AI Article Synopsis
- Gut dysbiosis, particularly involving Enterococcus faecalis, is linked to chronic liver diseases and liver cancer, though the exact mechanisms are not fully understood.* ! -
- Research showed that transplanting gut microbiota from hepatitis C patients into mice led to increased liver tumors and higher sensitivity to liver carcinogens.* ! -
- E. faecalis enhances liver tumor development by activating certain growth genes through a specific immune pathway, while also lowering levels of certain bile acids in feces.* !
Article Abstract
Gut dysbiosis is observed in chronic hepatobiliary diseases and is frequently associated with liver carcinogenesis; however, the extent and specific mechanisms triggered by alterations in the microbiota mediating tumorigenesis in these patients remain unclear. Here we show that Enterococcus faecalis is abundant in the microbiota of patients with hepatitis C virus-related chronic liver disease. Xenotransplantation of gut microbiota from these patients increased the number of spontaneous liver tumors in mice and enhanced susceptibility to liver carcinogens. Hepatic colonization by gelE-positive E. faecalis increased liver expression of proliferative genes in a TLR4-Myd88-dependent manner, leading to liver tumorigenesis. Moreover, decreased fecal deoxycholic acid levels were associated with colonization by E. faecalis. Overall, these data identify E. faecalis as a key promoter of liver carcinogenesis.
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| http://dx.doi.org/10.1038/s43018-021-00251-3 | DOI Listing |
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