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Abstract <p>Air pollution remains a major environmental challenge, largely driven by urban dust composed of suspended solid particles of diverse origins and chemical compositions. Particulate matter (PM<sub>2.5</sub>) and ultrafine urban dust nanoparticles (NPs), with diameters smaller than 2.5&#xa0;μm and 100&#xa0;nm, respectively, pose a particular threat to human health. In this study, we present the first evidence that NPs induce pro-inflammatory activation of human bronchial epithelial cells. Exposure to non-cytotoxic concentrations of NPs led to a significant increase in the mRNA levels of pro-inflammatory markers IL-8, IL-1β, IL-6, and ICAM-1, accompanied by increased secretion of the cytokines IL-8 and IL-6. Heat treatment of NPs, which removed their organic components, completely abolished their ability to stimulate cytokine secretion. NP-induced upregulation of pro-inflammatory gene expression depended on both surface-adsorbed organic compounds and inorganic particle constituents.</p>

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Urban Dust Nanoparticles Induce Proinflammatory Activation of Human Bronchial Epithelial Cells

  • 期刊论文

  • 发表日期：

    2026年2月1日

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  • Anna A. Dashkevich,
  • Lyudmila A. Zinovkina,
  • Alexander I. Ivaneev,
  • Mikhail S. Ermolin,
  • Petr S. Fedotov,
  • Boris V. Chernyak,
  • Roman A. Zinovkin

摘要

Abstract

Air pollution remains a major environmental challenge, largely driven by urban dust composed of suspended solid particles of diverse origins and chemical compositions. Particulate matter (PM2.5) and ultrafine urban dust nanoparticles (NPs), with diameters smaller than 2.5 μm and 100 nm, respectively, pose a particular threat to human health. In this study, we present the first evidence that NPs induce pro-inflammatory activation of human bronchial epithelial cells. Exposure to non-cytotoxic concentrations of NPs led to a significant increase in the mRNA levels of pro-inflammatory markers IL-8, IL-1β, IL-6, and ICAM-1, accompanied by increased secretion of the cytokines IL-8 and IL-6. Heat treatment of NPs, which removed their organic components, completely abolished their ability to stimulate cytokine secretion. NP-induced upregulation of pro-inflammatory gene expression depended on both surface-adsorbed organic compounds and inorganic particle constituents.