Potential Links Between Micro- and Nanoplastic Exposure, Enteric Neuropathy, and Gastrointestinal Dysmotility

Micro- and nanoplastics (MNPs) have emerged as ubiquitous environmental contaminants, with dietary ingestion serving as the primary route of human exposure. While their capacity to induce localized epithelial damage is well recognized, recent evidence suggests that MNPs can alter the complex regulatory networks governing gastrointestinal (GI) transit. The objective of this narrative review is to evaluate the role of MNP exposure as a possible pathogenic factor in GI dysmotility, assessing the intersection of neuromuscular toxicity, microbial dysbiosis, and barrier failure. A comprehensive literature search was conducted across major biomedical databases to synthesize emerging biomonitoring studies, preclinical models, and clinical correlations from the past five years characterizing MNP-mediated intestinal dysfunction. Ingestion of MNPs triggers a distinct, size-dependent, multifaceted, interconnected pathological triad characterized by ensuing oxidative stress, physical barrier dysfunction, and extensive microbiome reconfiguration. Rather than strict, isolated events, these insults interact in a self-perpetuating feedback loop. On a cellular level, nano-sized particles translocate across the intestinal lining via paracellular transport, persorption, or transcytosis, embedding into cell membranes and downregulating key tight junction (TJ) proteins (ZO-1, occludin, claudins). This mechanical and chemical disruption yields an overproduction of reactive oxygen species (ROS) and a concomitant reduction in anti-inflammatory, short-chain fatty acid (SCFA)-producing bacterial taxa (e.g., Bacteroidetes, Faecalibacterium, Roseburia). Crucially, this resulting mucosal disruption converges on the enteric nervous system (ENS). MNPs induce neuroendocrine derangements by perturbing cholinergic neurotransmission—characterized by acetylcholinesterase (AChE) inhibition, aberrant synaptic acetylcholine dynamics, and subsequent downregulation of muscarinic acetylcholine receptors (mAChRs)—ultimately resulting in uncoordinated smooth muscle contractility and delayed transit. In murine models, this enteric neuropathy manifests phenotypically as structural intestinal shortening, delayed gastric emptying, and chronic constipation. The intestinal defense network is susceptible to MNP bioaccumulation, wherein particle-induced barrier failure and microbial dysbiosis may contribute to downstream neuromuscular dysmotility. Understanding this interconnected oxidative-barrier–microbiome–neuromuscular axis is essential, positioning environmental plastic contamination as an emerging, potentially modifiable factor in the pathogenesis of functional bowel disorders.