The role of microplastics in the pathogenesis of inflammatory bowel diseases

Plastics and their degradation products — microplastics and nanoplastics — are regarded as emerging and significant environmental pollutants that widely penetrate the human food chain. In recent years, increasing evidence has accumulated regarding the potential adverse effects of microplastics (MPs) on human health, particularly on the gastrointestinal tract, which represents the first barrier upon their ingestion. Objective. To summarize current experimental and clinical evidence on the role of microplastics in the pathogenesis of inflammatory bowel diseases (IBD). Key points. This review discusses the principal sources and types of microplastics, routes of human exposure, and mechanisms of their interaction with the intestinal barrier. Microplastics have been shown to induce mechanical damage to the intestinal mucosa, trigger oxidative stress and inflammatory responses, disrupt intestinal epithelial permeability, and impair immune homeostasis. Particular attention is paid to the effects of microplastics on the composition and functional activity of the gut microbiota, including reduced microbial diversity, overgrowth of opportunistic pathogens, and alterations in microbial metabolites. The role of microplastics as carriers of organic pollutants, pathogenic microorganisms, and antibiotic resistance genes is also considered, as this may enhance their biological activity. Clinical and experimental studies demonstrating higher concentrations of microplastics in patients with IBD and their association with disease severity are reviewed. Conclusion. The available evidence suggests a potential role of microplastics as an environmental factor contributing to intestinal homeostasis disruption and the development of inflammatory bowel diseases. The limited clinical data and heterogeneity of experimental models highlight the need for further fundamental and clinical epidemiological studies to clarify the actual contribution of microplastics to IBD pathogenesis.