Environmental pollution (Barking, Essex : 1987)Jan 14, 2023

Polystyrene microplastics may cause lung damage in mice by activating immune response pathways

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 8, 2026

Abstract

Chronic exposure to small polystyrene microplastics (1-5 μm) causes severe inflammatory responses and lung damage in mice.

Histopathological analysis revealed significant inflammation, cell death, and collagen buildup in mouse lungs after exposure to polystyrene microplastics.
Smaller microplastic sizes (1-5 μm) caused more pronounced lung damage compared to larger sizes (10-20 μm).
Increased levels of TLR2 mRNA were observed, indicating a potential role in the inflammatory response triggered by microplastics.
Polystyrene microplastics heightened inflammation in human kidney cells identified by TLR2 expression.
Exposure to small microplastics led to increased oxidative stress and cell death, promoting lung fibrosis.
Blocking the NF-κB signaling pathway reduced inflammation and oxidative stress, limiting cell death and fibrosis progression.

Simplified

Microplastics are ubiquitous pollutants with a wide range of plastic applications. More recently, microplastics are in the air and can be inhaled into the lungs, causing respiratory diseases. Knowledge of the underlying mechanisms by which microplastics may induce respiratory disease is still limited. This study used intranasal instillation to develop a model of lung injury. The histopathology result showed that the mouse lung had severe inflammatory responses, apoptosis and collagen deposition with chronic exposure to different sizes (Small: 1-5 μm and Large: 10-20 μm) of polystyrene microplastics (PS-MPS), and the damage of smaller sizes was obvious. The expression levels of the Toll-like receptors (TLRs) family, evolutionarily conserved pattern recognition receptors, were detected, and the levels of TLR2 mRNA was significantly increased. In transfection experiments, PS-MPS increased the inflammatory response in HEK293 cells with TLR2 expression. Furthermore, exposure to small polystyrene microplastics promoted oxidative stress and apoptosis, and accelerated the process of fibrosis. Interestingly, inhibition of the NF-κB signal relieves inflammation and oxidative stress, reduces apoptosis, and thus controls the fibrosis process. These results suggested that PS-MPS targeted binding to TLR2 and further exacerbated fibrosis by facilitating inflammation, oxidative stress, and apoptosis with the activation of NF-κB signal.

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Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

PubMed

Polystyrene microplastics may cause lung damage in mice by activating immune response pathways

Abstract

Full Text

Funding

Competing interests

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Abstract

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