We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Bifidobacterium Pseudolongum‐Derived Inosine Mitigates Polystyrene Nanoplastics‐Induced Hepatic Injury by Inhibiting the Polarization of M1 Macrophages
Original title: Bifidobacterium Pseudolongum‐ Derived Inosine Mitigates Polystyrene Nanoplastics‐Induced Hepatic Injury by Inhibiting the Polarization of M1 Macrophages
AI summary Read the abstract
Tiny plastic particles from everyday exposure can damage the liver, and this mouse study found that they do so partly by wiping out a helpful gut bacterium and its byproduct, a molecule called inosine, that normally keeps liver inflammation in check. When researchers restored this bacterium or gave the mice inosine directly, it calmed down the inflammatory immune cells and protected the liver from plastic-related damage. While this research is still in the early animal-testing stage, it points to a promising future strategy—boosting specific gut bacteria—that could help protect our livers from the health effects of the microplastics we're increasingly ex
Nanoplastics (NPs) exposure can cause severe hepatic injuries. Gut microbiota is considered a contributing factor to multiple hepatic injuries. However, its role in NPs-induced hepatic injuries remains unclear, and microbial intervention strategies are required. Our results reveal that oral exposure to polystyrene NPs reduces gut probiotic Bifidobacterium pseudolongum (B.p) and its metabolite inosine. Gut microbiota from NPs-administered mice partially reproduces NPs-related impairment of gut homeostasis and hepatic injury in recipient mice. Moreover, B.p colonization improves NPs-induced gut homeostasis impairment and hepatic injury, and its protective effects are reproduced by supplementation with inosine. Mechanically, B.p colonization increases hepatic level of inosine and subsequently normalizes the expression of its target A2AR. Meanwhile, increased inosine inhibits the miR155/SOCS1/NF-κB pathway and represses NPs-induced M1 macrophage polarization. CGS21680, an agonist of A2AR, effectively represses lipopolysaccharide (LPS)-induced M1 macrophage polarization and inhibits the miR155/SOCS1/NF-κB pathway in vitro. Further, miR155 knockout inhibits NPs-induced M1 macrophage polarization, but does not influence the suppression of NPs on A2AR. These findings suggest that B.p-derived inosine can repress NPs-induced M1 macrophages polarization by inhibiting the miR155/SOCS1/NF-κB pathway via targeting A2AR. Altogether, this study further clarifies the role of gut microbiota in NPs-induced hepatic injury and provides a potential microbial therapeutic strategy.
More Papers Like This
Gut microbiota and liver metabolomics reveal the potential mechanism of Lactobacillus rhamnosus GG modulating the liver toxicity caused by polystyrene microplastics in mice
AI summary Read the abstract
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.
Gut dysbiosis exacerbates inflammatory liver injury induced by environmentally relevant concentrations of nanoplastics via the gut-liver axis
AI summary Read the abstract
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.
Lactiplantibacillus plantarum ZP-6 mitigates polystyrene nanoplastics-induced liver damage in colitis mice via the gut-liver axis
AI summary Read the abstract
The probiotic strain Lactiplantibacillus plantarum ZP-6 mitigated polystyrene nanoplastic-induced liver injury in an animal model through multiple mechanisms including toxin binding, barrier enhancement, and anti-inflammatory activity, suggesting probiotics as a potential strategy for reducing nanoplastic health impacts.
Inulin-modified nano selenium biocomposite with dual-targeting capability mitigates polystyrene nanoplastic-induced hepatic ferroptosis
AI summary Read the abstract
Tiny plastic particles that we're increasingly exposed to (called nanoplastics) can damage the liver by triggering a harmful type of cell death, partly by throwing off the balance of gut bacteria. In this mouse study, researchers found that a specially modified selenium supplement helped protect the liver from this damage, both by boosting the body's natural antioxidant defenses and by restoring healthy gut bacteria function. While this is early-stage animal research, it points to a promising future strategy for protecting ourselves from the health effects of plastic pollution that's now nearly impossible to avoid.
Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice
AI summary Read the abstract
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.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.