We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Top-down generated microplastics differentially induce neutrophil cell death associated with phagocytosis
AI summary Read the abstract
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.
More Papers Like This
Polystyrene microplastics induce activation and cell death of neutrophils through strong adherence and engulfment
AI summary Read the abstract
Researchers found that neutrophils (key immune cells that fight infections) strongly bind to and swallow polystyrene microplastics, mistaking them for bacteria. This triggers inflammation and eventually kills the neutrophils, and the same response was confirmed in both mouse and human immune cells. The findings suggest that microplastics accumulating in the body could weaken immune defenses by destroying these important infection-fighting cells.
Generation of Eroded Nanoplastics from Domestic Wastes and Their Impact on Macrophage Cell Viability and Gene Expression
AI summary Read the abstract
Researchers created nanoplastics from common household plastic waste like water bottles, styrofoam, and plastic bags, then tested their effects on immune cells. All types of nanoplastics killed immune cells in a dose-dependent way and triggered changes in genes related to inflammation, with polystyrene, polyethylene, and polypropylene being the most toxic. This study shows that the tiny plastic particles shed from everyday items can harm immune cells, which could weaken the body's ability to fight infection and disease.
Micro- and nanoplastics reduce the phagocytosis and intracellular killing of E. coli by THP1-Blue™ NFκB monocytes
AI summary Read the abstract
Researchers exposed human immune cells to micro- and nanoplastic particles and then measured their ability to engulf and kill bacteria. They found that plastic exposure reduced both phagocytosis (the ability to capture bacteria) and intracellular killing in a dose-dependent manner, without directly killing the immune cells. The study suggests that microplastic exposure could weaken the body's first line of immune defense against bacterial infections.
Detrimental effects of micro- and nanoplastics (MNPs) on platelet and neutrophil immunity: Recent findings and emerging insights
AI summary Read the abstract
Researchers reviewed how micro- and nanoplastics (MNPs) harm the immune system, finding that tiny plastic particles can trigger dangerous inflammation in platelets and neutrophils — immune cells that control clotting and infection defense. These effects could disrupt normal blood vessel function and immune balance, though the exact mechanisms by which cells take up MNPs remain poorly understood.
Micro- and nanoplastics remodel the autophagy-lysosomal axis and mitochondrial function in primary human monocytes
AI summary Read the abstract
Scientists found that when human immune cells (monocytes) engulf tiny plastic particles, it disrupts the cells' internal "cleanup crew" (a process called autophagy) and damages their energy-producing mitochondria, with smaller plastic particles (0.5-1 micron) causing more harm than larger ones. This matters because monocytes are frontline defenders in your immune system, so if microplastics are impairing how they function and produce energy, this could have knock-on effects for immune health over time, though more research is needed to understand the long-term consequences.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.