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Human Turbinate Mesenchymal Stromal Cell-Derived Exosomes Alleviate PM2.5-Induced Pyroptosis via Promoting Mitophagy
Jooin Bang1, Hyunsu Choi2, Yaegi Song1
1Department of Otolaryngology-Head and Neck Surgery, College of Medicine, The Catholic University of Korea. Eunpyeong St. Mary's Hospital, 1021 Tongil-ro, Eunpyeong-gu, Seoul, Republic of Korea.
Abstract:
Chronic laryngitis is a persistent inflammatory disorder that has recently been linked to air pollution. Fine particulate matter (PM2.5) is a major air pollutant capable of inducing pyroptosis, a caspase-1-dependent inflammatory form of programmed cell death characterized by gasdermin D cleavage, plasma membrane rupture, and the release of proinflammatory cytokines. However, the mechanisms underlying PM2.5-induced pyroptosis in the larynx and the potential therapeutic strategies remain unclear. In this study, we investigated the protective effects of human turbinate mesenchymal stromal cell-derived exosomes (hTMSC-exos) on PM2.5-induced pyroptosis in human vocal fold fibroblasts (hVFFs). PM2.5 exposure triggered pyroptotic cell death, as evidenced by increased LDH release, PI positivity, GSDMD-N expression, and IL-1β and IL-18 secretion. It also induced excessive reactive oxygen species (ROS) production, disrupted mitochondrial function, and impaired mitophagy, as indicated by p62 accumulation and suppressed PINK1/Parkin expression. Treatment with hTMSC-exos significantly alleviated these effects, reducing pyroptosis markers, lowering ROS production, and preserving mitochondrial membrane potential. Mechanistically, hTMSC-exos restored mitophagy activity suppressed by PM2.5, as demonstrated by increased LC3-II, PINK1, and Parkin expression and decreased p62 levels. Fluorescence imaging further confirmed enhanced co-localization of mitochondria with LC3-II. Importantly, the protective effects of hTMSC-exos were abolished by the mitophagy-specific inhibitor cyclosporin A, confirming that mitophagy activation is essential for exosome-mediated protection. These findings suggest that hTMSC-exos attenuate PM2.5-induced pyroptosis through a mitophagy-dependent mechanism, providing new insight into the pathogenesis of environmentally induced laryngeal injury and highlighting the therapeutic potential of exosome-based approaches for chronic laryngitis.
Insights
Human turbinate mesenchymal stromal cell-derived exosomes (hTMSC-exos) protect against air pollution-induced chronic laryngitis. hTMSC-exos mitigate pyroptosis and restore mitophagy in vocal fold cells damaged by fine particulate matter (PM2.5).
Area of Science:
- Cell Biology
- Environmental Health
- Toxicology
Background:
- Chronic laryngitis is linked to air pollution, specifically fine particulate matter (PM2.5).
- PM2.5 induces pyroptosis, a programmed cell death pathway, in laryngeal cells.
- Mechanisms of PM2.5-induced laryngeal pyroptosis and potential therapies are not well understood.
Purpose of the Study:
- To investigate the protective effects of human turbinate mesenchymal stromal cell-derived exosomes (hTMSC-exos) against PM2.5-induced pyroptosis in human vocal fold fibroblasts (hVFFs).
- To elucidate the underlying mechanisms of hTMSC-exos-mediated protection, focusing on mitophagy.
Main Methods:
- PM2.5 exposure was used to induce pyroptosis in hVFFs.
- hTMSC-exos treatment was administered to PM2.5-exposed hVFFs.
- Pyroptosis markers (LDH, PI, GSDMD-N, IL-1β, IL-18), reactive oxygen species (ROS), mitochondrial function, and mitophagy markers (p62, PINK1, Parkin, LC3-II) were assessed.
- The role of mitophagy was confirmed using a specific inhibitor (cyclosporin A).
Main Results:
- PM2.5 exposure induced pyroptosis, increased ROS, disrupted mitochondrial function, and impaired mitophagy in hVFFs.
- hTMSC-exos treatment significantly reduced pyroptosis markers, ROS levels, and preserved mitochondrial function.
- hTMSC-exos restored mitophagy by increasing key protein expression and mitochondrial-LC3-II co-localization.
- Inhibition of mitophagy abolished the protective effects of hTMSC-exos.
Conclusions:
- hTMSC-exos attenuate PM2.5-induced pyroptosis in laryngeal cells via a mitophagy-dependent mechanism.
- This study provides insights into environmentally induced laryngeal injury pathogenesis.
- hTMSC-exos represent a potential therapeutic strategy for chronic laryngitis linked to air pollution.
