Abstract
BackgroundDespite significant advances in organ preservation, surgical techniques and perioperative care, primary graft dysfunction is a serious medical problem in transplantation medicine in general and a specific problem in patients undergoing lung transplantation. As a result, patients develop lung edema, causing reduced tissue oxygenation capacity, reduced lung compliance and increased requirements for mechanical ventilatory support. Yet, there is no effective strategy available to protect the grafted organ from stress reactions induced by ischemia/reperfusion and by the surgical procedure itself.MethodsWe assessed the effect of a cingulin-derived peptide, XIB13 or a random peptide in an established rat model of allogeneic lung transplantation. Donor lungs and recipients received therapeutic peptide at the time of transplantation and outcome was analyzed 100min and 28 days post grafting.ResultsXIB13 improved blood oxygenation and reduced vascular leak 100min post grafting. Even after 28 days, lung edema was significantly reduced by XIB13 and lungs had reduced fibrotic or necrotic zones. Moreover, the induction of an allogeneic T cell response was delayed indicating a reduced antigen exchange between the donor and the host.ConclusionsIn summary, we provide a new tool to strengthen endothelial barrier function thereby improving outcomes in lung transplantation.
Highlights
Lung transplantation (LTX) has become an effective treatment option for end-stage lung diseases, with 1-year survival rates around 80%
We assessed the effect of a cingulin-derived peptide, XIB13 or a random peptide in an established rat model of allogeneic lung transplantation
Even after 28 days, lung edema was significantly reduced by XIB13 and lungs had reduced fibrotic or necrotic zones
Summary
Lung transplantation (LTX) has become an effective treatment option for end-stage lung diseases, with 1-year survival rates around 80%. In the lung, edema between pulmonary capillaries and alveoli reduces gas exchange damaging the lung itself, and causing systemic hypoxia and inflammation [4]. This may lead to delayed organ function or even dysfunction requiring extended mechanical ventilation or extracorporeal membrane oxygenation [5, 6]. This results in higher perioperative mortality and morbidity such as infections, bleeding, or prolonged intensive care. There is no effective strategy available to protect the grafted organ from stress reactions induced by ischemia/reperfusion and by the surgical procedure itself
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