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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
Summary
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.