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Top-down generated microplastics differentially induce neutrophil cell death associated with phagocytosis
Summary
Tiny plastic particles from everyday sources like PVC pipes and polyester (PET) can be swallowed up by neutrophils, white blood cells that act as your body's first line of defense against germs. When these immune cells "eat" the plastic bits, it can trigger their death, and in some cases, a type of cell death linked to inflammation, especially with certain plastic types and sizes. Since neutrophils can't actually break down plastic like they would bacteria, this research suggests microplastics circulating in our blood may quietly stress and disrupt our immune system's frontline defenders, though more research is needed to understand what this means for long
Abstract Micro- and nanoplastics (MNPs) are able to cross the epithelial barriers, enter the circulation and encounter immune cells. Unlike bacteria or viruses, MNPs cannot be degraded by immune cells and may therefore pose a potential risk to human health. Neutrophils are the most predominant circulatory immune cells and the first responders to tissue injury and invading pathogens. The aim of this study was to examine the dose-dependent effects of environmentally relevant virgin and UV-aged polyvinyl chloride (PVC), nylon 6.6 or polyamide 6.6 (PA6.6), and polyethylene terephthalate (PET) fragments of different size fractions on human neutrophil phagocytosis and their potential to induce pro-inflammatory cell death. Three different size fractions (<1, 1–5 and 5–10 µm) were tested at mass-based concentrations ranging from 1 to 100 µg/mL and compared to the control. Particle size distributions were determined in culture medium, and the number of particles settling onto the cells was modeled. As controls, neutrophils were also exposed to particle leachates and to spherical monodisperse polystyrene particles (PS; 1 and 10 µm) that are widely tested but not representative of environmental particles. All particles were pretreated in human pooled serum. Live-cell imaging captured neutrophil phagocytosis and distinct forms of cell death. Nine out of fourteen particle fractions induced significantly increased neutrophil death of which three triggered pro-inflammatory cell death when compared to the control. Increased neutrophil death correlated with the extent of neutrophils that had phagocytosed. However, phagocytic uptake was strongly influenced by the modelled number of particles deposited onto the cells. Especially 10 µm PS, virgin <1 µm and 5–10 µm PVC induced significant pro-inflammatory cell death. Overall, our findings suggest that while phagocytic uptake is associated with neutrophil cell death, different MNP polymers preferentially induce distinct forms of cell death when compared to the control.