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Enterohepatic Circulationof Polystyrene NanoplasticsPromotes Intestinal Inflammation by Impairing Enteric Neurons
Summary
New research in mice found that tiny plastic particles (nanoplastics) don't just pass through your gut and leave — instead, once absorbed, they get sent to the liver, stored in the gallbladder, and recycled back into the intestines through bile, essentially getting trapped in a loop inside the body. This repeated exposure damaged the gut lining, disrupted healthy gut bacteria, and harmed the nerve cells that help control digestion, all of which drove inflammation. While this was shown in mice rather than humans, it suggests that everyday plastic exposure could build up and cause lasting gut damage in ways scientists h
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.