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20 resultsShowing papers similar to Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut–Liver Axis
ClearGut microbiota and liver metabolomics reveal the potential mechanism of Lactobacillus rhamnosus GG modulating the liver toxicity caused by polystyrene microplastics in mice
Researchers found that the probiotic Lactobacillus rhamnosus GG helped protect mice from liver damage caused by polystyrene microplastic exposure. The probiotic worked by restoring healthy gut bacteria and normalizing liver metabolic pathways disrupted by the microplastics. The study suggests that supporting gut health through beneficial bacteria may help mitigate some of the toxic effects microplastics have on the liver.
Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice
Mice exposed to polyethylene microplastics developed liver damage that was traced back to disrupted gut bacteria -- the microplastics increased harmful bacteria while decreasing beneficial ones, triggering inflammation through the TLR2/NF-kB/NLRP3 immune pathway. This study provides new evidence that microplastics may harm the liver not just through direct contact, but indirectly by first throwing off the balance of gut bacteria.
Gut dysbiosis exacerbates inflammatory liver injury induced by environmentally relevant concentrations of nanoplastics via the gut-liver axis
This mouse study found that swallowing nanoplastics at levels found in the environment disrupted gut bacteria and damaged the intestinal barrier, allowing toxins to leak into the bloodstream and cause liver inflammation. When researchers transplanted gut bacteria from nanoplastic-exposed mice into healthy mice, those mice also developed liver damage. This demonstrates that nanoplastics may harm the liver indirectly by first disrupting the gut, a finding relevant to understanding how everyday plastic exposure could affect human health.
Polystyrene microplastics exacerbated liver injury from cyclophosphamide in mice: Insight into gut microbiota
Researchers developed a mouse model to investigate whether chronic pre-exposure to polystyrene microplastics worsens liver injury caused by the drug cyclophosphamide. The study found that mice with 90 days of microplastic exposure showed significantly more severe liver damage when subsequently treated with cyclophosphamide, with changes linked to gut microbiota disruption. The findings suggest that chronic microplastic exposure may reduce the liver's resilience to additional chemical stressors.
Environmentally Relevant Concentrations of Microplastic Exposure Cause Cholestasis and Bile Acid Metabolism Dysregulation through a Gut-Liver Loop in Mice
Mice exposed to environmentally realistic levels of polystyrene microplastics for 30 days developed damaged intestinal barriers, liver injury, and disrupted bile acid metabolism. The study revealed a gut-liver feedback loop where microplastics alter gut bacteria, which changes bile acid production, which in turn causes further liver damage, suggesting a mechanism by which everyday microplastic exposure could harm digestive health.
Gut microbiota dysbiosis exacerbates polystyrene microplastics-induced liver inflammation via activating LPS/TLR4 signaling pathway in ducks
This study found that polystyrene microplastics exacerbate gut microbiota dysbiosis in ducks, and that this disruption of the gut microbial community amplifies liver inflammation through the gut-liver axis, revealing a mechanism by which MP exposure causes hepatic injury.
Polystyrene microplastics induce gut microbiota dysbiosis and hepatic lipid metabolism disorder in mice
Researchers fed mice two sizes of polystyrene microplastics for five weeks and observed significant disruption of gut bacteria and changes in liver fat metabolism. The microplastics decreased mucus production in the gut and shifted the balance of key bacterial populations at multiple taxonomic levels. The study suggests that microplastic ingestion can trigger gut microbiota imbalance in mammals, which may in turn affect metabolic health.
Disturbed Gut-Liver axis indicating oral exposure to polystyrene microplastic potentially increases the risk of insulin resistance
Researchers found that oral exposure to polystyrene microplastics in mice disrupted the gut-liver axis, causing intestinal inflammation and liver metabolic dysfunction that together increased the risk of insulin resistance. The study showed that microplastics damaged the intestinal barrier, allowing harmful substances to reach the liver and trigger metabolic disturbances. These findings suggest a potential pathway by which microplastic ingestion could contribute to metabolic health problems.
Oral exposure to polyethylene microplastics of adult male mice fed a normal or western-style diet: impact on gut and gut-liver axis homeostasis
Researchers exposed adult male mice to polyethylene microplastics on normal or Western diet for 90 days, examining synergistic effects between plastic and dietary stress on gut and liver health. Microplastic exposure disrupted gut barrier integrity, altered the microbiome, and affected liver homeostasis, with some effects differing between normal and Western diet groups.
Microplastic-mediated new mechanism of liver damage: From the perspective of the gut-liver axis
This review describes how microplastics can damage the liver through the gut-liver axis: they first disrupt the gut's protective barrier and beneficial bacteria, allowing harmful substances to leak through the weakened intestinal wall into the bloodstream and travel to the liver. Once there, these substances cause inflammation, metabolic problems, and oxidative stress, offering a new explanation for how microplastic exposure could lead to liver disease.
Polystyrene microplastic exposure modulates gut microbiota and gut-liver axis in gilthead seabream (Sparus aurata)
Researchers fed gilthead seabream diets containing polystyrene microplastics and found that the particles disrupted the communication between the gut and liver, known as the gut-liver axis. The microplastics altered gut bacteria composition, increased liver inflammation markers, and changed bile acid metabolism. The study highlights how microplastic ingestion can trigger a chain of interconnected effects across multiple organ systems in fish.
Chronic exposure to polyethylene terephthalate microplastics induces gut microbiota dysbiosis and disordered hepatic lipid metabolism in mice
Researchers found that mice exposed to PET microplastics (the type commonly found in plastic bottles) over 17 weeks developed liver damage, including fat buildup, oxidative stress, and cell death. The study revealed that the damage was driven by changes in gut bacteria that altered lipid metabolism, and when researchers depleted the gut bacteria, the liver damage was reduced. This suggests the gut microbiome plays a key role in how microplastics cause harm to internal organs.
Impacts of polystyrene microplastic on the gut barrier, microbiota and metabolism of mice
Researchers exposed mice to polystyrene microplastics for six weeks and found that the particles accumulated in the gut, reduced protective mucus secretion, and damaged the intestinal barrier. The microplastics also significantly altered the composition of gut bacteria, decreasing beneficial species and increasing harmful ones. The study suggests that microplastic ingestion could disrupt gut health in mammals by simultaneously impairing the physical barrier and reshaping the microbiome.
Polystyrene microplastics exacerbate experimental colitis in mice tightly associated with the occurrence of hepatic inflammation
Researchers found that polystyrene microplastics worsened experimentally induced colitis in mice, causing greater intestinal inflammation, reduced mucus secretion, and increased gut permeability. The study also revealed that microplastic exposure in mice with colitis increased the risk of secondary liver inflammation, suggesting that individuals with pre-existing gut conditions may be more vulnerable to microplastic exposure.
Polystyrene microplastics exposure: Disruption of intestinal barrier integrity and hepatic function in infant mice
Researchers found that even low concentrations of polystyrene microplastics caused significant gut barrier damage and liver injury in infant mice. The microplastics disrupted the intestinal lining, allowed particles to leak into the bloodstream, and triggered liver fat accumulation and altered gut bacteria colonization. The study raises concerns about microplastic exposure during early life, when developing digestive and liver systems may be especially vulnerable.
Obesogenic polystyrene microplastic exposures disrupt the gut-liver-adipose axis
Mice that drank water containing polystyrene microplastics for 13 weeks developed signs of obesity and metabolic dysfunction, with disruptions across the gut, liver, and fat tissue. The microplastics caused intestinal bacteria changes, liver inflammation, and altered fat storage, affecting the entire gut-liver-fat tissue communication system. These findings suggest that chronic microplastic ingestion through contaminated water and food could contribute to obesity and metabolic disease in humans.
Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice
In a mouse study, oral exposure to high concentrations of polystyrene microplastics caused fatty liver disease and abnormal blood lipid levels even without prior gut leakiness. The microplastics triggered intestinal inflammation through immune cells, disrupted gut bacteria, and altered how the body processes nutrients. These results suggest that swallowing microplastics could contribute to metabolic problems and liver disease in humans.
Gut–Liver Axis Mediates the Combined Hepatointestinal Toxicity of Triclosan and Polystyrene Microplastics in Mice: Implications for Human Co-Exposure Risks
Mice co-exposed to the antimicrobial triclosan and polystyrene microplastics showed markedly worse intestinal and liver damage than those exposed to either contaminant alone, with gut microbiome disruption identified as a key mediating mechanism.
Microbiota-mediated metabolic perturbations in the gut and brain of mice after microplastic exposure
In a mouse study, oral exposure to polystyrene microplastics of two sizes altered the gut bacteria community and caused metabolic changes in both the intestines and the brain. The disrupted gut bacteria appeared to drive changes in bile acid, energy, and other metabolic pathways. These findings support the idea that microplastics in food and water could affect brain health indirectly by first disrupting the gut microbiome and its chemical signals.
Polystyrene nanoplastics exacerbate aflatoxin B1-induced hepatic injuries by modulating the gut−liver axis
Mice exposed to both polystyrene nanoplastics and aflatoxin B1, a common food contaminant from mold, suffered worse liver damage than from either pollutant alone. The nanoplastics disrupted gut bacteria and weakened the intestinal barrier, allowing more toxins to reach the liver through the gut-liver axis. This study is concerning because it shows that microplastics can amplify the harmful effects of other food contaminants people are already exposed to.