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Fig. 8 | BMC Microbiology

Fig. 8

From: Defining the temporal evolution of gut dysbiosis and inflammatory responses leading to hepatocellular carcinoma in Mdr2 −/− mouse model

Fig. 8

The temporal evolution of the gut microbiome, its functionality and inflammatory responses in Mdr2 −/− model of HCC. Schema summarizing key findings. The Mdr2 −/− mouse models exemplifies the process of inflammation mediated hepatocarcinogenesis as seen in humans. Dysbiosis and altered function of the microbiome occur with progression of liver injury/disease and hepatocarcinogenesis. A shift in functionality is seen with changes in intestinal barrier function early, followed by increased LPS biosynthesis and altered metabolic pathways with progressive liver disease. These changes occur in parallel with increased serum LPS levels, and a shift towards a Th1/Th17 cytokine milieu. In HCC there is a switch in microbiota function from carbohydrate to amino acid metabolism which may support hepatocarcinogenesis through direct and/or indirect mechanisms. The findings suggest that gut-based interventions should be timed early in the disease process to halt hepatocarcinogenesis. Figure was created with Biorender.com

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