Gut Microbiota Contributes to the Development of Selenium-Deficiency-Induced Gut-Liver Inflammation

Little is known about the factors that drive the gut-liver axis changes in selenium (Se)-deficiency-induced gut and liver injury. We tested Se deficiency in mice to determine whether or not it would break the intestinal bacteria balance as well as induce liver injury. Serum Se status, LPS, and liver injury biomarkers were tested by a biochemical method. Liver and jejunum pathological changes were observed by H & E stains, and a fluorescence spectrophotometer was used for the evaluation of the intestinal permeability. Tight-junction-related and toll like receptor (TLR) signaling pathway genes and proteins were tested using qPCR, WB or IHC. 16S rRNA gene-targeted sequencing of jejunum microorganisms was done. Se deficiency significantly decreased GPx activity and disrupted intestinal flora, with the most significant decrease in Lactobacillus reuteri. Expression of tight-junction-related genes and proteins was significantly decreased with increasing treatment time, while supplementation with Se, feces microbiota transplantation, or L. reuteri reversed these decreases. Signs of liver injury and LPS were significantly increased after the intestinal flora imbalance and jejunum injury. The levels of TLR-signaling-related genes were significantly increased. The results indicate that Se deficiency disrupts the balance of microbiota, decreases expression of intestinal tight junction factors, and increases intestinal permeability. LPS by Se deficiency-induced liver injury was shown to increase via activation of the TLR4/MyD88/NF-kB signaling pathway.