Microplastics and nanoplastics in inflammatory bowel disease: Mechanistic plausibility, human evidence and future research priorities

Figure 1 Overview of the main pathways contributing to human exposure to microplastics and nanoplastics. Plastic products from a wide range of industrial and domestic uses undergo fragmentation to generate microplastics and nanoplastics (MNPs). These particles, along with primary MNPs, contaminate air, aquatic systems and agricultural environments, which may subsequently be ingested by human via airborne particles, drinking water and dietary sources. Once the MNPs enter the human body they can pass through the gastrointestinal tract where they can interact with the intestinal immune system. MNPs: Microplastics and nanoplastics; UV: Ultraviolet. The image created in BioRender (Supplementary material).

Figure 2 Proposed intestinal mechanisms through which micro- and nanoplastics may influence inflammation relevant to inflammatory bowel disease. Schematic illustration of how microplastics and nanoplastics (MNPs) may interact with the intestinal mucosa and contribute to pathways relevant to intestinal inflammation. In inflamed mucosa, disruption of protective barriers may increase mucosal exposure to MNPs, facilitate uptake, permit passage into the lamina propria and subsequently systemic circulation. MNPs exposure may contribute to intestinal inflammation through multiple pathways including dysbiosis, impairment of the mucus layer, increased epithelial permeability, and activation of mucosal immune pathways. Numbered labels indicate the proposed sequence of MNPs uptake. Lettered labels indicate key mechanisms linking MNP exposure to intestinal inflammation. These pathways are based predominantly on in vitro and animal-model evidence. MNPs: Microplastics and nanoplastics; IL: Interleukin; TNF: Tumour necrosis factor. The image created in BioRender (Supplementary material).