Aug 2026· Veterinární Medicína· Vol 71, pp. 295 - 309· 0 citations· 87 references
Medicine
TL;DR
Plastic-induced dysbiosis was confirmed, characterised by reduced microbial diversity, depletion of beneficial taxa (e.g., Bacteroidota, Actinobacteriota), and shifts in short-chain fatty acid–producing bacteria, and highlights the vulnerability of freshwater species to environmental microplastics.
Abstract
This study examined the intestinal effects of polyethylene (PE; size 46.6 ± 11.3 μm) and polystyrene (PS; size 52.5 ± 11.5 μm) microparticles at three different concentrations (0.5%, 2%, and 5%) on juvenile rainbow trout (Oncorhynchus mykiss) using an integrative approach combining transcriptomics, proteomics, and microbiome analysis. After a six-week experiment, molecular analyses identified concentration-dependent transcriptional responses, including downregulation of genes involved in ion exchange (slc9a1b) and appetite regulation (ghrl), alongside upregulation of immune- and stress-related genes (il10, tfa), particularly at higher concentrations. Proteomic profiling showed a more pronounced effect of PS compared to PE, including suppression of digestive enzymes, disruption of lipid and energy metabolism, and activation of proteins associated with oxidative stress and immune responses. Microbiome analysis confirmed plastic-induced dysbiosis, characterised by reduced microbial diversity, depletion of beneficial taxa (e.g., Bacteroidota, Actinobacteriota), and shifts in short-chain fatty acid–producing bacteria. By integrating multiple levels of biological organisation, this study provides new insights into how microplastics interfere with intestinal physiology, beyond acute toxicity. The findings emphasise the relevance of polymer type and exposure concentration in shaping biological responses and highlight the vulnerability of freshwater species to environmental microplastics.
It is suggested that ciprofloxacin primarily impaired nutrient assimilation through abundance shifts in multiple bacterial classes of the gut microbiome, and thiacloprid reduced feeding potentially through neurophysiological mechanisms, with secondary effects on the microbiome.
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