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Long-term polystyrene nanoplastics exposure aggravates retinal inflammation and photoreceptor degeneration through microglial SPP1 signaling and neutrophil extracellular traps formation
Summary
Scientists found that when mice drank water containing nanoplastics (tiny plastic particles) for two months, it made eye damage from retinal detachment significantly worse by triggering harmful inflammation and immune cell activity in the retina. This matters because it's one of the first studies showing nanoplastics can cross into the eye and worsen a specific eye disease process, adding to growing evidence that everyday plastic pollution may have real consequences for our health beyond just general toxicity.
BACKGROUND: Micro/nanoplastics (MNPs), as emerging environmental contaminants, present a growing concern for human health. This study aims to investigate the effects of polystyrene nanoplastics (PS-NPs) exposure on retinal pathology and underlying mechanisms. METHODS: Retinal detachment (RD) model was established on adult mice following PS-NPs exposure (10 and 50 mg/L) through drinking water for two months. In vitro, oxygen glucose deprivation (OGD) model was established on BV2 microglia-661W photoreceptor co-culture system following PS-NPs exposure (100 mg/L) for 24 h. SPP1 neutralizing antibody and recombinant protein were administrated by subretinal injection. DNase I and Cl-amidine were utilized to achieve neutrophil extracellular traps (NETs) inhibition. Electroretinogram was used to assess retinal function. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), immunofluorescent staining, western blot analysis and enzyme activity assays were used to analyze photoreceptor apoptosis, microglial responses and oxidative stress. Microglia were purified with CD11b MicroBeads. Transcriptomic profiles of PS-NPs-exposed microglia and human retinas of proliferative vitreoretinopathy (PVR) were analyzed. RESULTS: PS-NPs were able to breach the blood-retina barrier, disrupt phototransduction, aggravate oxidative stress and apoptosis in RD-induced photoreceptor degeneration model dose-dependently. Mechanistically, PS-NPs exposure triggered retinal inflammation, microglial activation and microglial SPP1-mediated peripheral neutrophil recruitment. SPP1 neutralization mitigated PS-NPs-aggravated chemokine secretion, neutrophil infiltration and NETs formation. Recombinant SPP1 protein treatment heightened neutrophil-driven retinal damage, while this could be partially reversed by chemokine receptor inhibition. NETs inhibition alleviated PS-NPs-exacerbated microglial proinflammatory activation and photoreceptor degeneration. Furthermore, transcriptomic profiling showed parallels between PS-NPs-exposed microglia and human PVR specimens in SPP1 signaling and stress/stimulus response pathways. CONCLUSIONS: Our findings demonstrated that PS-NPs exposure aggravated retinal inflammation and photoreceptor degeneration by microglial SPP1 signaling activation and NETs formation, underscoring new insights into the effects and potential targets of MNPs exposure on retinal disorders.