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Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism
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Mice given long-term exposure to micro and nanoplastics showed that immune cells in the liver, called Kupffer cells, absorbed these particles, changing their activity and disrupting liver metabolism. Microplastics reduced the liver cells' ability to clear bacteria and worsened fat buildup in obese mice, while nanoplastics affected blood sugar control and reached the brain in small amounts without causing inflammation or behavior changes.
Abstract Plastic pollution is an emerging yet understudied environmental risk to the immune system. Once ingested, nano- and microplastic particles (MNPs) can translocate from the gut to internal organs, with macrophages serving as primary targets. Kupffer cells (KCs), the liver-resident macrophages, play a central role in immune surveillance and metabolism, yet their response to MNPs remains unclear. Here, using a chronic plastic exposure model in mice, we identify KCs as the primary hepatic reservoir for MNPs. Long-term exposure alters their transcriptional profile and impairs phagocytic function, leading to metabolic dysregulation of hepatocytes. Microplastics, but not nanoplastics, reduce KC-mediated clearance of circulating cells and bacteria. Under diet-induced obesity, microplastics exacerbates hepatic lipid accumulation, while nanoplastics impair systemic glucose metabolism. Although the blood-brain barrier limits microplastic infiltration, a small fraction of ingested nanoplastics reaches the brain, where it is taken up by microglia, the brain-resident macrophages. However, we observe no signs of neuroinflammation or behavioral deficits. These findings demonstrate that chronic MNP exposure disrupts macrophage function in a size-dependent manner, with distinct consequences for liver and systemic metabolism, while the brain remains largely protected. Understanding tissue-specific vulnerabilities to MNPs is crucial for assessing their long-term health impact.
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Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism
AI summary Read the abstract
Using a chronic plastic exposure mouse model, researchers identified Kupffer cells—liver-resident macrophages—as the primary immune cells affected by micro- and nanoplastic ingestion. Smaller particles reached the liver at higher concentrations than larger ones, disrupted Kupffer cell lipid metabolism and immune function, and altered liver-specific metabolic pathways in a size-dependent manner.
Image data related to publication "Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism"
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This dataset accompanied a study investigating how nano- and microplastic particle size affects macrophage function and tissue-specific metabolism, with a focus on liver Kupffer cells. Size-dependent differences in macrophage immune responses and metabolic disruption were documented, adding to evidence that particle dimensions critically determine the biological impact of ingested plastics.
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Researchers found that long-term exposure to polystyrene microplastics in drinking water caused significant fat accumulation in the livers of mice over 9 to 12 weeks. The microplastics triggered an imbalance in immune cells in the liver called Kupffer cells, shifting them toward a pro-inflammatory state. The study identifies a specific signaling pathway through which microplastics may disrupt fat metabolism and contribute to liver problems.
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This review summarizes how microplastics and nanoplastics can damage the gastrointestinal tract and disrupt liver metabolism when they enter the human body. The particles trigger oxidative stress, inflammation, and cell death in gut tissues, and can interfere with how the liver processes glucose and fats. As plastics continue to break down into ever-smaller particles, the potential for harm increases because nanoplastics can penetrate cells more easily.
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