Oral administration of Lactobacillus brevis 23017 combined with ellagic acid attenuates intestinal inflammatory injury caused by Eimeria infection by activating the Nrf2/HO-1 antioxidant pathway

AbstractThe aim of this study was to investigate whether oral administration ofLactobacillus brevis 23017 (LB) alone and in combination with ellagic acid inhibits ChTLR15/ChNLRP3/ChIL-1 β by activating the Nrf2/HO-1 pathway to attenuate intestinal inflammatory injury. Two animal experiments were performed. In Experiment 1, chickens were allocated into 7 groups: PBS, and low, medium and high dosages of live and heat-killed LB, named L/LB(+), M/LB(+) and H/LB(+), and L/LB(−), M/LB (−) and H/LB(−), respectively. In Experiment 2, chickens were divided into 5 groups: PBS, challenge control, and low, medium and high dosages of ellagic acid combined with LB(+), named L/EA + L/LB(+), M/EA + M/LB(+) and H/EA + H/LB(+), respectively. Chickens were gavaged with LB with or without ellagic acid once a day. Then, the mRNA and protein levels of the components of the Nrf2/HO-1 pathway found in the caecal tissues were quantified. On Day 7 post-infection withE. tenella, the levels of the components of the ChTLR15/NLRP3/IL-1 β pathway in the caeca were again quantified, and the anticoccidial effects were assessed. The results showed that the levels of the genes in the Nrf2/HO-1 pathway in the chickens in the LB(+) groups were higher than those in the LB(−) groups (p <  0.001); those in the H/LB(+) group were higher than those in the M/LB(+) and L/LB(+) groups (p <  0.001); and those in the H/EA + H/LB(+) group showed the highest expression levels compared...
Source: Veterinary Research - Category: Veterinary Research Source Type: research