Postbiotic sequestration of micro- and nanoplastics: in vitro intestinal epithelial protection and proof of concept in the human mouth

Micro- and nanoplastics (MNPs) are ubiquitous dietary contaminants, yet practical strategies to reduce gastrointestinal exposure remain limited. We evaluated whether Qi601, a heat-inactivated Limosilactobacillus fermentum biofilm-derived postbiotic, could sequester fluorescent 100-nm polystyrene nanoplastics (PSNPs) and reduce their interaction with Caco-2 intestinal epithelial monolayers using sequential simulated digestion, protection, post-exposure rescue, and transfer assays. Consistent with particle sequestration, Qi601 produced approximately 92% depletion of free PSNP-associated fluorescence from the supernatant during sequential digestion. In protection assays, Qi601 reduced surface-associated and intracellular PSNP fluorescence by 65% and 67%, respectively, at 5 h, and by 41% and 33% at 24 h. In monolayers previously exposed to PSNPs for 24 h, Qi601 reduced surface-associated and intracellular PSNP fluorescence by 77% and 43%, respectively. Transfer of PSNP fluorescence from Qi601–PSNP agglomerates to Caco-2 cells remained ≤ 0.057%. Atomic force, scanning electron, and confocal microscopy demonstrated close physical association between Qi601 and PSNPs with predominantly extracellular localization of Qi601-associated PSNPs. In a qualitative human proof-of-concept chewing-gum experiment, microscopy of saliva showed heterogeneous, Nile Red-positive polymers within or closely associated with Qi601 agglomerates. Laser direct infrared (LDIR) chemical imaging showed that the number of rubber-class particles from the gum-plus-Qi601 saliva sample was 43% lower than from the gum-only sample (2,562 versus 4,529 particles; hit quality index ≥ 0.70); after procedural-control subtraction, the background-adjusted rubber particle count was approximately 91% lower (185 versus 2,152 particles; hit quality index ≥ 0.70). These findings establish proof of concept for postbiotic-mediated sequestration of dietary MNPs and support a model in which Qi601 limits their epithelial association and intracellular burden. To our knowledge, this represents the first human in vivo proof-of-concept study directly demonstrating physical association between an administered intervention designed to capture microplastics and microplastic particles. Further studies should define the molecular basis of Qi601–MNP interactions, characterize their gastrointestinal fate, and validate these findings in larger studies.