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61,005 resultsShowing papers similar to Why do microplastics aggravate cholestatic liver disease? The NLRP3-mediated intestinal barrier integrity damage matter
ClearEnvironmentally 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 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.
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.
Polystyrene nanoplastics induce intestinal and hepatic inflammation through activation of NF-κB/NLRP3 pathways and related gut-liver axis in mice
In a mouse study, ingested polystyrene nanoplastics accumulated in the gut and liver and triggered inflammation through specific immune pathways, damaging the intestinal lining and allowing bacterial toxins to leak into the liver. This gut-liver connection suggests that swallowing nanoplastics could set off a chain reaction of inflammation affecting multiple organs in the body.
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.
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.
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 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.
Proinflammatory properties and lipid disturbance of polystyrene microplastics in the livers of mice with acute colitis
Researchers studied the effects of polystyrene microplastics on the livers of mice fed a high-fat diet and found that the particles triggered significant inflammatory responses and disrupted lipid metabolism. The microplastics worsened fat accumulation in the liver and activated inflammatory signaling pathways. The findings suggest that microplastic exposure combined with a high-fat diet may amplify liver damage and metabolic disturbances.
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.
Prolonged oral ingestion of microplastics induced inflammation in the liver tissues of C57BL/6J mice through polarization of macrophages and increased infiltration of natural killer cells
Researchers found that prolonged oral ingestion of polystyrene microplastics caused liver inflammation in mice by polarizing macrophages and increasing natural killer cell infiltration, revealing how microplastics disrupt the liver immune microenvironment.
Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut–Liver Axis
This mouse study showed that polystyrene microplastics cause liver damage partly through disrupting gut bacteria, which then triggers harmful signals along the gut-liver connection. When researchers eliminated gut bacteria with antibiotics, liver damage from microplastics was reduced, confirming the gut microbiome plays a key role. Green tea extract (EGCG) helped protect the liver by restoring healthy gut bacteria, suggesting diet may help counteract some effects of microplastic exposure.
Low-dose polystyrene microplastics exposure increases susceptibility to obesity-induced MASLD via disrupting intestinal barrier integrity and gut microbiota homeostasis
A mouse study found that even low doses of polystyrene microplastics made fatty liver disease significantly worse when combined with a high-fat diet, creating a "double hit" effect. The microplastics damaged the gut lining, disrupted beneficial gut bacteria, and triggered inflammation that spread to the liver, and these harmful effects were difficult to reverse even after two weeks of stopping exposure.
Polystyrene microplastics aggravate inflammatory damage in mice with intestinal immune imbalance
Researchers found that polystyrene microplastics caused significantly worse inflammatory damage in mice that already had compromised intestinal immune systems compared to healthy mice. The microplastics increased inflammatory markers, disrupted gut bacteria, and caused more severe tissue damage in the vulnerable animals. The study suggests that individuals with pre-existing gut health issues may be more susceptible to the harmful effects of microplastic exposure.
Chronic PET‐Microplastic Exposure: Disruption of Gut–Liver Homeostasis and Risk of Hepatic Steatosis
Researchers exposed mice to PET microplastics ground from plastic bottles over 29 weeks and found that the particles caused obesity, liver enlargement, fatty liver disease, and early-stage scarring of liver tissue. The microplastics also disrupted gut bacteria and bile acid metabolism, pointing to damage along the gut-liver connection. The findings raise concerns about the long-term health effects of chronic exposure to the type of microplastics commonly found in food and beverages.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
Exposure to submicroplastics promotes the progression of nonalcoholic fatty liver disease in ApoE-deficient mice
Researchers found that exposing mice to submicron-sized polystyrene plastics in their drinking water for 12 weeks accelerated the progression of nonalcoholic fatty liver disease. The tiny plastic particles accumulated in the liver, worsened fat buildup, increased inflammation, and disrupted cholesterol metabolism. This study suggests that people who already have risk factors for liver disease may be especially vulnerable to health effects from microplastic exposure.
Chronic environmental exposure to polystyrene microplastics increases the risk of nonalcoholic fatty liver disease
A mouse study found that long-term exposure to polystyrene microplastics increased the risk of developing non-alcoholic fatty liver disease. The microplastics accumulated in the liver and disrupted fat metabolism, causing inflammation and liver damage, which is concerning because most previous studies only looked at short-term exposure effects.
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.
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.
Impact of microplastics and nanoplastics on liver health: Current understanding and future research directions
This review summarizes what scientists know about how micro- and nanoplastics affect the liver, which is one of the first organs exposed because it processes everything absorbed from the gut. The particles trigger oxidative stress, disrupt energy metabolism, cause cell death, and promote inflammation, and may contribute to conditions like fatty liver disease and liver fibrosis. The paper also highlights how plastics can disturb the gut microbiome, which communicates with the liver through the gut-liver axis and may amplify liver damage.
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.
Gut 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.
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.