Characterizing the impact of neonatal sepsis on mitochondrial respiration and cellular metabolism in the developing heart and kidney
Sepsis (blood poisoning) in early-life leads to 1.4 million deaths annually. Preterm babies are at a higher risk of developing early-life sepsis than term-born infants due to an underdeveloped immune system. Even after recovery, sepsis can adversely affect heart and kidney development and function, subjecting them to health complications throughout life. Our goal is to study how exposure to sepsis early in life affects heart and kidney development and function by examining its impact on tissue mitochondria, which are the powerhouses of the cell. Importantly, we are interested in studying why health complications persist even after these neonates recover from sepsis. We will induce abdominal sepsis in rat pups, which models pre-term babies (who are most susceptible to sepsis). Pups will be monitored for heart (cardiac) and kidney (vascular) mitochondrial function at various timepoints after insult. Moreover, we will study the lasting effects of early-life sepsis on heart and kidney health after pups recover and grow into adulthood. To study the immediate and lasting effects of sepsis, we will use metabolomics, which enables us to simultaneously measure thousands of chemicals involved in mitochondrial function and energy metabolism. Due to the high prevalence of early-life sepsis in pre-term newborns, these health issues are likely important contributors to the global burden of cardiovascular disease. Our aim is to lay a foundation upon which we can devise new treatments for this condition to improve survival and promote better health outcomes for future children as they grow into young adults.