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Bifidobacterium Pseudolongum-Derived Inosine Mitigates Polystyrene Nanoplastics-Induced Hepatic Injury by Inhibiting
Kaikai Zhang1,2, Yuchuan Chen1, Jiayuan Wan1
1Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, State Key Laboratory of Multi-Organ Injury Prevention and Treatment, Key Laboratory of Infectious Diseases Research in South China, Ministry of Education, Guangdong Provincial Key Laboratory for Prevention and Control of Major Liver Diseases, Guangdong Provincial Clinical Research Center for Viral Hepatitis, Guangdong Institute of Hepatology, Guangdong Provincial Research Center for Liver Fibrosis Engineering and Technology, Southern Medical University, Guangzhou, China.
Abstract:
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.
Insights
Nanoplastics (NPs) exposure harms the liver by reducing beneficial gut bacteria like Bifidobacterium pseudolongum (B.p). Restoring B.p or its metabolite inosine protects against liver injury.
Area of Science:
- Environmental Health
- Microbiology
- Toxicology
- Hepatology
Background:
- Nanoplastics (NPs) exposure is linked to severe hepatic injuries.
- The gut microbiota's role in NP-induced liver damage is not fully understood.
- Microbial interventions are needed for NP-related hepatic injuries.
Purpose of the Study:
- To investigate the role of gut microbiota, specifically Bifidobacterium pseudolongum (B.p), in nanoplastics-induced hepatic injury.
- To explore the protective mechanisms of B.p and its metabolite inosine against liver damage.
- To identify potential microbial therapeutic strategies for nanoplastics exposure.
Main Methods:
- Oral administration of polystyrene nanoplastics to mice.
- Analysis of gut microbiota composition and metabolite levels (inosine).
- Fecal microbiota transplantation experiments.
- Colonization with B.p and supplementation with inosine.
- Investigation of molecular pathways including A2AR, miR155/SOCS1/NF-κB, and macrophage polarization.
Main Results:
- Oral nanoplastics exposure reduced B.p abundance and inosine levels, impairing gut homeostasis and causing liver injury.
- B.p colonization or inosine supplementation ameliorated nanoplastics-induced gut and liver damage.
- B.p-derived inosine normalized A2AR expression, inhibited the miR155/SOCS1/NF-κB pathway, and repressed M1 macrophage polarization.
Conclusions:
- Gut microbiota, particularly B.p, plays a crucial role in mediating nanoplastics-induced hepatic injury.
- B.p-derived inosine protects the liver by modulating the A2AR and miR155/SOCS1/NF-κB pathway, suppressing M1 macrophage polarization.
- B.p represents a promising microbial therapeutic strategy for mitigating nanoplastics-induced liver damage.
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