Deficiency of neutrophil high-mobility group box-1 in liver transplant recipients exacerbates early allograft injury in mice
To investigate the role of recipient neutrophil intracellular HMGB1 in early allograft injury after liver transplant. Using a mouse orthotopic liver transplant model, as well as LPS injection, we found that neutrophils significantly infiltrate the liver after liver transplant and LPS challenge. Deficiency of neutrophil HMGB1 enhances their activation, boosts their pro-oxidant and pro-inflammatory phenotype, and hinders biosynthesis and metabolism of inositol polyphosphates. Overall, these events exacerbate early allograft injury after liver transplant. Overall design: Comparative gene expression profiling analysis of RNA-seq data from neutrophils of WT and Hmgb1?Mye mice treated with saline or LPS.