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Mucin2 regulated by Ho1/p38/IL-10 axis plays a protective role in polystyrene nanoplastics-mediated intestinal toxicity
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Researchers discovered that nanoscale polystyrene particles damage the intestinal barrier in both cell models and mice, but the gut simultaneously activates a protective response by increasing mucin production. This defense mechanism is regulated through a specific signaling pathway involving the HO1, p38, and IL-10 molecules. The study suggests the body has a built-in protective response to nanoplastic exposure in the gut, though the long-term adequacy of this defense remains unclear.
Micro/nano-plastics (MPs/NPs) are a newly discovered environmental pollutant that can be ingested by humans through food and drinking water. In this study we evaluated the impact of MPs/NPs on the intestinal barrier and its mechanism. Doses of MPs/NPs were used to treat Caco-2/HT29-MTX in-vitro model and in-vivo model. In in-vitro model, 20 nm polystyrene nanoplastics (PS-NPs) had higher cytotoxicity than larger particles (200 nm and 2000 nm), and led to the increase of the permeability along with the decreased expression of tight junction proteins. Intriguingly, 20 nm PS-NPs elevated the expression of MUC2 simultaneously. Further studies revealed that PS-NPs increased the expression of HO1 through ROS generation, and then activated p38 to elevate IL-10 secretion in Caco-2 cell. The IL-10 secreted by Caco-2 cell promoted the expression of MUC2 in HT29-MTX cell through STAT1/3. Elevated MUC2 expression alleviates the cytotoxicity of PS-NPs. Besides, increased intestinal permeability and up-regulation of MUC2 through Ho1/p38/IL-10 pathway was also observed in 20 nm PS-NPs treated mouse model. In conclusion, PS-NPs can induce the intestinal toxicity and result in the increased adaptive expression of MUC2 to resist this adverse effect. People with inadequate mucin expression need to pay more attention to the toxicity of PS-NPs. This study provided a valuable insight for clarifying the mechanism and potential risk of intestinal toxicity induced by nanoplastics.
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Researchers found that polystyrene nanoplastics disrupt the gut lining in mice by altering tiny RNA molecules that control the production of protective proteins in the intestinal barrier. The nanoplastics also caused an imbalance in gut bacteria, creating a chain reaction where damaged gut cells release particles that further weaken the intestinal barrier and change the microbiome.
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Researchers found that quercetin, a natural compound found in fruits and vegetables, protected mice from gut damage and immune system disruption caused by polystyrene nanoplastics. The nanoplastics damaged the small intestine and disrupted immune balance, but quercetin reversed much of this harm by restoring healthy gut bacteria and gene activity. This suggests that dietary compounds like quercetin might help counteract some negative health effects of nanoplastic exposure.
Toxicity and absorption of polystyrene micro-nanoplastics in healthy and Crohn’s disease human duodenum-chip models
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Using an advanced gut-on-a-chip model built from human intestinal cells, researchers found that 25-nanometer polystyrene particles could cross the intestinal barrier through both passive leaking and active cell transport. The nanoplastics also turned down a gene involved in immune defense (IFI6), suggesting that even without causing obvious cell damage, nanoplastics may weaken the gut's ability to fight off infections.
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.
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