Immune Mechanisms and Immunomodulation in Sepsis and Injury Sepsis and multiple organ failure are leading causes of death in the Intensive Care Unit. They result from a complex inflammatory response that is initiated by activation of the innate immune system by interactions between host cells and microbes or endogenous host factors that are released during injury or cell death. Non-infectious processes can also cause tissue injury, dysfunction, and long-term complications, such as chronic pain, through the activation of innate immune signaling and inflammation. The Hellman laboratory uses in vitro and in vivo system to define immunologic mechanisms and to explore immunomodulation in sepsis and in acute and non-acute injury. Current research focuses include understanding the role of Toll-like receptor (TLR) signaling in different cell populations (e.g.: endothelial cells, leukocytes) in sepsis and injury, defining the mechanisms of endothelial activation and dysfunction in sepsis and critical illness, and delineating the immune and functional effects of activation of the endocannabinoid and endovanilloid systems in sepsis, acute inflammation and pain.
