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Polystyrene nanoplastics perturb macrophage mitochondrial homeostasis and inflammatory responses: Evidence implicating CPEB4.
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This study exposed mouse immune cells (macrophages) to polystyrene nanoplastics in lab tests. The particles increased oxidative stress and inflammatory signals, altered mitochondrial function, and reduced levels of a protein called CPEB4, though a direct cause-and-effect role for CPEB4 was not established.
Polystyrene nanoplastics (NPs) may affect macrophage function, but the relationships between inflammatory responses and mitochondrial alterations remain unclear. We combined exploratory analysis of public zebrafish intestinal single-cell RNA-sequencing data with transcriptomic, metabolomic, and experimental studies in RAW264.7 cells and primary mouse macrophages. In RAW264.7 cells, NPs increased reactive oxygen species (ROS), nitric oxide (NO), and the secretion of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). ROS and cytokine responses occurred at concentrations below those causing significant cytotoxicity in this cell line. A complex I-associated activity assay detected changes at lower NP concentrations than assays of cellular adenosine triphosphate (ATP) and the NAD+/NADH ratio. MitoSOX and JC-1 measurements further indicated changes in mitochondrial oxidant-sensitive fluorescence and membrane-potential-associated signals. Primary mouse macrophages showed concentration- and time-dependent responses, including increased TNF-α secretion. NPs exposure was also associated with reduced CPEB4 and INO80B protein abundance. CPEB4 knockdown increased ROS and reduced ATP at a later time point, whereas cellular thermal shift assay showed altered CPEB4 thermal behavior after NPs exposure. These findings identify inflammatory and mitochondrial responses associated with NPs exposure and implicate CPEB4 as a candidate contributor. However, they do not establish direct binding of intact NPs to CPEB4 or a causal role for CPEB4 or INO80B.
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Polystyrene nanoplastics impair mitochondrial function, quality control, and ER–mitochondria crosstalk in HeLa cells
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Researchers exposed human HeLa cells (grown in the lab) to polystyrene nanoplastics and measured effects on mitochondria, the cell's energy-producing structures. The nanoplastics disrupted mitochondrial energy production, increased oxidative stress markers, and interfered with communication between mitochondria and another cell structure called the endoplasmic reticulum.
C70-26 Transcriptional Regulators of Mitochondrial Biogenesis Are Attenuated in Macrophages by Polystyrene Exposure
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Scientists exposed immune cells (macrophages) to tiny polystyrene microplastic particles—the kind found in styrofoam food containers and inhaled from the air—and found that the plastics reduced key proteins these cells need to keep their energy-producing mitochondria healthy. Since macrophages rely on properly functioning mitochondria to fight off infections and clean up debris in the body, this suggests that breathing in microplastics could weaken our immune system's ability to protect us. This early lab study used mouse cells, so more research is needed to confirm these effects happen the same way in humans.
Toxicological profiling of polystyrene microplastics in raw 264.7 macrophages: Linking microplastic exposure to immune cell impairment
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Researchers exposed immune cells called macrophages to polystyrene microplastics and found that the cells rapidly absorbed the particles within two hours. Higher concentrations caused mitochondrial damage, disrupted cellular recycling processes, and triggered inflammation-related signaling. The study provides evidence that microplastics can impair the function of key immune cells responsible for defending the body against foreign threats.
Polystyrene Nanoplastics Induce Inflammasome Activation in Nasal Epithelial Cells via ROS ‐Mediated Mitochondrial Dysfunction
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Researchers exposed human nasal epithelial cells to polystyrene nanoplastics and found that the particles triggered NLRP3 inflammasome activation by inducing mitochondrial oxidative stress, depleting ATP, depolarizing mitochondrial membranes, and downregulating SIRT1-AMPK signaling—effects that were substantially reversed by the antioxidant N-acetylcysteine, pointing to oxidative damage as the primary driver of nanoplastic-induced nasal inflammation.
Hazard assessment of different-sized polystyrene nanoplastics in hematopoietic human cell lines
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Researchers tested how different sizes of polystyrene nanoplastics (50, 200, and 500 nm) affect human blood cell lines. While none of the sizes caused direct cell death, all three were taken up by cells and disrupted mitochondrial function in immune-related cell types. The study suggests that even without killing cells outright, nanoplastics may interfere with important cellular energy processes, with effects varying by particle size and cell type.
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