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61,005 resultsShowing papers similar to Multi-Omics Analysis of the Gut-Liver Axis Reveals the Mechanism of Liver Injury in Colitis Mice
ClearGut 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.
Integrated multi-omics of gut-liver axis to dissect the mechanism underlying hepatotoxicity induced by sub-chronic tire wear particles exposure in mice
Researchers gavaged female mice with tire wear particles (a major microplastic source) at three doses and performed integrated gut-liver multi-omics analysis, finding that sub-chronic exposure disrupted lipid metabolism, promoted liver inflammation, and altered gut microbial communities in a dose-dependent manner.
Chronic exposure to polyvinyl chloride microplastics induces liver injury and gut microbiota dysbiosis based on the integration of liver transcriptome profiles and full-length 16S rRNA sequencing data
Researchers exposed mice to polyvinyl chloride microplastics for 60 days and found significant liver damage accompanied by changes in gut bacteria composition. Gene expression analysis revealed that the liver injury involved inflammatory and metabolic pathways, while the gut microbiome shifted toward disease-associated bacterial profiles. The study suggests a connection between chronic microplastic exposure, gut health disruption, and liver toxicity.
Multiomics Reveals Nonphagocytosable Microplastics Induce Colon Inflammatory Injury via Bile Acid-Gut Microbiota Interactions and Barrier Dysfunction
Researchers used multi-omics analysis to understand how large microplastics that cannot be absorbed by intestinal cells still cause colon inflammation in mice. They found that long-term oral exposure to polystyrene microplastics disrupted bile acid metabolism and gut barrier function, leading to the accumulation of specific bile acids that triggered cell death in colon tissue. The study reveals a novel mechanism linking microplastic exposure to intestinal inflammation through bile acid-gut microbiota interactions.
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.
Research progress on the role of gut microbiota dysbiosis in the pathogenesis of immune−mediated liver diseases
This research review shows that an unhealthy gut microbiome (the bacteria living in your intestines) can trigger serious liver diseases where your immune system attacks your own liver. When gut bacteria are out of balance, harmful substances can leak into your bloodstream and cause dangerous inflammation in the liver. The good news is that treatments like probiotics and fecal transplants that restore healthy gut bacteria are showing promise for preventing and treating these liver diseases.
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.
Single-cell transcriptome analysis of liver immune microenvironment changes induced by microplastics in mice with non-alcoholic fatty liver
Using advanced single-cell analysis, researchers showed that microplastics worsened non-alcoholic fatty liver disease in mice fed a high-fat diet by changing how immune cells behaved in the liver. Microplastic exposure amplified inflammatory responses and altered the communication between different liver cell types. This study is important because it reveals specific immune mechanisms by which microplastics could worsen liver disease, a condition already affecting roughly one in four adults worldwide.
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.
Dose-effect of polystyrene microplastics on digestive toxicity in chickens (Gallus gallus): Multi-omics reveals critical role of gut-liver axis
Researchers fed chickens different doses of polystyrene microplastics and used multi-omics analysis to study digestive system damage through the gut-liver axis. They found that microplastics disrupted gut barrier function, altered liver metabolism, and changed gut bacterial communities in a dose-dependent manner. The study provides detailed molecular evidence of how microplastics can damage the digestive health of poultry, which may have implications for food safety.
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.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Proteomic and lipidomic profiling of mouse livers after polypropylene microplastic exposure revealed crosstalk between hepatic lipid fluctuations, nutrient metabolism disorders, and energy pathway disarrangements, providing mechanistic insight into microplastic-induced liver toxicity.
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.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Mouse liver studies with polypropylene microplastics revealed interconnected disruptions in lipid metabolism, nutrient processing, and energy balance, with proteomic and transcriptomic data highlighting the complexity of hepatic responses to chronic microplastic exposure.
Dysbiosis of gut microbiota in C57BL/6-Lepem1hwl/Korl mice during microplastics-caused hepatic metabolism disruption
Researchers administered polypropylene microplastics orally to obese mice for 9 weeks and found disruption of hepatic lipid, glucose, and amino acid metabolism alongside structural changes in gut microbiota, with microplastic-treated mice showing decreased hepatic lipid accumulation and altered abundance of specific bacterial genera.
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.
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.
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.
A probiotic for preventing microplastic toxicity: Clostridium dalinum mitigates microplastic-induced damage via microbiota-metabolism-barrier interactions
Using metagenomics and metabolomics, this study found that the probiotic bacterium Clostridium dalinum reduced microplastic-induced gut damage in mice by modulating gut microbiota composition, metabolic pathways, and intestinal barrier integrity.
Multi-omics association pattern between gut microbiota and host metabolism of a filter-feeding fish in situ exposed to microplastics
Scientists exposed filter-feeding fish to environmentally realistic levels of microplastics and found that the particles reshaped gut bacteria communities, which in turn altered the fish's liver metabolism through changes in amino acid processing. This gut-microbiome-to-organ connection matters because it shows microplastics may affect human health not just through direct toxicity but by disrupting the beneficial bacteria in our digestive systems.
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.
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.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study examined how polypropylene microplastics accumulate in and damage the mouse liver, using integrated lipidomics and transcriptomics to map the molecular landscape of microplastic-induced lipid disruption and metabolic dysfunction.
Nano‐plastics disrupt systemic metabolism by remodeling the bile acid–microbiota axis and driving hepatic–intestinal dysfunction
Mice were exposed to polyethylene terephthalate nanoparticles, and researchers used histopathology, metabolomics, and metagenomics to track downstream effects. Nanoplastic ingestion caused severe metabolic disruption—including weight loss, organ atrophy, and liver-intestinal dysfunction—by remodeling the bile acid–gut microbiota axis.