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Inhalation of Microplastics Induces Inflammatory Injuries in Multiple Murine Organs via the Toll-like Receptor Pathway
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After mice inhaled polystyrene microplastics, the particles spread to the brain, liver, kidneys, spleen, and other organs within days, triggering widespread inflammation through a specific immune signaling pathway called TLR/NF-kB. These findings suggest that breathing in microplastics could cause inflammatory damage across multiple organ systems in the body.
Previous studies have detected microplastics (MPs) in human biological samples, such as lungs, alveolar lavage fluid, and thrombus. However, whether MPs induce health effects after inhalation are unclear. In this study, fluorescent polystyrene microplastics (PS-MPs) were found in the thymus, spleen, testes, liver, kidneys, and brain on day 1 or day 3 after one intratracheal instillation. Furthermore, mice showed inflammation in multiple organs, manifested as obvious infiltration of neutrophils and macrophages, increased Toll-like receptors (TLRs), myeloid differentiation primary response protein 88 (MyD88) and nuclear factor-κB (NF-κB), as well as proinflammatory cytokines (tumor necrosis factor (TNF)-α and interleukin (IL)-1β) in the lungs, thymus, spleen, liver, and kidneys after four intratracheal instillations of PS-MPs at once every 2 weeks. Hepatic and renal function indexes were also increased. Subsequently, the inflammatory response in multiple murine organs was significantly alleviated by TLR2 and TLR4 inhibitors. Unexpectedly, we did not find any elevated secretion of monocyte chemotactic protein (MCP)-1 or TNF-α by RAW264.7 macrophages in vitro. Thus, PS-MPs induced inflammatory injuries in multiple murine organs via the TLRs/MyD88/NF-κB pathway in vivo, but not macrophages in vitro. These results may provide theoretical support for healthy protection against PS-MPs and their environmental risk assessment.
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Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice
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This mouse study found that inhaling polystyrene microplastics caused serious lung damage, including inflammation, cell death, and scar tissue buildup. Smaller microplastics (1-5 micrometers) caused more harm than larger ones, and the damage worsened with longer exposure. The study identified a specific immune pathway (TLR2/NF-kB) through which inhaled microplastics trigger lung injury, raising concerns about the respiratory effects of airborne microplastics on humans.
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In a mouse study, ingested polystyrene nanoplastics accumulated in the gut and liver and triggered inflammation through specific immune pathways, damaging the intestinal lining and allowing bacterial toxins to leak into the liver. This gut-liver connection suggests that swallowing nanoplastics could set off a chain reaction of inflammation affecting multiple organs in the body.
Tissue accumulation of microplastics in mice and biomarker responses suggest widespread health risks of exposure
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Researchers fed mice polystyrene microplastics of two sizes and tracked where the particles accumulated in the body, finding them in the liver, kidneys, and gut with distribution patterns depending on particle size. Biochemical analysis revealed that microplastic exposure disrupted energy and fat metabolism, caused oxidative stress, and altered markers of neurotoxicity in the blood. The study provides evidence that microplastics can accumulate in mammalian tissues and may pose widespread health risks.
Systematic toxicity evaluation of polystyrene nanoplastics on mice and molecular mechanism investigation about their internalization into Caco-2 cells
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Researchers fed mice polystyrene nanoplastics (about 100 nm) for 28 days and found the particles accumulated in multiple organs including the spleen, lungs, kidneys, intestines, testes, and brain. The nanoplastics caused cell death, inflammation, and tissue damage in these organs, as well as disrupted fat metabolism and blood cell counts. This study demonstrates that ingested nanoplastics can spread throughout the body and cause widespread harm, raising concerns about long-term human exposure.
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Researchers orally administered polystyrene nanoplastics to mice for two weeks and tracked their distribution and biological effects. The nanoplastics accumulated primarily in the intestine, kidneys, and liver, triggering significant inflammatory responses and oxidative stress in these organs despite no visible tissue damage. The study provides evidence that even short-term oral exposure to nanoplastics can cause meaningful inflammatory changes in multiple organ systems.
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