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IDDF2026-ABS-0347 Uncovering potential pro-carcinogenic effects of microplastics in colonic polyps and their association with gut dysbiosis and intestinal permeability dysfunction
Original title: IDDF2026-ABS-0347 Uncovering potential pro-carcinogenic effects of microplastics in colonic polyps and their association with gut dysbiosis and intestinal permeability dysfunction
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Researchers found higher levels of microplastics (tiny plastic particles from packaging, containers, and other everyday products) in colon polyps—growths that can sometimes turn into cancer—compared to healthy colon tissue. These microplastics were linked to an imbalanced gut microbiome and weakened connections between intestinal cells, both of which could make it easier for harmful changes to take hold. While this doesn't prove microplastics cause colon cancer, it adds to growing evidence that reducing plastic exposure may be worth taking seriously for gut health.
Background Emerging evidence suggests that environmental contaminants, such as microplastics (MPs), may accelerate colonic polyp progression by disrupting gut homeostasis. MPs have been detected in human stool and colonic tissue, raising concerns about their potential role in gastrointestinal diseases. This study investigates the presence and impact of MPs in polyps, exploring their association with gut dysbiosis and barrier dysfunction that may contribute to polyp-to-cancer progression. Methods Colonic tissues and stool from 35 healthy controls and 35 patients with colonic polyps were analysed for MPs using Laser Direct Infrared (LDIR) Chemical Imaging Spectroscopy with a spectral matching threshold >0.80. Gut microbiota composition was assessed by 16S rRNA amplicon sequencing. The ultrastructural integrity of epithelial junctions (tight junctions, adherens junctions, and desmosomes) was evaluated via transmission electron microscopy (TEM). Gene expression of proinflammatory cytokines and transmembrane proteins was measured using RT-qPCR. Results Polyp tissues and stool samples showed significantly higher levels of carcinogenic polyurethane (53.95±5.56) and polyvinyl chloride (5.48±2.42) respectively (IDDF2026-ABS-0347 Figure 1). MPs found in colonic polyps were more solid and spherical with smaller height, width, area, and perimeter. Gut microbiome composition differed significantly between colonic polyp and healthy individuals, with reduced richness and evenness observed in polyp patients (p<0.05) (IDDF2026-ABS-0347 Figure 2). Both mucin-degrading bacteria (Parabacterioides_B_distasonis, Phocaeicola_A_vulgatus, Bacteroides_H_thetaiotaomicron) and mucin-producing bacteria (Blautia sp.) were enriched in polyps, indicating a dynamic microbial response to maintain mucosal homeostasis (IDDF2026-ABS-0347 Figure 3). Fusobacterium, a genus with known pathogenic potential, was frequently detected in polyp tissues. The presence of pathogenic bacteria corresponded with reduced propanoic acid levels (6.82±5.05; p<0.05) (IDDF2026-ABS-0347 Figure 4). TEM analysis revealed widened tight junctions (10.5±0.96nm), adherens junctions (20.38 ±1.98nm), and desmosomes (26.98±2.06nm) in polyp tissues (p<0.05), indicating epithelial barrier disruption (IDDF2026-ABS-0347 Figure 5). Furthermore, an immunosuppressive environment was evidenced by downregulation of IFN-γ and upregulation of CDH1 and CLDN1 in colonic polyps (IDDF2026-ABS-0347 Figure 6). Conclusions These findings suggest that MPs may influence gut microbiota composition and compromise epithelial barrier integrity, potentially contributing to precancerous changes in colonic polyps. The correlation between MP abundance in colonic polyp tissues and microbial dysbiosis underscores their potential role in colorectal cancer (CRC) development and the urgent need to clarify the underlying mechanisms linking MP exposures to CRC risk.
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