Gut microbiota contribution to selenium deficiency-induced gut-liver inflammation.

There is limited knowledge about the factors that drive gut-liver axis changes after selenium (Se) deficiency-induced gut or liver injuries. Thus, we tested Se deficiency in mice to determine its effects on intestinal bacterial balance and whether it induced liver injury. Serum Se concentration, lipopolysaccharide (LPS) level, and liver injury biomarkers were tested using a biochemical method, while pathological changes in the liver and jejunum were observed via hematoxylin and eosin stain, and a fluorescence spectrophotometer was used to evaluate intestinal permeability. Tight junction (TJ)-related and toll-like receptor (TLR) signaling-related pathway genes and proteins were tested using quantitative polymerase chain reaction, western blotting, immunohistochemistry, and 16S ribosomal ribonucleic acid gene-targeted sequencing of jejunum microorganisms. Se deficiency significantly decreased glutathione peroxidase activity and disrupted the intestinal flora, with the most significant effect being a decrease in Lactobacillus reuteri. The expression of TJ-related genes and proteins decreased significantly with increased treatment time, whereas supplementation with Se, fecal microbiota transplantation, or L. reuteri reversed these decreases. Signs of liver injury and LPS content were significantly increased after intestinal flora imbalance or jejunum injury, and the levels of TLR signaling-related genes were significantly increased. The results indicated that Se deficiency disrupted the microbiota balance, decreased the expression of intestinal TJ factors, and increased intestinal permeability. By contrast, LPS increased due to a bacterial imbalance, which may induce inflammatory liver injury via the TLR4 signaling pathway.

Selenium Deficiency via the ROS/NLRP3/IL-1ß Signaling Pathway Leads to Pyroptosis Injury in Pig Spleen.

The aim of the present study was to investigate the effect of selenium (Se) deficiency on the relationship between the pyroptosis and MAPK signaling pathway in spleen injury. A total of 10 two-month-old Sus scrofa domesticus specimens were allocated to two groups. The control group was fed a basal diet (0.15-mg/kg Se), and the experimental group was fed a 0.03-mg/kg Se-deficient diet for 2 months. The pig-spleen histopathological changes were observed with hematoxylin-eosin staining. Frozen sections were prepared to detect the content of ROS in pig-spleen cells. The oxidation stress related indexes were determined using a spectrophotometer. The levels of pyroptosis- and MAPK signaling pathway-related factors were detected via quantitative real-time polymerase chain reaction (qPCR) and western blotting (WB). The results of sections showed that the lymphocytes decreased in number, the spacing of cells widened, and some cells were necrotic in the spleen tissue of pigs fed a low-selenium diet. The content of ROS, malondialdehyde, nitric oxide, H2O2, and catalase activity in the low-selenium group was significantly higher than that in the control group, and SOD activity was decreased. The protein-ratio-levels of p-Nrf2 to Nrf2 were decreased. The expression levels of nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3), IL-1ß, IL-18, ASC, gasdermin D, and caspase-1, the protein-ratio-levels of p-AKT serine/threonine kinase (p-AKT) to AKT, p-extracellular regulated protein kinases (ERK) to ERK, p-P38 MAPK to p-P38, and p-c-Jun N-terminal kinase (p-JNK) to JNK were significantly increased in the Se-deficient group compared with the control group. These results suggested that Se deficiency can induce oxidant stress, which increases pyroptosis- and inflammation-related factors of pig-spleen injury.