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Enterohepatic Circulationof Polystyrene NanoplasticsPromotes Intestinal Inflammation by Impairing Enteric Neurons
Summary
Scientists discovered that tiny plastic particles (nanoplastics) we swallow don't just pass through our gut and leave—they get absorbed, travel to the liver, get concentrated in bile, and get recycled back into the intestines, causing them to build up over time. In mice, this repeated exposure damaged the gut lining, disrupted healthy gut bacteria, and even harmed the nerve cells that help control digestion. This matters because it suggests plastic pollution in our food and water could cause more lasting gut damage than previously thought, since our bodies may be unintentionally recirculating these particles instead of clearing them out
Microplastics (MPs) are emerging contaminants of increasing concern, yet their in vivo fate and mechanisms of intestinal toxicity remain poorly defined. Here, we demonstrate that polystyrene nanoplastics (PS-NPs) undergo a previously overlooked enterohepatic recirculation pathway that markedly enhances their intestinal retention. Using oral exposure and a Zombie mouse model with intravenous PS-NPs delivery, we show that systemically absorbed PS-NPs are efficiently captured by the liver, concentrated in the gallbladder, and subsequently reintroduced into the intestine via bile. Chronic PS-NPs exposure caused pronounced epithelial injury, including goblet cell loss, tight-junction disruption, and robust cytokine-mediated inflammation. Multiomics analyses revealed gut microbial dysbiosis, extensive shifts in metabolite profiles, and enrichment of neuroactive signaling pathways, suggesting microbiome-metabolite contributions to toxicity. We further identified significant enteric neurotoxicity characterized by reduced expression of vasoactive intestinal peptide, increased expression of tyrosine hydroxylase, and downregulation of the mechanosensitive PIEZO1 channel. Together, these findings establish hepatobiliary recycling as a key driver of intestinal PS-NPs accumulation and demonstrate that epithelial damage, microbiome-metabolite imbalance, and enteric nervous system dysfunction collectively mediate PS-NPs-induced gut pathology. This work provides mechanistic insights essential for evaluating the health risks of environmental PS-NPs exposure.