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Polystyrene nanoplastics exacerbate systemic lupus erythematosus via neutrophil extracellular traps (NETs) formation
Summary
Tiny plastic particles called nanoplastics—found widely in our environment—may make autoimmune diseases like lupus worse, according to new research in mice and human blood samples. Scientists found that these plastic particles cause certain immune cells (neutrophils) to release web-like traps that trigger inflammation, worsening organ damage and disease symptoms at exposure levels similar to what people encounter in daily life. While this study was done in mice and lab-grown cells, it raises real concerns about how ordinary environmental plastic exposure could impact people already living with autoimmune conditions.
Nanoplastics (NPs) are ubiquitous environmental pollutants capable of penetrating biological barriers and disrupting immune homeostasis. However, their immunotoxic potential to trigger or exacerbate autoimmune diseases (AIDs), such as systemic lupus erythematosus (SLE), remains largely unexplored. Herein, using polystyrene NPs (PS-NPs) as a model, we systematically investigated their immunotoxicity and underlying mechanisms exacerbating SLE progression via neutrophil extracellular traps (NETs). Initiating with human data, we observed that SLE patients exhibited significantly decreased neutrophils and increased serum NETs, closely correlating with disease activity. In vitro toxicological assessments revealed that neutrophils rapidly internalized PS-NPs, triggering concentration- and time-dependent cell death specifically driven by NET formation. In vivo, using environmentally relevant, human-equivalent exposure doses, orally administered PS-NPs heavily accumulated in the liver and kidneys of lupus-prone mice. This exposure dose-dependently elevated systemic NET levels and profoundly aggravated SLE manifestations, including severe renal lesions, hepatosplenomegaly, and elevated autoantibodies levels. Furthermore, serum metabolomic profiling uncovered that PS-NPs amplified lipid and amino acid dysregulation, highlighting a metabolic dimension to NP-induced immunotoxicity. Crucially, pharmacological inhibition of this pathway using cyclophosphamide (CTX) or dihydroartemisinin (DHA) successfully mitigated the PS-NPs-exacerbated phenotypes, supporting the potential involvement of NETs in this environmental toxicity. Collectively, our findings identify environmental PS-NP exposure as a significant risk factor for AID exacerbation, providing critical mechanistic evidence to inform human health risk assessments for susceptible populations.