The long-term research interest in my lab is to investigate the function and mechanism of glucose metabolism and mitochondrial metabolism in the innate immune function during pathogen infection and inflammatory diseases. Sepsis, pathogen infection including bacteria, DNA or RNA viruses, are our main disease focuses. 1. For glucose metabolism studies, we are currently focusing on two glucose metabolism pathways, the hexosamine biosynthesis pathway (HBP) and the pentose phosphate pathway (PPP). Using the combined biochemical, genetic, metabolomics and animal modeling strategies, our recent studies show that 1) HBP-associated O-GlcNAc signaling negatively regulates TLR-mediated innate immune activation in sepsis; 2) PPP is critical for inflammasome activation and bacterial killing in septic inflammation; 3) O-GlcNAc signaling in required for MAVS-mediated antiviral innate immunity. 2. For mitochondrial metabolism pathway, we are interested in the role of mitochondrial calcium uniporter (MCU)-mediated mitochondrial metabolism in the innate immune response. We found that MCU deletion in myeloid cells results in enhanced bacterial killing during bacterial challenge.