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Exposure to polystyrene nanoplastics induces abnormal activation of innate immunity via the cGAS-STING pathway
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Polystyrene nanoplastics triggered an abnormal immune response in mouse cells by activating a specific signaling pathway called cGAS-STING, which normally defends against viruses and damaged DNA. This activation led to inflammation through the NF-kB pathway, and when researchers silenced the STING gene, the inflammatory response was significantly reduced. The study reveals a new mechanism by which nanoplastics could cause chronic inflammation in the body.
Endogenous immune defenses provide an intrinsic barrier against external entity invasion. Microplastics in the environment, especially those at the nanoscale (nanoplastics or NPs), may pose latent health risks through direct exposure. While links between nanoplastics and inflammatory processes have been established, detailed insights into how they may perturb the innate immune mechanisms remain uncharted. Employing murine and macrophage (RAW264.7) cellular models subjected to polystyrene nanoplastics (PS-NPs), our investigative approach encompassed an array of techniques: Cell Counting Kit-8 assays, flow cytometric analysis, acridine orange/ethidium bromide (AO/EB) fluorescence staining, cell transfection, cell cycle scrutiny, genetic manipulation, messenger RNA expression profiling via quantitative real-time PCR, and protein expression evaluation through western blotting. The results showed that PS-NPs caused RAW264.7 cell apoptosis, leading to cell cycle arrest, and activated the cGAS-STING pathway. This resulted in NF-κB signaling activation and increased pro-inflammatory mediator expression. Importantly, PS-NPs-induced activation of NF-κB and its downstream inflammatory cascade were markedly diminished after the silencing of the STING gene. Our findings highlight the critical role of the cGAS-STING pathway in the immunotoxic effects induced by PS-NPs. We outline a new mechanism whereby nanoplastics may trigger dysregulated innate immune and inflammatory responses via the cGAS/STING pathway.
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Researchers exposed mice to polystyrene nanoplastics through nasal administration and studied the resulting lung damage over seven days. They found that the nanoplastics triggered oxidative stress, programmed cell death, and inflammatory responses in lung tissue through activation of the cGAS-STING-NLRP3 signaling pathway. The study provides evidence that inhaled nanoplastics can cause acute lung injury through specific molecular mechanisms involving both apoptosis and pyroptosis.
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Researchers found that tiny polystyrene microplastics (0.1 micrometers) can enter liver cells and cause DNA damage that triggers a chain reaction leading to liver scarring, known as fibrosis. The microplastics activated a specific immune signaling pathway called cGAS/STING, which caused inflammation that progressively damaged liver tissue even at low concentrations. This study reveals a specific mechanism by which long-term microplastic exposure could lead to serious liver disease in humans.
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