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Inhaled polystyrene microplastics impaired lung function through pulmonary flora/TLR4-mediated iron homeostasis
Huiwen Kang1, Danyang Huang1, Wei Zhang1
1Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China.
Abstract:
Microplastics (MPs) have been found in the air, human nasal cavity, and lung, suggesting that the respiratory tract is one of the important exposure routes for MPs. The lung is a direct target organ for injury from inhaled MPs, but data on lung injury from longer-term exposure to environmental doses of MPs are limited, and the mechanisms remain unclear. Here, C57BL/6 J mice were treated with 5 μm polystyrene (PS)-MPs by intratracheal instillation (0.6, 3, and 15 mg/kg) for 60 days to establish MPs exposure model. We found that PS-MPs lead to increased collagen fibers and decreased lung barrier permeability and lung function in lung tissue. Mechanistically, the abundance of gram-negative bacteria in the pulmonary flora increased after inhalation of PS-MPs, causing lipopolysaccharide (LPS) release. The expression of Toll-like receptor 4 (TLR4), the key receptor of LPS, was increased, and ferroptosis occurred in lung tissue cells. Further in vitro intervention experiments were performed, pulmonary flora/TLR4-induced imbalance of lung iron homeostasis is an important mechanism of PS-MPs-induced lung injury. Our study provides new evidence for lung injury caused by environmental doses of MPs and strategies to prevent it through longer-term dynamic observation.
Insights
Inhaled microplastics (MPs) cause lung injury by altering gut bacteria and triggering inflammation via Toll-like receptor 4 (TLR4). This research reveals ferroptosis as a key mechanism in MP-induced lung damage.
Area of Science:
- Environmental Health
- Toxicology
- Pulmonary Medicine
Background:
- Microplastics (MPs) are increasingly detected in the respiratory system, indicating inhalation as a significant exposure route.
- While the lungs are a direct target for inhaled MPs, data on long-term, environmentally relevant exposure effects and underlying mechanisms are scarce.
Purpose of the Study:
- To investigate the long-term effects of environmental doses of microplastics on lung injury.
- To elucidate the mechanisms behind microplastic-induced lung damage, focusing on pulmonary flora and cellular responses.
Main Methods:
- Establishment of a 60-day microplastic exposure model in C57BL/6J mice using intratracheal instillation of 5 μm polystyrene (PS)-MPs at varying doses (0.6, 3, 15 mg/kg).
- Assessment of lung tissue for collagen fiber content, barrier permeability, lung function, bacterial abundance, lipopolysaccharide (LPS) levels, Toll-like receptor 4 (TLR4) expression, and ferroptosis.
- In vitro experiments to confirm the role of pulmonary flora and TLR4 in microplastic-induced lung injury and iron homeostasis imbalance.
Main Results:
- PS-MPs exposure led to increased collagen fibers, reduced lung barrier permeability, and impaired lung function.
- Inhalation of PS-MPs increased gram-negative bacteria in pulmonary flora, leading to lipopolysaccharide (LPS) release.
- Increased TLR4 expression and ferroptosis were observed in lung tissue cells, indicating a mechanism involving LPS/TLR4 signaling and iron dysregulation.
Conclusions:
- Longer-term exposure to environmental doses of microplastics induces lung injury.
- Pulmonary flora alterations, LPS release, TLR4 activation, and subsequent ferroptosis due to imbalanced lung iron homeostasis are key mechanisms in microplastic-induced lung injury.
- This study provides critical evidence for microplastic-induced lung damage and suggests potential preventative strategies.
