Determining the cellular and molecular pathophysiology of the pulmonary response to thermal injury and its association with infection will elucidate possible therapeutic strategies to reduce the pulmonary sequelae following burns. Using a murine "knock out" model deficient in apoptosis and resistant to pulmonary injury following burns and a model deficient in IL-10, a down regulator of the immune response, the differences in the histopathology, predisposition to infection, and the cytokine profile (both protein and mRNA) will demonstrate those factors central to the pulmonary response to injury. The studies will include attempts to alter the inflammatory process using organ-specific cytokine gene therapies.