<?xml version='1.0' encoding='UTF-8'?><metadata xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns="http://dublincore.org/documents/dcmi-terms/"><dcterms:title>Image data related to publication "Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism"</dcterms:title><dcterms:identifier>https://doi.org/10.60507/FK2/M42B8O</dcterms:identifier><dcterms:creator>Makdissi, Nikola</dcterms:creator><dcterms:creator>Viola, Maria Francesca</dcterms:creator><dcterms:creator>Mass, Elvira</dcterms:creator><dcterms:publisher>bonndata</dcterms:publisher><dcterms:issued>2026-01-21</dcterms:issued><dcterms:modified>2026-01-21T10:52:46Z</dcterms:modified><dcterms:description>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.</dcterms:description><dcterms:subject>Medicine, Health and Life Sciences</dcterms:subject><dcterms:IsSupplementTo>Nikola Makdissi, Maria Francesca Viola, Lisa Steinheuer et al. Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism, PREPRINT (Version 1) available at Research Square, doi, 10.21203/rs.3.rs-6204281/v1, https://doi.org/10.21203/rs.3.rs-6204281/v1</dcterms:IsSupplementTo><dcterms:date>2026-01-21</dcterms:date><dcterms:contributor>Makdissi, Nikola</dcterms:contributor><dcterms:contributor>Dagmar Wachten</dcterms:contributor><dcterms:contributor>Virginia Aliprandi</dcterms:contributor><dcterms:contributor>Marina Mayer</dcterms:contributor><dcterms:contributor>Katharina Sieckmann</dcterms:contributor><dcterms:contributor>Nele Kronau</dcterms:contributor><dcterms:dateSubmitted>2025-12-20</dcterms:dateSubmitted><dcterms:license>CC BY 4.0</dcterms:license></metadata>