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<p>Nanoplastics (NP) are emerging environmental pollutants with potential risks to human health. This study investigates how polystyrene-NP exposure disrupts the intestinal microenvironment and barrier function through bacteria-host interactions. Using in vivo models and bacterial sorting technology, we show that NP accumulation in the mouse intestine alters the expression of intestinal miR-501-3p and miR-700-5p, compromising tight junction protein ZO-1 and mucin (MUC)−13 expression, thereby increasing intestinal permeability. NP increases miR-98-3p, miR-548z, miR-548h-3o, miR-548d-3p, miR-548az-5p, miR-12136, and miR-101-3p levels in extracellular vesicles (EVs) derived from goblet-like cells, which can interfere with ZO-1 expression. NP also induces gut microbiota dysbiosis, characterized by elevated <i>Ruminococcaceae</i> abundance and altered EV characteristics from goblet cells. <i>Lachnospiraceae</i> internalize NP, and their EVs suppress MUC-13 expression. These findings reveal a mechanism by which NP compromises intestinal integrity and indirectly alters intestinal microbiota composition, potentially leading to adverse health outcomes.</p>

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Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月10日

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  • Wei-Hsuan Hsu,
  • You-Zuo Chen,
  • Yi-Ting Chiang,
  • Yi-Tsen Chang,
  • Yi-Wen Wang,
  • Kung-Ting Hsu,
  • Yi-Yun Hsu,
  • Pei-Ting Wu,
  • Bao-Hong Lee

摘要

Nanoplastics (NP) are emerging environmental pollutants with potential risks to human health. This study investigates how polystyrene-NP exposure disrupts the intestinal microenvironment and barrier function through bacteria-host interactions. Using in vivo models and bacterial sorting technology, we show that NP accumulation in the mouse intestine alters the expression of intestinal miR-501-3p and miR-700-5p, compromising tight junction protein ZO-1 and mucin (MUC)−13 expression, thereby increasing intestinal permeability. NP increases miR-98-3p, miR-548z, miR-548h-3o, miR-548d-3p, miR-548az-5p, miR-12136, and miR-101-3p levels in extracellular vesicles (EVs) derived from goblet-like cells, which can interfere with ZO-1 expression. NP also induces gut microbiota dysbiosis, characterized by elevated Ruminococcaceae abundance and altered EV characteristics from goblet cells. Lachnospiraceae internalize NP, and their EVs suppress MUC-13 expression. These findings reveal a mechanism by which NP compromises intestinal integrity and indirectly alters intestinal microbiota composition, potentially leading to adverse health outcomes.