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Polystyrene nanoparticle-induced keratinocyte death compromises skin barrier integrity and augments antigen-driven allergic skin inflammation in NC/Nga mice.
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Tiny 20-nanometer polystyrene plastic particles killed skin cells and weakened the skin barrier in lab tests on mouse skin cells. In mice, applying these particles with an allergen worsened allergic skin inflammation, increasing skin thickness, immune markers, and antibody levels compared to allergen alone.
BACKGROUND: Micro- and smaller plastic particles have been detected in human tissues, raising health concerns. Whereas some micro-sized particulates induce cell death through phagocytosis-dependent mechanisms, nanoparticulates-particularly those smaller than 100 nm-often exhibit marked phagocytosis-independent cytotoxicity. Given that the skin is exposed to environmental plastic particles, keratinocyte injury may impair barrier function and increase susceptibility to allergic diseases. We therefore investigated the size-dependent cytotoxicity of polystyrene (PS) particles in keratinocytes and their role in the development of allergic skin disease. METHODS: Mouse keratinocytes were exposed to 20-, 200-, or 2,000-nm PS particles (PS20, PS200, and PS2000), and cell death was analyzed. Barrier dysfunction was evaluated by 40-kDa dextran (FD40) permeability across PS20-treated keratinocyte monolayers. In vivo, PS20 and mite antigen were repeatedly co-applied to NC/Nga mouse skin and atopic dermatitis (AD)-like lesions, Th cytokine expression, skin permeability, and plasma mite antigen-specific IgE were assessed. RESULTS: PS20, not PS200 or PS2000, induced phagocytosis-independent keratinocyte death and increased FD40 flux across keratinocyte monolayer. In NC/Nga mice, repeated co-application of PS20 and mite antigen exacerbated AD-like lesions and increased ear thickness relative to antigen-only treatment. This co-application elevated ear interleukin (IL)-4 mRNA expression and plasma mite antigen-specific IgE levels. In this group, enhanced FD40 permeability was observed in areas with inflamed and collapsed epidermis as well as in histologically intact epidermis. CONCLUSIONS: PS nanoparticles approximately 20 nm in diameter induce phagocytosis-independent keratinocyte death, which may compromise the keratinocyte barrier and amplify antigen-driven Th2-skewed skin inflammation during co-exposure to antigens, potentially increasing AD susceptibility.
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