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Polystyrene nanoplastics deteriorate LPS-modulated duodenal permeability and inflammation in mice via ROS drived-NF-κB/NLRP3 pathway
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Researchers found that polystyrene nanoplastics worsened intestinal inflammation and increased gut permeability in mice already exposed to bacterial endotoxin. The combined exposure triggered higher levels of oxidative stress and activated inflammatory pathways, leading to greater damage to the intestinal lining than either substance alone. The study suggests that nanoplastic exposure could make the gut more vulnerable to inflammation and barrier breakdown when other stressors are present.
The widespread occurrence of nanoplastics (NPs), has markedly affected the ecosystem and has become a global threat to animals and human health. There is growing evidence showing that polystyrene nanoparticles (PSNPs) exposure induced enteritis and the intestinal barrier disorder. Lipopolysaccharide (LPS) can trigger the inflammation burden of various tissues. Whether PSNPs deteriorate LPS-induced intestinal damage via ROS drived-NF-κB/NLRP3 pathway is remains unknown. In this study, PSNPs exposure/PSNPs and LPS co-exposure mice model were duplicated by intraperitoneal injection. The results showed that exposure to PSNPs/LPS caused duodenal inflammation and increased permeability. We evaluated the change of duodenum structure, oxidative stress parameters, inflammatory factors, and tight junction protein in the duodenum. We found that PSNPs/LPS could aggravate the production of ROS and oxidative stress in cells, activate NF-κB/NLRP3 pathway, decrease the expression tight junction proteins (ZO-1, Claudin 1, and Occludin) levels, promote inflammatory factors (TNF-α, IL-6, and IFN-γ) expressions. Duodenal oxidative stress and inflammation in PS + LPS group were more serious than those in single exposure group, which could be alleviated by NF-kB inhibitor QNZ. Collectively, the results verified that PSNPs deteriorated LPS-induced inflammation and increasing permeability in mice duodenum via ROS drived-NF-κB/NLRP3 pathway. The current study indicated the relationship and molecular mechanism between PSNPs and intestinal injury, providing novel insights into the adverse effects of PSNPs exposure on mammals and humans.
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Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen
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Researchers found that polystyrene nanoplastics worsened the inflammatory damage caused by bacterial toxins in the spleens of mice. The nanoplastics triggered oxidative stress that activated inflammatory signaling pathways, leading to cell death, and these effects were significantly amplified when nanoplastics were combined with bacterial endotoxin. The study suggests that nanoplastic exposure may compromise the immune system's ability to handle infections and inflammation.
Polystyrene microplastic-induced oxidative stress triggers intestinal barrier dysfunction via the NF-κB/NLRP3/IL-1β/MCLK pathway
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Mice that swallowed polystyrene microplastics for 28 days developed oxidative stress and inflammation in their colons, leading to a weakened intestinal barrier with reduced protective mucus and loosened cell connections. The largest microplastics (5 micrometers) caused the most severe gut damage through a specific inflammatory pathway (NF-kB/NLRP3/MLCK), and antioxidant treatment was able to partially reverse the effects.
Polystyrene nanoplastics induce intestinal and hepatic inflammation through activation of NF-κB/NLRP3 pathways and related gut-liver axis in mice
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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.
Underestimated health risks: polystyrene micro- and nanoplastics jointly induce intestinal barrier dysfunction by ROS-mediated epithelial cell apoptosis
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This mouse study found that when micro-sized and nano-sized polystyrene particles were present together, as they would be in the real world, they caused more intestinal damage than either size alone. The combined exposure increased gut permeability by killing intestinal lining cells through oxidative stress, weakening the barrier that keeps harmful substances out of the bloodstream. This is important because real-world microplastic exposure always involves a mix of particle sizes, meaning health risks may be greater than single-size lab studies suggest.
Co-exposure to polystyrene nanoplastics and glyphosate exacerbates NETs-mediated pyroptosis by activating the NLRP3 inflammasome in mouse liver
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Researchers found that co-exposing mice to polystyrene nanoplastics and the herbicide glyphosate caused significantly worse liver damage than either pollutant alone. The combined exposure triggered a chain of inflammatory events including immune cell infiltration, formation of neutrophil traps, and cell death in liver tissue, all driven by activation of a key inflammatory pathway called NLRP3. The study suggests that nanoplastics may amplify the harmful effects of common agricultural chemicals when they enter the body together.
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