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Long-term exposure to nanoparticles alters senescence-associated markers and immune responses in human monocyte-derived macrophages
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Long-term exposure to polyethylene terephthalate (PET) nanoparticles modulates CDKN2A gene expression in human macrophages, while gold nanoparticles trigger strong pro-inflammatory responses, demonstrating material-specific effects on immune senescence. These findings are directly relevant to microplastic research as PET is one of the most abundant plastic polymers found in human tissues, and macrophage dysfunction is a plausible mechanism linking microplastic exposure to chronic inflammation.
Background: Macrophages are essential in maintaining tissue homeostasis. However, their functionality and phenotype can be impaired by senescence, which impacts immune competence and inflammatory responses. Despite the growing use of engineered nanoparticles (NPs) in biomedical applications or chronic exposure to environmental NPs, their impact on macrophage senescence and immune function remains poorly understood, particularly in the context of prolonged NP exposure. Results: Here, we first confirm that human monocyte-derived macrophages (MDMs) undergo senescence in vitro, as indicated by a panel of senescence-associated markers that increased within 10 days of culture. Then, we investigate how gold (AuNPs), silica (SiO2 NPs), and polyethylene terephthalate (PET NPs) influence senescence-associated markers, and immunocompetence in MDMs. By examining key markers such as senescence-associated beta-galactosidase (SA-β-gal), CDKN2A (p16), and senescence-associated secretory phenotype (SASP) cytokines, e.g., interleukin (IL)-6 and IL-8, over extended exposure periods up to 10 days, we revealed material-specific effects: AuNPs induce a strong pro-inflammatory response, SiO2 NPs demonstrate low inflammatory potential, and PET NPs modulate the gene expression level of CDKN2A involved in cell cycle regulation. Conclusion: Our findings underscore the need to characterize long-term NP behavior in biological systems and reveal material-specific effects on macrophage senescence-associated traits and immune function. Rather than assessing NP-induced senescence, this study defines how prolonged NP exposure modulates selected senescence-associated signatures in non-proliferative macrophages, offering valuable insights into the functional consequences of chronic NP accumulation.
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Researchers review how micro- and nanoplastics trigger cellular senescence — a state of permanent cell cycle arrest — through oxidative stress and DNA damage, activating pathways like cGAS-STING and NF-κB that elevate risk for age-related diseases, and survey potential therapeutic strategies to counter these effects.
Micro- and Nanoplastics as Potential Chronic Abiotic Stressors: Cellular Senescence, Hallmarks of Ageing, and an Oxidative–Mitochondrial–Inflammatory Framework
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This review summarizes existing lab research on tiny plastic particles and cell ageing processes. Studies found effects on cell energy production, DNA, and inflammation signals, with strongest evidence for mitochondrial problems and cell senescence, but most used high doses and short exposures, so links to human ageing remain unconfirmed.
Effects of true to life polyethylene terephthalate and polycaprolactone nanoparticles on macrophages under a repeated exposure mode
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Researchers compared how macrophages respond to repeated low-dose exposure to persistent PET nanoparticles versus biodegradable polycaprolactone nanoparticles. They found that cells adapted over repeated exposures, showing less dramatic changes than in single-dose experiments, but PET nanoparticles still induced oxidative stress, reduced phagocytic ability, and triggered pro-inflammatory responses. The study suggests that the biopersistence of conventional plastic nanoparticles like PET may pose more sustained immune system effects compared to biodegradable alternatives.
Effects of polystyrene and polylactide nanoparticles on macrophages under a repeated exposure mode
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This study compared the responses of macrophages to repeated low-dose exposure to persistent polystyrene nanoparticles and biodegradable polylactide (PLA) nanoparticles, finding that proteome changes were reduced (PS) or similar (PLA) compared to acute single-dose exposure, indicating cell adaptation. However, PLA particles induced mitochondrial dysfunction and suppressed immune responses to bacterial danger signals, while PS caused slight immune function alterations, indicating harmful effects persisting even under repeated low-dose exposure.
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