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The impact of polystyrene nanoplastics on the chicken gut and liver: Based on transcriptomics and microbiomics
Summary
Researchers fed polystyrene nanoplastics to chickens for 21 days and found that the particles triggered inflammation and oxidative stress in the gut and liver, damaged the intestinal lining, and disrupted the gut microbiome — with some effects persisting even after exposure stopped. Because poultry is a major protein source for humans globally, these findings raise concerns about nanoplastic contamination in the food supply.
Nanoplastics, an emerging environmental pollutant, pose potential hazards to organisms. The impact of nanoplastics on poultry health, a crucial protein source for humans, has raised considerable concern. This study evaluated the multidimensional toxic effects of nanoplastic exposure on 240 Sanhuang chickens over a 21-day oral administration period followed by a 21-day recovery period. While nanoplastics did not affect average daily gain and average daily feed intake, they induced cardiac index elevation, indicating myocardial compensatory hypertrophy, with partial functional recovery post-exposure. Serum analysis revealed that reduced antioxidant enzyme activities and increased lipid peroxidation, and pro-inflammatory cytokines levels rose during exposure. Oxidative stress and inflammatory responses were alleviated, but IgG levels significantly declined in recovery. Transcriptome sequencing showed disrupted mitochondrial complex I function and inhibited cholesterol synthesis through abnormal expression of key genes, exacerbating cytotoxicity. Mechanistic studies confirmed toll-like receptor 4 (TLR4)/ nuclear factor kappa B (NF-κB) pathway activation driving hepatic/jejunal inflammation, alongside elevated pro-apoptotic Bax/Caspase-3, reduced anti-apoptotic B-cell lymphoma-2, and suppressed autophagy and nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Post-exposure, the TLR4/NF-κB pathway remained activated, and autophagy and the Nrf2 pathway remained inhibited. Intestinal barrier function was impaired via downregulated tight junction proteins, increasing jejunal permeability. Jejunal villi height was abnormally elevated in the low-dose group during exposure, which decreased in the villus height / crypt depth ratio during recovery. Microbiome analysis revealed increased Proteobacteria/Escherichia-Shigella abundance during exposure and reduced beneficial bacteria. Harmful bacteria such as Flavobacteriaceae_uncultured remained highly abundant post-exposure. This study systematically demonstrates that NPs compromise avian health via two primary mechanisms: inducing inflammation, oxidative stress, apoptosis, and autophagy inhibition in the liver and jejunum; disrupting mitochondrial respiration in the liver and causing intestinal barrier dysfunction accompanied by dysbiosis. These findings offer critical evidence for evaluating the potential risks of environmental nano-pollutants in livestock and poultry industry.
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