Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism
Published in: Nat Metab, 2026
Type: preprint
Citation
Nikola Makdissi, Maria Francesca Viola, Lisa Maria Steinheuer, Nelli Blank-Stein, Ronja Kardinal, Fabrizio Musacchio, Eliana Franco Taveras, Virginia Aliprandi, Katharina Sieckmann, Akram Abdulkadyrov, Marina L. Mayer, Marie-Louise Diefenbach-Wilke, Diana Fink, Hannes Beckert, Stefan Böhmdorfer, Quentin Deveuve, Frederike J. Graelmann, Katharina Mauel, Nele Kronau, Jake Thomas, David Bejarano, Andreas Schlitzer, Sandra Högler, Mohamed H. Yaghmour, Joerg Heeren, Christoph Thiele, Lukas Kenner, Felix Meissner, Falk Nimmerjahn, Martin Fuhrmann, Dagmar Wachten, Kevin Thurley, and Elvira Mass, "Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism" (2026). Nat Metab, https://doi.org/10.1038/s42255-026-01615-8
Abstract
Plastic pollution is an emerging yet understudied environmental risk to the immune system. Once ingested, microplastic and nanoplastic particles (MNPs) can translocate from the gut to internal organs, with macrophages serving as primary targets. Kupffer cells (KCs), the liver-resident macrophages, have a central role in immune surveillance and metabolism, yet their response to MNPs remains unclear. Here we identify KCs as the primary hepatic reservoir for MNPs in young male mice. Chronic plastic exposure over 12 weeks alters their transcriptional profile, impairs phagocytic function and is associated with metabolic dysregulation of hepatocytes. Microplastics, but not nanoplastics, reduce KC-mediated clearance of circulating cells. Under diet-induced obesity, microplastics exacerbate hepatic lipid accumulation, while nanoplastics alter systemic glucose metabolism and energy expenditure. These findings demonstrate that chronic MNP exposure disrupts macrophage function in a size-dependent manner, with subsequent distinct consequences for liver and systemic metabolism.
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