We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene microplastic-induced pathophysiology is driven by disruption of efferocytosis
Summary
Researchers discovered that polystyrene microplastics accumulate in immune cells and disrupt efferocytosis, the process by which macrophages clear dead cells from the body. This disruption was linked to a buildup of the toxic metabolite methylglyoxal, which impaired the cellular machinery needed to digest dead cells. The study found that microplastic-driven efferocytosis failure caused damage in the lungs, liver, and testes of exposed mice.
Microplastics (MPs), microparticles from plastic degradation, pose a substantial threat to human health. Macrophages, the body's immune sentinels, are unable to break down MPs, suggesting that MP accumulation could impair essential functions, such as removal of apoptotic cells (ACs), termed efferocytosis. We found that polystyrene MP (PS-MP) accumulation disrupted efferocytosis by impairing AC digestion in multiple types of macrophages and Sertoli cells, specialized testes phagocytes, in vitro. PS-MP exposure also suppressed efferocytosis and caused damage in the lungs, liver, and testes in vivo. Mechanistically, PS-MP-loaded efferocytotic macrophages had dysregulated metabolic and phagolysosome processes, including accumulation of methylglyoxal (MGO) and increased MGO glycation of glucose-6-phosphate dehydrogenase, an enzyme required for AC digestion. Consistently, we found that overexpression of the MGO detoxification glyoxalase-1 rescued PS-MP-induced defects in AC digestion in vitro and in vivo. Collectively, we demonstrate that PS-MPs directly disrupt efferocytosis, which negatively affects the function and health of multiple organs.
Sign in to start a discussion.
More Papers Like This
Toxicological profiling of polystyrene microplastics in raw 264.7 macrophages: Linking microplastic exposure to immune cell impairment
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 microplastics induce an immunometabolic active state in macrophages
Researchers investigated how macrophages, the immune cells that act as first-line defense in the gut and lungs, respond metabolically to polystyrene microplastic particles. The study found that phagocytosis of microplastics induced an immunometabolic active state in macrophages, suggesting that microplastic exposure may alter immune cell metabolism in ways relevant to understanding potential health effects.
Polystyrene microplastics induce an immunometabolic active state in macrophages
Researchers found that polystyrene microplastics taken up by macrophages — immune cells lining the gut and lungs — triggered a metabolic shift toward an inflammatory state. This finding suggests microplastics reaching human tissues may alter immune function in ways that could contribute to inflammation-related diseases.
Ingestion of micro- and nanoplastic perturbs tissue homeostasis and macrophage core functions
Researchers fed mice polystyrene particles chronically and found that micro- and nanoplastics breached intestinal barriers and accumulated in multiple organs, disrupting tissue homeostasis and impairing core macrophage functions including phagocytosis and inflammatory regulation.
Microplastics induced apoptosis in macrophages by promoting ROS generation and altering metabolic profiles
This study found that polystyrene microplastics trigger cell death in macrophages, key immune cells that serve as the body's first line of defense against harmful substances. Smaller microplastics (0.5 micrometers) were more damaging than larger ones because they can enter the cells directly, where they generate harmful reactive oxygen species and disrupt normal cell metabolism.