Intestinal inflammation caused by selenium (Se) deficiency is one of the causes of broiler diarrhea, which can harm the health of poultry. The addition of Se is the current method to relieve this problem, but it has not fundamentally resolved intestinal inflammation. Therefore, we are looking for new strategies to alleviate intestinal inflammation by studying the specific mechanisms underlying Se deficiency. By replicating the Se-deficient broiler model and establishing a chicken small intestinal epithelial cell (CSIEC) model, we determined that Se deficiency caused intestinal inflammation in broilers by decreasing glutathione peroxidase (GPX) 3 expression. Recently discovered competing endogenous RNAs (ceRNAs) form novel regulatory networks, which were found that selenoproteins are involved in ceRNA regulation. This study aimed to explore the mechanism through which Se deficiency regulates intestinal inflammation in broilers through ceRNAs. In previous studies, the ceRNA regulatory relationship between long non-coding RNA (lncRNA)WSF27, miR-1696, and GPX3 has been determined. To further determine the mechanism underlying this axis in intestinal inflammation in Se-deficient broilers, we established CSIEC models with GPX3 knockdown/overexpression, lncRNAWSF27 knockdown, and miR-1696 knockdown/overexpression to simulate intestinal injury. The results showed that Se deficiency reduced GPX3 expression through the lncRNAWSF27/miR-1696 axis, activated oxidative stress, and caused necroptosis, inflammatory responses, and tight junction damage.

Read the full article in the Journal of Animal Science.