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Chemokine–complement cascade in glial–vascular units protects neurons from non-biogenic nanoparticles
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Researchers discovered that the developing mouse brain mounts a coordinated immune defense against non-biogenic nanoparticles — including polystyrene — through a vascular-glial signaling cascade where endothelial CCL17 triggers astrocytic complement production, enabling microglia to engulf nanoparticles; disrupting this pathway increased neuronal loss and anxiety-like behavior.
Non-biogenic nanoparticles (NPs), including silica and polystyrene, are major components of environmental particulate pollution and can accumulate in the brain, especially during development when the blood-brain barrier is immature, leading to neurotoxicity. However, protective responses within the brain to these NPs remain poorly understood. Here, using a developing mouse model, we show that microglia phagocytose non-biogenic NPs through a complement-dependent mechanism involving C3 tagging. This process is regulated by a chemokine cascade in which vascular endothelial cells release CCL17, activating CCR4 on perivascular astrocytes to promote astrocytic C3 production. Inhibition of CCR4 signaling suppresses C3 production, impairs microglial phagocytosis, increases neuronal loss, and exacerbates anxiety-like behaviors. Our data establish a protective role for the vascular-glial chemokine-complement axis in limiting neurotoxicity during brain development. These findings reveal a coordinated immune response to non-biogenic environmental NPs and uncover a vascular-glial mechanism that mitigates NP-induced brain injury.
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Exposure to microplastics/ nanoplastics induces responses of microglia and astrocytes: roles of oxidative stress and autophagy
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This study investigated how microplastic and nanoplastic exposure affects glial cells including microglia and astrocytes in the central nervous system, which are essential for neurological immune defense and homeostasis. Exposure triggered reactive responses in both cell types, raising concern that plastic particle accumulation in the brain could contribute to neuroinflammation.
Primary astrocytes as a cellular depot of polystyrene nanoparticles
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Researchers found that astrocytes — support cells in the brain — absorb polystyrene nanoplastics far more efficiently than neurons and act as a cellular buffer to protect nerve cells, but become overactivated when the particle load is too high, losing their protective function and potentially contributing to neurological harm.
Exposure to microplastics/ nanoplastics induces responses of microglia and astrocytes: roles of oxidative stress and autophagy
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This study examined how microplastic and nanoplastic exposure affects glial cells in the central nervous system, specifically investigating responses of microglia and astrocytes, which are the brain's primary immune and support cells. Results showed that micro- and nanoplastic exposure triggered inflammatory-type responses in these cells, raising concern for neurological effects.
Neurotoxic potential of polystyrene nanoplastics in primary cells originating from mouse brain
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Researchers exposed three types of primary mouse brain cells to 100 nm polystyrene nanoplastics and found that neurons underwent apoptosis while astrocytes survived but developed reactive astrocytosis with elevated inflammatory markers, suggesting that neuronal vulnerability to nanoplastic accumulation may be amplified by astrocyte-driven neuroinflammation.
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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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.