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Polystyrene Nanoplastics Accumulate in Murine Cortex and Induce Transient Microglial Activation via Endolysosomal Retention
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Polystyrene nanoplastics accumulated in mouse cerebral cortex after 60 days of exposure and triggered microglial activation and thousands of differentially expressed genes, including downregulation of synaptic signaling genes, in a particle-size-dependent manner. These findings provide mechanistic evidence that nanoplastics can cross the blood-brain barrier, activate neuroinflammation, and disrupt neural function, raising serious concerns about long-term neurological health impacts from chronic plastic exposure.
Abstract Environmental degradation and accumulation of plastics results in micro- and nanoplastics (MNPLs) that are small enough to cross biological barriers, including the blood–brain barrier. Microglia, resident immune cells of brain, are critical regulators of neuroimmune homeostasis and represent a cellular target of nanoplastic exposure. In this study, we assessed the neurotoxic effects of two sizes of polystyrene nanoplastics (PS-NPs; 100 nm and 500 nm) using integrated in vivo and in vitro exposure and washout paradigms. In vivo exposure in mice (60 days; 0.15 or 1.5 mg/day) showed the accumulation of both PS-NP sizes in the cerebral cortex without histopathological damage. However, cortical microglia showed pronounced morphological remodeling, observed as increased expression of Iba1 and GFAP. Transcriptomic profiling of cortical tissue revealed a strong size-dependent response. The 100 nm PS-NP group revealed 18 DEGs (|log 2 FC| ≥ 2, padj < 0.05), whereas the 500 nm PS-NPs showed more than 4,000 DEGs, including upregulation of immune- and microglia-associated genes (CCL5, CXCL10, LCN2, LYZ2) and downregulation of synaptic and neuronal signaling genes (GRIN2B, SYN1, STX1B, MAP1B, ITPR1/2). In vitro assessment, using BV2 microglia cells, showed internalization of PS-NPs via the endolysosomal pathway, with strong co-localization to Rab7- and LAMP2-positive compartments and prolonged intracellular retention following exposure washout. Also, microglial activation markers (Iba1, CD68) exhibited a transient, size- and concentration-dependent increase, correlated with intracellular particle burden rather than cumulative exposure. Overall, these findings demonstrate that PS-NPs accumulate in brain, driving size-dependent microglia activation and transcriptomic reprogramming, even after cessation of exposure to PS-NPs. Highlights PS-NPs (100 nm and 500 nm) reach mouse cerebral cortex following 60-day oral exposure. PS-NPs were internalized by microglia; accumulated in endolysosomal compartments. PS-NP exposure induced transient microglial activation without sustained cytotoxicity. Microglial activation was correlated with intracellular PS-NPs burden. Transcriptomics revealed disruption of neuroimmune and microglial regulatory pathways.
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