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

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This review pulls together what scientists currently know about tiny plastic particles (microplastics and nanoplastics) and their possible link to inflammatory bowel disease (IBD), a condition that causes chronic gut inflammation. Lab studies suggest these plastic particles could disrupt gut bacteria, damage the intestinal lining, and trigger immune responses—all things that matter in IBD—but so far there's no solid proof from human studies that plastics actually cause or worsen the disease. In short: the theory is plausible and worth watching, but we need better research before drawing firm conclusions about how the plastics in our food and environment

Microplastics and nanoplastics (MNPs) are increasingly recognized as ubiquitous environmental contaminants with unavoidable human exposure through ingestion and inhalation.The gastrointestinal tract is an important interface between MNPs and the intestinal microbiota, epithelium and immune system.Interest in the effects of MNPs on human health has been increasing particularly in inflammatory bowel disease (IBD), a chronic immune-mediated disease in which environmental factors are thought to contribute to disease pathogenesis.Experimental studies have suggested that intestinal MNP exposure may promote several pathways relevant in IBD including dysbiosis, mucus disruption, impaired epithelial integrity, intestinal permeability and activation of immune pathways.Current evidence is largely translational and is dominated by experimental models that do not reflect real world human exposures.Human studies in IBD are currently limited to a small number of observational studies with data vulnerable to confounding and reverse causation.Despite increasing mechanistic plausibility, there is still no direct evidence that MNPs cause IBD or alter the disease course.In this narrative review we summaries the current knowledge on human MNPs exposures, we examine experimental evidence for biologically plausible pathways through which MNPs may influence intestinal inflammation and the emerging human evidence in IBD.We also explore the major analytical and methodological limitations in the field.

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