BIRC3 RNA Editing Modulates Lipopolysaccharide-Induced Liver Inflammation: Potential Implications for Animal Health

Animals and humans are frequently infected by bacteria or exposed to bacterial derivatives in contaminated food, drinking water, or air, which significantly impacts their health. Among these bacterial sources, LPS (lipopolysaccharide) is the primary culprit. While it is widely known that LPS can cause liver inflammation and damage in animals, few studies have investigated this mechanism from the perspective of RNA editing. In this study, we administered LPS to mice via gavage to induce a liver injury model. We then used RNA editing omics approaches (RE-seq) to analyze RNA editing events potentially leading to liver inflammation following LPS administration, aiming to reveal the crucial role of RNA editing in LPS-induced processes. At the RNA editing level, we observed significant differences between the LPS group and the control (CON) group. Specifically, we identified 354 differentially edited genes, with 192 upregulated and 162 downregulated. These differentially edited genes were significantly enriched in pathways related to apoptosis, mTOR signaling, oxidative stress, and Nf-Kappa B signaling. By further integrating gene expression profiles and using a nine-quadrant analysis, we identified an important gene, Birc3, which showed significantly higher editing and expression levels in the LPS group. This gene is directly linked to liver inflammation and damage. The RNA editing of Birc3 represents a significant potential mechanism underlying LPS-induced liver damage, providing a novel approach for addressing animal and human health issues.