PLGA from PolySciTech used in development of Mito-TEMPO loaded nanoparticle treatment for COPD

 

Chronic obstructive pulmonary disease (COPD) is an ongoing lung condition caused by damage to the lungs. The damage results in swelling and irritation, also called inflammation, inside the airways. Researchers at University of Newcastle used PLGA (AP041) from PolySciTech division of Akina, Inc. (www.PolySciTech.com) to generate antioxidant loaded nanoparticles for therapy of this chronic disease. Read more: Adams, Thomas J., Michael Schuliga, Su Ling Loo, Shan Mohanan, Nyoaki Pearce, Punnam C. Veerati, Andrew T. Reid, Nathan W. Bartlett, and Mingtao Liang. "A targeted antioxidant nanomedicine regulates mitochondrial ROS and antiviral immunity in rhinovirus-infected human bronchial epithelial cells." Drug Delivery and Translational Research (2026): 1-16. https://link.springer.com/article/10.1007/s13346-026-02182-x

“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.”

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