MICRO- AND NANOPLASTICS IN INFLAMMATORY BOWEL DISEASE: FROM EXPERIMENTAL MODELS TO HUMAN EVIDENCE
DOI:
https://doi.org/10.31435/ijitss.4(52).2026.6481Keywords:
Microplastics, Nanoplastics, Inflammatory Bowel Disease, Ulcerative Colitis, Crohn’s DiseaseAbstract
Research objectives: Micro- and nanoplastics (MNPs) are pervasive environmental contaminants that may affect gastrointestinal health. This narrative review aimed to evaluate current mechanistic, experimental, and human evidence concerning the potential relationship between MNP exposure and inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease.
Methods: PubMed, Scopus, and Google Scholar were searched for human, animal, and in vitro studies investigating MNP exposure in IBD, experimental colitis, ileitis, intestinal inflammation, or mechanisms relevant to IBD pathogenesis. Studies addressing epithelial barrier dysfunction, mucus alterations, oxidative stress, immune activation, dysbiosis, and epithelial cell death were included. The evidence was synthesized descriptively because of substantial methodological heterogeneity.
Key findings: Experimental studies indicate that MNPs can impair the intestinal mucus layer and epithelial junctions, increase permeability, promote oxidative and mitochondrial stress, activate inflammatory pathways, alter the gut microbiota and microbial metabolites, and disturb epithelial regeneration. In healthy animals, these effects were generally mild, subclinical, or inconsistent, and MNP exposure alone did not reliably produce an IBD-like phenotype. In contrast, most chemically induced colitis models showed greater mucosal injury, inflammation, permeability, delayed healing, fibrosis, or colitis-associated tumorigenesis after MNP exposure. Human studies reported higher fecal microplastic concentrations in IBD and associations with disease activity and Crohn’s disease-related fibrosis, but evidence remains limited.
Conclusions: MNPs should currently be regarded as potential environmental modifiers of IBD rather than established etiological agents. Prospective studies using standardized exposure assessment and separate analyses of ulcerative colitis and Crohn’s disease are required to clarify causal relationships.
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