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Polystyrene nanoplastics induce transient microglial activation via endolysosomal retention in the mouse cortex
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Tiny plastic particles from everyday pollution can reach the brain and temporarily rev up its immune cells, according to a mouse study, with larger particles causing more disruption to genes involved in brain signaling. This suggests that as microplastics build up in our environment, they may quietly affect brain health, even after exposure stops, making plastic pollution a growing concern worth watching.
Environmental degradation and accumulation of plastics results in micro- and nanoplastics that are small enough to cross biological barriers, including the blood-brain barrier. Microglia, resident immune cells of the 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; 1.5 mg/day) showed the presence of both PS-NPs sizes in the cerebral cortex without overt histopathological damage. However, cortical microglia showed pronounced morphological remodeling, assessed by Sholl and Skeleton analyses. Transcriptomic profiling of cortical tissue revealed a strong size-dependent response. The 100 nm PS-NPs group revealed 18 DEGs (|log₂FC= ≥ 2, padj < 0.05), whereas the 500 nm PS-NPs showed more than 4000 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). Using BV2 microglial cells, data indicate size dependent internalization of PS-NPs via the endolysosomal pathway. While both the 100 and 500 nm particles were present in late endosomes, only the 100 nm particles were found in lysosomes. 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 reached cortical regions of the brain, driving size-dependent microglial activation and transcriptomic reprogramming, even after cessation of exposure to PS-NPs.
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Adverse interactions of plastic nanoparticles with cultured primary microglial cells.
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Tiny plastic particles from broken-down polystyrene (a common plastic) can get absorbed into brain immune cells called microglia, causing stress damage and triggering inflammation, according to lab tests on these cells. This matters because microglia act as the brain's cleanup crew and first line of defense, so if microplastics cause them to malfunction, it could contribute to brain inflammation linked to neurological problems—though this study was done in isolated cells, not in living people, so more research is needed to know exactly what this means for human brain health.
Neurotoxic effects of polystyrene nanoplastics on memory and microglial activation: Insights from in vivo and in vitro studies
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In a mouse study, tiny nanoplastics (30-50 nanometers) that were swallowed reached the brain and caused memory problems by activating the brain's immune cells, called microglia, which triggered inflammation. This is concerning because it shows that nanoplastics small enough to be found in everyday products like cosmetics could cross into the brain and impair cognitive function.
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.
Polystyrene nanoplastics penetrate across the blood-brain barrier and induce activation of microglia in the brain of mice
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Researchers demonstrated that 50-nanometer polystyrene nanoplastics can cross the blood-brain barrier in mice, accumulate in brain tissue, and activate immune cells called microglia that then damage neurons. The nanoplastics disrupted the tight junctions that normally protect the brain, creating openings for the particles to pass through. This study provides direct evidence that nanoplastics can reach the brain and trigger inflammation, raising concerns about potential neurological effects of long-term nanoplastic exposure in humans.
Microglial phagocytosis of polystyrene microplastics results in immune alteration and apoptosis in vitro and in vivo
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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.
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