Ischemia-reperfusion injury

In the field of lung and heart transplantation, one focus is on research into so-called ischemia/reperfusion injury (cooperation with Prof. Dr. G. Warnecke, Dr. B. Wiegmann, HTTG). The cold, ex vivo preservation of the organ before transplantation and its warm reperfusion after vascularization cause organ damage, mainly triggered by the innate immune system, which is directly related to the recipient's inflammatory reaction and, in the case of lung transplantation, is involved in primary graft dysfunction. Various molecular mechanisms are currently being discussed in the literature, which could be used to identify biomarker candidates for the degree of organ damage on the one hand and target structures for improving organ preservation by blocking these mechanisms on the other. The rapid responsiveness of the innate immune system predestines it for involvement in ischemia/reperfusion injury, a connection that we are currently investigating in the context of ex vivo perfusion of the lung (Prof. Dr. G. Warnecke, Dr. B. Wiegmann, HTTG). By closely monitoring patients directly before and in the first 24 hours after lung transplantation, we want to identify central mechanisms of activation of the innate stress response and demonstrate that it represents a template for the cascade-like development of a later allo-specific T cell-mediated immune response and donor-specific antibodies (DSA). Elucidation of this pathway could open a therapeutic window for targeted intervention during organ preservation to reduce primary ischemia/reperfusion injury, thereby improving long-term survival by reducing chronic rejection and other complications.