was assessed by immunofluorescence, flow cytometry and stable isotopes analysis. Epithelial barrier alterations were examined via transepithelial electrical resistance, dextran permeability, and tight junctions (TJ) analysis. In ALI-cultured 16HBE, epithelial integrity, goblet cells, ZO-1 and CXCL8 release were measured. CSE reduced epithelial barrier function through a decrease in TJ proteins which may account for the increased percentage of PS-NPs- positive cells observed in submerged conditions. Similar findings were also observed in ALI-cultured 16HBE cells, supporting the hypothesis that CSE is able to impair epithelial integrity. Moreover, CSE and PS-NPs led to a significant increase in goblet cell number but not an increase in CXCL8 release in ALI-16HBE. Our results suggest that combined exposure to CS and PS-NPs has a profound detrimental effect on the airway epithelium, which could facilitate lung diseases onset.</p>

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Cigarette smoke drives polystyrene nanoparticles-associated airway epithelial damage and chronic obstructive pulmonary disease-like features

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月28日

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  • Davida Mirra,
  • Francesca Panico,
  • Yiannis De Meersman,
  • Giuseppe Spaziano,
  • Simona Altieri,
  • Eleonora Caiazzo,
  • Ken R. Bracke,
  • Pasquale Iovino,
  • Raffaele Marfella,
  • Carmine Lubritto,
  • Giuseppe Paolisso,
  • Tania Maes,
  • Bruno D’Agostino

摘要

Cigarette smoke (CS) is a major driver of chronic obstructive pulmonary disease (COPD), however also exposure to polystyrene nanoparticles (PS-NPs) may contribute to COPD development. This study investigated how cigarette smoke extract (CSE) influences epithelial responses to PS-NPs in vitro using BEAS-2B cells and human bronchial epithelial cells (16HBE). Cytotoxicity was evaluated through metabolic activity and lactate dehydrogenase (LDH) release. The proportion of PS-NP-positive cells after CSE exposure was assessed by immunofluorescence, flow cytometry and stable isotopes analysis. Epithelial barrier alterations were examined via transepithelial electrical resistance, dextran permeability, and tight junctions (TJ) analysis. In ALI-cultured 16HBE, epithelial integrity, goblet cells, ZO-1 and CXCL8 release were measured. CSE reduced epithelial barrier function through a decrease in TJ proteins which may account for the increased percentage of PS-NPs- positive cells observed in submerged conditions. Similar findings were also observed in ALI-cultured 16HBE cells, supporting the hypothesis that CSE is able to impair epithelial integrity. Moreover, CSE and PS-NPs led to a significant increase in goblet cell number but not an increase in CXCL8 release in ALI-16HBE. Our results suggest that combined exposure to CS and PS-NPs has a profound detrimental effect on the airway epithelium, which could facilitate lung diseases onset.