Microplastics (MPs) have emerged as pervasive environmental contaminants with increasing relevance to human health. Beyond their role as inert particulate pollutants, accumulating evidence suggests that MPs may act as biologically active modulators of the gastrointestinal ecosystem. The gut represents a major interface for MP exposure, where ingested particles interact with intestinal epithelial cells, mucus layers, immune components, and resident microbial communities. This review summarizes current evidence on MPs' capacity to alter gut microbiota composition, impair intestinal barrier integrity, disrupt microbial metabolite production, and promote inflammatory and metabolic disturbances. Experimental studies indicate that MP exposure may reduce microbial diversity, shift the abundance of key bacterial taxa, impair tight junction proteins, and increase intestinal permeability. These changes may facilitate the translocation of bacterial products such as lipopolysaccharide, thereby activating inflammatory pathways including TLR4/NF-κB signaling. In parallel, MP-associated dysbiosis may alter short-chain fatty acids, bile acid metabolism, and tryptophan-derived metabolites, suggesting plausible biological pathways relevant to insulin resistance, hepatic lipid dysregulation, cardiometabolic risk, and gut-brain axis disruption. However, most available evidence is derived from animal and in vitro models, and causal relationships in humans remain insufficiently established. Major limitations include heterogeneous exposure protocols, non-standardized particle characterization, limited human longitudinal data, and difficulty separating particle-specific effects from those of associated chemical contaminants. Future studies integrating environmentally realistic exposure models, standardized microbiome analyses, multi-omics approaches, and human cohort designs are needed. Overall, the gut microbiota may represent a critical biological interface through which MPs interact with host physiology; however, further evidence is required before definitive conclusions can be drawn regarding their role in human chronic disease susceptibility.
