High-salt diet leads to liver fibrosis with enterococcus pathway

The protein expression levels of TGF-β, TNF-α, and MCP-1 were significantly higher in the HSD group than in the normal group. These factors are known to be involved in the development of liver fibrosis.

The study also found that HSD altered the gut microbiota composition, impaired the intestinal barrier function, and promoted the translocation of bacteria, particularly Enterococcus.

In vitro experiments showed that Enterococcus induced macrophage activation through the NF-κB pathway, leading to the expression of fibrosis-related genes and the development of liver fibrogenesis. The study also found that Enterococcus disrupted the gut microbiome in vivo and significantly increased the expression of fibrotic markers in the liver.

These findings have important implications for liver fibrosis therapy and gut microbiota management. The study suggests that an HSD can exacerbate liver fibrosis by altering the gut microbiota composition, and that this may serve as a new target for liver fibrosis therapy. The study also highlights the importance of  and other related health problems.

Source:

Zhang, X., Liang, Y., Jiang, J., Lu, C., Shi, F., Cao, Q., Zhang, Y., & Diao, H. (2023). A High-Salt Diet Exacerbates Liver Fibrosis through Enterococcus -Dependent Macrophage Activation. In Y. Fu (Ed.), Microbiology Spectrum. American Society for Microbiology. https://doi.org/10.1128/spectrum.03403-22