Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice.

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.