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Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through
Jinming Zhang1, Jiangzhou Du1, Dongyu Liu1
1Chronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Abstract:
Polystyrene microplastics (PS-MPs) are new types of environmental pollutant that have garnered significant attention in recent years since they were found to cause damage to the human respiratory system when they are inhaled. The pulmonary fibrosis is one of the serious consequences of PS-MPs inhalation. However, the impact and underlying mechanisms of PS-MPs on pulmonary fibrosis are not clear. In this study, we studied the potential lung toxicity and PS-MPs-developed pulmonary fibrosis by long-term intranasal inhalation of PS-MPs. The results showed that after exposing to the PS-MPs, the lungs of model mouse had different levels of damage and fibrosis. Meanwhile, exposing to the PS-MPs resulted in a markedly decrease in glutathione (GSH), an increase in malondialdehyde (MDA), and iron overload in the lung tissue of mice and alveolar epithelial cells (AECs). These findings suggested the occurrence of PS-MP-induced ferroptosis. Inhibitor of ferroptosis (Fer-1) had alleviated the PS-MPs-induced ferroptosis. Mechanically, PS-MPs triggered cell ferroptosis and promoted the development of pulmonary fibrosis via activating the cGAS/STING signaling pathway. Inhibition of cGAS/STING with G150/H151 attenuated pulmonary fibrosis after PS-MPs exposure. Together, these data provided novel mechanistic insights of PS-MPs-induced pulmonary fibrosis and a potential therapeutic paradigm.
Insights
Inhaled polystyrene microplastics (PS-MPs) cause lung damage and fibrosis by inducing ferroptosis. Inhibiting ferroptosis or the cGAS/STING pathway may offer therapeutic strategies for PS-MP lung toxicity.
Area of Science:
- Environmental Science
- Toxicology
- Pulmonary Medicine
Background:
- Polystyrene microplastics (PS-MPs) are emerging environmental pollutants.
- Inhalation of PS-MPs can lead to respiratory system damage, including pulmonary fibrosis.
- The precise mechanisms of PS-MP-induced lung toxicity remain unclear.
Purpose of the Study:
- To investigate the lung toxicity and mechanisms of pulmonary fibrosis induced by long-term intranasal inhalation of PS-MPs.
- To explore the role of ferroptosis in PS-MP-induced lung injury.
- To elucidate the signaling pathways involved in PS-MP-mediated pulmonary fibrosis.
Main Methods:
- Long-term intranasal inhalation exposure of model mice to PS-MPs.
- Assessment of lung damage and fibrosis.
- Measurement of glutathione (GSH), malondialdehyde (MDA), and iron levels in lung tissue and alveolar epithelial cells (AECs).
- Administration of ferroptosis inhibitor (Fer-1) and cGAS/STING inhibitors (G150/H151).
Main Results:
- PS-MP exposure caused significant lung damage and fibrosis in mice.
- PS-MPs induced ferroptosis, evidenced by decreased GSH, increased MDA, and iron overload in lung tissues and AECs.
- Inhibition of ferroptosis with Fer-1 alleviated PS-MP-induced lung injury.
- PS-MPs activated the cGAS/STING signaling pathway, promoting ferroptosis and pulmonary fibrosis.
- Inhibition of cGAS/STING attenuated PS-MP-induced pulmonary fibrosis.
Conclusions:
- PS-MPs induce pulmonary fibrosis through ferroptosis, involving the cGAS/STING signaling pathway.
- Ferroptosis and cGAS/STING pathway inhibition represent potential therapeutic strategies for PS-MP-induced lung toxicity.
- This study provides novel mechanistic insights into the pulmonary effects of microplastic inhalation.
