Micro- and nanoplastics (MNPs) are ubiquitous environmental contaminants and a growing public health concern(1). Oral ingestion is considered a major route of MNP exposure(2). As MNPs have been detected in human stool(3), they may alter the gut microbiome and disrupt intestinal homeostasis. Rodent models are widely used to study gut microbial responses under controlled conditions. However, findings from experimental studies are inconsistent, and substantial variation in study design and analytical approaches limits interpretation. This systematic review and meta-analysis aimed to determine the effects of MNP exposure on the gut microbiome and host responses in rodent models.
Peer-reviewed rodent studies investigating MNP exposure and gut microbiome outcomes were systematically identified from four databases up to November 2025 (PROSPERO: CRD420251179715). Where raw 16S rRNA sequencing data were available, data were re-analysed using a standardised bioinformatics pipeline (nf-core/ampliseq). Alpha diversity was assessed using the Shannon index, while beta diversity was evaluated using Bray–Curtis dissimilarity. Random-effects meta-analyses were conducted for sufficiently comparable microbiome and host biomarker outcomes.
A total of 117 studies were included. Following author contact, raw sequencing data were obtained for 15 studies (13%). Standardised re-analysis showed no significant overall effect of MNP exposure on Shannon diversity (mean difference = −0.26, 95% confidence interval: −0.66 to 0.14; p = 0.16). Beta-diversity and taxonomic findings were heterogeneous across studies, with no consistent pattern of microbiome alteration observed. In contrast, meta-analyses of host biomarkers extracted from the included studies showed more consistent responses. Markers of gut epithelial barrier integrity were reduced at both the mRNA and protein levels. Significant decreases were observed in Tjp1 (encoding zonula occludens-1 [ZO-1]) and Ocln (encoding occludin [OCLN]) mRNA expression (effect sizes: −2.18 and −2.04, respectively), as well as in ZO-1 and OCLN protein expression (−2.19 and −4.88, respectively) (all p < 0.05). In the gut, MNP exposure increased pro-inflammatory markers at the mRNA (Tnfa: 2.59, p < 0.05; Il1b: 2.38, p < 0.05), and protein level (TNF-α: 3.33, p < 0.01; IL-1β: 3.31, p < 0.05). Lastly, decreased superoxide dismutase (−3.36, p < 0.05), alongside non-significant alterations in other oxidative stress markers, suggested increased oxidative stress following MNP exposure. Experimental conditions varied substantially across studies, while environmental conditions were often poorly reported, limiting assessment of background MNP exposure.
Overall, we found no consistent evidence that MNP exposure alters gut microbial diversity or composition in rodent models; however, exposure disrupted markers of gut epithelial barrier integrity and promoted inflammatory signalling and oxidative stress. Broader quantitative synthesis and cross-study comparison was limited due to data availability and accessibility. Based on these findings and limitations, we developed a research checklist to improve the consistency, transparency and reproducibility of future studies and strengthen their translation to human health.