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Microglial phagocytosis of polystyrene microplastics results in immune alteration and apoptosis in vitro and in vivo
Summary
Researchers found that polystyrene microplastics can cross the blood-brain barrier in mice after oral exposure and accumulate in brain tissue, where they are engulfed by microglia, the brain's immune cells. This engulfment triggered inflammatory responses and cell death in the microglia both in cell cultures and in living mice. The study suggests that microplastic exposure may affect brain immune function, with potential implications for neurological health.
The remarkable increase in plastic usage and widespread microplastic (MP) pollution has emerged as a substantial concern today. Many recent studies have revealed MPs as potentially hazardous substances in mammals. Despite several reports on the impact of small MPs in the brain and behaviors in aquatic animals, it is still unclear how small MPs affect the brain and its underlying cellular physiology in terrestrial animals. In this study, we investigated the accumulation of polystyrene MPs (PS-MPs) in mouse brain after oral treatment using three types of fluorescent PS-MPs of different sizes (0.2,2 and 10 μm). We found that PS-MPs were deposited in microglial cells of the brain. Following differential treatment of PS-MPs in human microglial HMC-3 cells, we identified changes in cellular morphology, immune responses, and microglial apoptosis induced by phagocytosis of 0.2 and 2 μm PS-MPs. By analyzing the PS-MP-treated HMC-3 cell transcriptome, we showed that PS-MPs treatment altered the expression of clusters of immune response genes, immunoglobulins, and several related microRNAs. In addition, we confirmed alterations in microglial differentiation marker expression with the activation of NF-κB, pro-inflammatory cytokines and apoptotic markers in PS-MP-treated human microglial cells and in mouse brain. Our findings suggest a potential risk of small PS-MPs in microglial immune activation, which leads to microglial apoptosis in murine and human brains.