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61,005 resultsShowing papers similar to Polystyrene microplastic-induced pathophysiology is driven by disruption of efferocytosis
ClearToxicological 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.
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
Polystyrene nanoplastics dysregulate lipid metabolism in murine macrophages in vitro
Researchers investigated the effects of polystyrene nanoplastics on immune cell metabolism and found that macrophages exposed to nanoplastics transformed into lipid-laden foam cells. The study suggests that nanoplastic exposure dysregulates lipid metabolism in immune cells, with implications for understanding how these particles may interact with the immune system at the cellular level.
Exposure to polystyrene nanoplastics impairs lipid metabolism in human and murine macrophages in vitro
Researchers exposed human and mouse macrophages to polystyrene nanoplastics and found that the particles disrupted lipid metabolism in these immune cells. The study observed that nanoplastic exposure altered how macrophages process and store fats, which could affect their ability to function properly. These findings suggest that nanoplastic accumulation in immune cells may interfere with normal metabolic processes at the cellular level.
Size-dependent plastic exposure disrupts macrophage function and tissue-specific metabolism
Using a chronic plastic exposure mouse model, researchers identified Kupffer cells—liver-resident macrophages—as the primary immune cells affected by micro- and nanoplastic ingestion. Smaller particles reached the liver at higher concentrations than larger ones, disrupted Kupffer cell lipid metabolism and immune function, and altered liver-specific metabolic pathways in a size-dependent manner.
Polystyrene microplastics promote liver inflammation by inducing the formation of macrophages extracellular traps
Researchers discovered that polystyrene microplastics trigger liver inflammation by causing immune cells called macrophages to release web-like structures (extracellular traps) that damage surrounding liver cells. The mechanism involves microplastics generating harmful reactive oxygen species inside macrophages, disrupting their internal recycling systems and ultimately causing them to burst, which highlights how microplastics may drive organ inflammation in the body.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Effects of micro- and nanoplastic exposure on macrophages: a review of molecular and cellular mechanisms
This review details how macrophages, key immune cells, respond when they engulf micro- and nanoplastics. The particles trigger inflammatory signaling, damage mitochondria and lysosomes, cause excessive production of harmful reactive oxygen species, and can lead to cell death, while in fat tissue they promote fat buildup and insulin resistance.
Polystyrene microparticle distribution after ingestion by murine macrophages
Researchers tracked what happens to polystyrene microparticles after they are ingested by mouse immune cells called macrophages. They found that the particles were distributed unevenly during cell division in a cell-type-specific manner, and no active excretion of the microplastics was observed. The study suggests that once immune cells take up microplastic particles, the particles may persist inside cells and accumulate over successive generations of cell division.
Mitigating microplastic-induced organ Damage: Mechanistic insights from the microplastic-macrophage axes
This review is the first comprehensive examination of how microplastics interact with macrophages, the immune cells responsible for engulfing and removing foreign particles from the body. When macrophages absorb microplastics, the resulting oxidative stress disrupts their normal function, leading to inflammation and organ damage, with gut bacteria potentially playing a role in this harmful process.
Acute exposure to polystyrene nanoparticles promotes liver injury by inducing mitochondrial ROS-dependent necroptosis and augmenting macrophage-hepatocyte crosstalk
Researchers discovered that very small polystyrene nanoparticles (20 nanometers) cause liver damage in mice by accumulating inside immune cells called macrophages, disrupting their energy-producing structures (mitochondria), and triggering a form of cell death that then spreads damage to liver cells. This study reveals a specific mechanism by which nanoplastic exposure could harm the liver, an organ critical for filtering toxins from the body.
Polystyrene microplastics induce activation and cell death of neutrophils through strong adherence and engulfment
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.
Microglial phagocytosis of polystyrene microplastics results in immune alteration and apoptosis in vitro and in vivo
Researchers found that polystyrene microplastics can cross the blood-brain barrier in mice after oral exposure and accumulate in brain tissue, where they are engulfed by microglia, the brain's immune cells. This engulfment triggered inflammatory responses and cell death in the microglia both in cell cultures and in living mice. The study suggests that microplastic exposure may affect brain immune function, with potential implications for neurological health.
Polystyrene nanoplastics target lysosomes interfering with lipid metabolism through the PPAR system and affecting macrophage functionalization
Researchers examined how polystyrene nanoplastics affect lysosomal function and lipid metabolism in macrophages through the PPAR signaling system. The study suggests that nanoplastics can interfere with cellular lipid processing by targeting lysosomes, which may affect immune cell function.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
Long-term exposure to polystyrene microplastics reduces macrophages and affects the microbiota–gut–brain axis in mice
Mice that consumed polystyrene microplastics over an extended period showed reduced immune cells called macrophages in their colons and changes in gut bacteria that were linked to altered brain chemistry. This study provides evidence for a gut-brain connection where microplastics may affect brain function indirectly by first disrupting gut health and the immune system.
Polystyrene microplastics-induced macrophage extracellular traps contributes to liver fibrotic injury by activating ROS/TGF-β/Smad2/3 signaling axis
In a mouse study, polystyrene microplastics caused liver scarring (fibrosis) by triggering immune cells called macrophages to release web-like traps that promoted inflammation. Smaller microplastic particles caused more severe liver damage than larger ones, and the damage involved a specific signaling pathway (ROS/TGF-beta/Smad2/3) that drives tissue scarring. This research reveals a new mechanism by which microplastics may contribute to chronic liver disease.
Microplastics and Metabolism: Physiological Responses in Mice Following Ingestion
Researchers found that mice orally exposed to microplastic microspheres showed changes in lipid metabolism and other metabolic pathways, with particles detected in tissues throughout the body. The effects were more pronounced when mice were exposed to mixed microplastic types compared to polystyrene alone, suggesting that real-world mixtures of microplastics may have broader physiological impacts.
Effect of micro- and nanoplastic particles on human macrophages
This study is the first to visualize polystyrene micro- and nanoparticles inside primary human immune cells (macrophages) from actual blood donors, showing that the particles increase cell death and generate harmful reactive oxygen species. The findings provide direct evidence that human immune cells react to plastic particles in ways that could contribute to inflammation and health problems.
Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice
In a mouse study, oral exposure to high concentrations of polystyrene microplastics caused fatty liver disease and abnormal blood lipid levels even without prior gut leakiness. The microplastics triggered intestinal inflammation through immune cells, disrupted gut bacteria, and altered how the body processes nutrients. These results suggest that swallowing microplastics could contribute to metabolic problems and liver disease in humans.