Li · Ecotoxicology and environmental safety 2024 · Controlled animal exposure experiment · n=?

Chronic exposure to polystyrene nanoplastics induces intestinal mechanical and immune barrier dysfunction in mice.

Cited 76 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Preclinical animal research (Oxford CEBM Level 5: bench or animal research)

PubMed 38039854 · doi:10.1016/j.ecoenv.2023.115749 · record verified 2026-08-26

What was done

Mice were administered drinking water containing polystyrene nanoplastics (PS-NPs) at concentrations of 0.1, 1, and 10 mg·L⁻¹ for up to 32 consecutive weeks alongside unexposed controls. At 28 weeks, intestinal tissue morphology, endocytosis markers (caveolin, clathrin), tight junction proteins (claudin-1, occludin, ZO-1), and lymphocyte subsets (B cells in MLNs; T cells in IELs and LPLs) were evaluated via immunohistochemistry, hematoxylin-eosin staining, and flow cytometry. Oxidative stress markers (ROS, MDA, SOD, GSH-Px) and pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) in intestinal tissues were quantified by ELISA at weeks 12, 16, 20, 24, and 32.

What was found

Oral PS-NPs accumulated in mouse intestinal tissues and upregulated clathrin and caveolin expression. At 1 and 10 mg·L⁻¹, PS-NPs induced structural abnormalities including villus erosion, reduced crypt numbers, inflammatory cell infiltration, and significant decreases in claudin-1, occludin, and ZO-1 proteins. Exposure to 0.1 mg·L⁻¹ decreased occludin without significantly altering claudin-1 or ZO-1. PS-NP exposure produced time- and dose-dependent increases in ROS, MDA, IL-1β, IL-6, and TNF-α, with concurrent reductions in SOD and GSH-Px. Immunologically, PS-NPs increased the proportion of B cells in MLNs and reduced CD8+ T cells in IELs and LPLs. The abstract reported directional shifts and statistical significance without exact numerical values.

Why it matters

This study shows that long-term ingestion of nanoplastics can trigger mechanical and immune barrier dysfunction in the mammalian gut via tight junction degradation and sustained oxidative inflammation.

Limits

Findings are derived entirely from an animal model and cannot be directly translated to human exposure risk without clinical validation. The abstract does not report the specific mouse strain, total sample size (n), particle size distribution, or quantitative numerical values for the measured outcomes.

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