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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."},"author":[{"citation:authorName":"Makdissi, Nikola","citation:authorAffiliation":"University of Bonn"},{"citation:authorName":"Viola, Maria Francesca","citation:authorAffiliation":"University of Bonn"},{"citation:authorName":"Mass, Elvira","citation:authorAffiliation":"University of Bonn"}],"publication":{"publicationCitation":"Nikola Makdissi, Maria Francesca Viola, Lisa Steinheuer et al. 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Need assistance? \n<br>\nGet in touch: <b> 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