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<p>Mitochondrial dysfunction and altered reactive oxygen species (ROS) production contribute to the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the role of mitochondrial ROS (mtROS) in regulating cellular responses in the airway epithelium during disease exacerbations remains poorly understood. Herein, live-cell imaging was used to characterise mtROS induction in primary human bronchial epithelial cells (BECs) infected with rhinovirus (RV), a major cause of COPD exacerbations. Excessive mtROS production was observed following RV infection in BECs from donors with COPD as well as from donors without airway disease. Using a design-of-experiments (DoE) approach to optimise formulation parameters, a targeted antioxidant nanomedicine (TNM) was developed to inhibit mtROS production. TNM treatment of BECs from a donor with COPD significantly reduced RV infection- induced mtROS production. This was associated with increased expression of antiviral interferon-β (IFN-β), interferon-λ (IFN-λ2/3) and antiviral interferon-stimulated genes (ISGs). Interleukin-6 (IL-6) production was also increased, while the production of other pro-inflammatory cytokines was unaffected by TNM treatment. Together, these findings demonstrate that BEC- targeted antioxidant delivery uncovers a mechanism by which mtROS suppression can achieve innate immune modulation, representing an innovative therapeutic approach in COPD exacerbations.</p> Graphical abstract <p></p>

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A targeted antioxidant nanomedicine regulates mitochondrial ROS and antiviral immunity in rhinovirus-infected human bronchial epithelial cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月8日

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  • Thomas J. Adams,
  • Michael Schuliga,
  • Su Ling Loo,
  • Shan Mohanan,
  • Nyoaki Pearce,
  • Punnam C. Veerati,
  • Andrew T. Reid,
  • Nathan W. Bartlett,
  • Mingtao Liang

摘要

Mitochondrial dysfunction and altered reactive oxygen species (ROS) production contribute to the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the role of mitochondrial ROS (mtROS) in regulating cellular responses in the airway epithelium during disease exacerbations remains poorly understood. Herein, live-cell imaging was used to characterise mtROS induction in primary human bronchial epithelial cells (BECs) infected with rhinovirus (RV), a major cause of COPD exacerbations. Excessive mtROS production was observed following RV infection in BECs from donors with COPD as well as from donors without airway disease. Using a design-of-experiments (DoE) approach to optimise formulation parameters, a targeted antioxidant nanomedicine (TNM) was developed to inhibit mtROS production. TNM treatment of BECs from a donor with COPD significantly reduced RV infection- induced mtROS production. This was associated with increased expression of antiviral interferon-β (IFN-β), interferon-λ (IFN-λ2/3) and antiviral interferon-stimulated genes (ISGs). Interleukin-6 (IL-6) production was also increased, while the production of other pro-inflammatory cytokines was unaffected by TNM treatment. Together, these findings demonstrate that BEC- targeted antioxidant delivery uncovers a mechanism by which mtROS suppression can achieve innate immune modulation, representing an innovative therapeutic approach in COPD exacerbations.

Graphical abstract