Polychlorinated biphenyls (PCBs) exposure is closely associated with the prevalence of metabolic diseases, including fatty liver and dyslipidemia. Emerging literature suggests that disturbance of gut microbiota is related to PCB126-induced metabolic disorders. However, the causal role of dysbiosis in PCB126-induced fatty liver is still unknown. To clarify the role of the gut microbiome in the detoxification of PCB126 in intestine or PCB126-induced toxicity in liver, mice were administrated with drinking water containing antibiotics (ampicillin, vancomycin, neomycin, and metronidazole) or Inulin. We showed that PCB126 resulted in significant hepatic lipid accumulation, inflammation, and fibrosis. PCB126, Antibiotics, and Inulin significantly affected the structure and shifted community membership of gut microbiome. 7 KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways at level 2 and 39 KEGG pathways at level 3 were significantly affected. Antibiotics alleviated PCB126-induced fibrosis in the liver but increased inflammation. Inulin treatment ameliorated both inflammation and fibrosis in the liver of PCB126-treated mice. Neither Antibiotics nor Inulin had significant effect on PCB126-induced hepatic steatosis. The more specific intervention of gut microbiota is needed to alleviate PCB126-induced fatty liver. These data demonstrate that homeostasis of gut microbiota is critical for the defense against PCB126 toxicity and dysbiosis plays a fundamental role in the development of inflammation and fibrosis in liver of PCB126-treated mice.
Keywords: Antibiotics; Dysbiosis; Fatty liver; Inulin; Polychlorinated biphenyl 126.
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