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Polystyrene nanoplastics promote colorectal tumorigenesis via gut microbiota-metabolite-Th17 cell axis
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In mice with chemically induced colorectal cancer, long-term feeding of polystyrene nanoplastics damaged the gut lining and altered gut bacteria, reducing a protective bacterium and its byproduct, propionic acid. This weakened an immune response linked to tumor fighting and increased tumor growth. Researchers also found microplastics in colorectal cancer patients' tissue and blood samples.
Nanoplastics (NPs) have emerged as pervasive environmental contaminants, yet their role in colorectal cancer (CRC) pathogenesis remains poorly understood. Here, we demonstrate that chronic oral exposure to polystyrene nanoplastics (PS-NPs) promotes colorectal tumorigenesis in a murine azoxymethane/dextran sulfate sodium (AOM/DSS)-induced CRC model through disruption of the gut microbiota–metabolite–immune axis. Mechanistically, PS-NPs accumulate predominantly in the colon and cause structural damage to intestinal epithelial microvilli. PS-NPs induce gut microbiota dysbiosis characterized by depletion of the beneficial bacterium Faecalibaculum rodentium ( F. rodentium ) and a consequent reduction in its protective metabolite, propionic acid. This metabolic perturbation attenuates Th17 cell differentiation and IL-17 A production, thereby impairing anti-tumor immunity. Clinically, we detected diverse microplastics in CRC patient tissues and blood. Collectively, our multi-omics and functional analyses delineate a mechanistic pathway linking environmental NPs exposure to colorectal carcinogenesis via the F. rodentium –propionic acid–Th17 cell axis, highlighting the gut microbiome and its metabolites as potential targets for intervention against pollution-associated cancer risks.
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In a mouse study, polystyrene nanoplastics accelerated the development of colon cancer linked to inflammatory bowel disease by disrupting fat metabolism and causing DNA damage in intestinal cells. The nanoplastics also altered gut bacteria and increased intestinal inflammation, suggesting that plastic particle exposure could worsen outcomes for people already at risk for colon cancer.
Microplastics’ Impact on the Development of AOM/DSS-Induced Colitis-Associated Colorectal Cancer in Mice
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Researchers used a mouse model of colitis-associated colorectal cancer and found that chronic polystyrene microplastic exposure (1.48 mg/kg/day for 12 weeks) increased tumor nodule number and promoted cancer development, providing experimental evidence linking microplastic ingestion to colorectal carcinogenesis.
Nanoplastics Shape Adaptive Anticancer Immunity in the Colon in Mice
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In a mouse study, researchers found that orally administered polyethylene nanoplastics disrupted the intestinal immune environment in ways that could favor tumor growth in the colon. The nanoplastics altered immune cell populations and promoted an immunosuppressive environment around colorectal tumors. The study suggests that nanoplastic exposure may influence how the immune system responds to abnormal cell growth in the gut.
A multi-omics signature of microplastic exposure and its clinical, metabolic, and microbial correlates in colorectal cancer
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Scientists found tiny plastic particles (from common plastics like PVC and polyethylene) built up more in colon tumors and the tissue around them than in blood samples from cancer patients. These plastic particles were linked to changes in blood chemistry and gut bacteria, suggesting microplastics might interact with the body's metabolism in ways connected to colorectal cancer. This is early evidence, not proof of cause and effect, but it highlights why reducing plastic exposure and further research into this link matter for gut health.
Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs
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Researchers found that polystyrene nanoplastics disrupt the gut lining in mice by altering tiny RNA molecules that control the production of protective proteins in the intestinal barrier. The nanoplastics also caused an imbalance in gut bacteria, creating a chain reaction where damaged gut cells release particles that further weaken the intestinal barrier and change the microbiome.
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