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Mucin2 regulated by Ho1/p38/IL-10 axis plays a protective role in polystyrene nanoplastics-mediated intestinal toxicity

Environmental Pollution 2023 23 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 55 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.

Qing Wang Qing Wang Liping Chen, Mengxing Cui, Qing Wang Qing Wang Mengxing Cui, Qing Wang Qing Wang Mengxing Cui, Qing Wang Qianmei He, Qianmei He, Qing Wang Ziwei Wang, Qing Wang Qing Wang Qing Wang Qing Wang Yongjiang Yu, Yongjiang Yu, Yongjiang Yu, Wen Chen, Qing Wang Qing Wang Yongjiang Yu, Qing Wang Huan Gao, Huan Gao, Ziqi Liu, Qing Wang Qing Wang Qing Wang Qing Wang Qing Wang Qing Wang Wen Chen, Huan Gao, Qing Wang Qing Wang Wen Chen, Qing Wang Qing Wang Qing Wang Qing Wang Xiumei Xing, Ziqi Liu, Qing Wang Honghao Peng, Qing Wang Qing Wang Qing Wang Qing Wang Honghao Peng, Qing Wang Qing Wang Qing Wang Qing Wang Wen Chen, Qing Wang Qing Wang Qing Wang Han Wang, Qing Wang Qing Wang Qing Wang Qing Wang Zhang Xue, Qing Wang Qing Wang Qing Wang Daochuan Li, Liping Chen, Qing Wang Qing Wang Qing Wang Xiumei Xing, Yongmei Xiao, Daochuan Li, Wen Chen, Liping Chen, Qing Wang Xiumei Xing, Yongmei Xiao, Qing Wang

Summary

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.

Polymers

Models

Mouse

Study Type In vivo

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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