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.