Dr. Coopersmith’s research examines the pathophysiology of sepsis. A major focus is the role of gut epithelial apoptosis. Gut apoptosis is increased in both animal models and human autopsy studies of sepsis. However, this observation cannot distinguish whether gut apoptosis is beneficial, detrimental, or an epiphenomenon in sepsis. Dr. Coopersmith’s laboratory has shown that gut-specific overexpression of the antiapoptotic protein Bcl-2 improves survival in murine models of ruptured appendicitis and Pseudomonas aeruginosa pneumonia. His laboratory has demonstrated that age, the adaptive immune system, disease severity, permeability, and proliferative status all have important roles in mediating sepsis-induced gut apoptosis. Ongoing research is currently aimed at understanding mechanisms underlying sepsis-induced gut apoptosis and translating these findings for potential therapeutic use in patients. Dr. Coopersmith’s research also focuses on the importance of comorbidities in the pathophysiology of sepsis. Notably, the presence of malignancy markedly increases the risk of developing sepsis and the risk of dying from sepsis. Both the adaptive immune system and gut integrity are different in cancer/septic hosts and previously healthy septic hosts, and understanding these differences may potentially allow us to exploit them for therapeutic gain.