The nature and severity of the inflammatory response influences the outcome of organ allotransplantation and xenotransplantation. In allotransplantation, the source of the allograft, for example, from a living, brain-dead, or circulatory death donor, influences the inflammatory response, as do such factors as the preexisting comorbidities and the length of the period of chronic kidney disease in the recipient and the management he/she has received. There is also inflammation associated with the transplant surgery, for example, as a result of ischemia-reperfusion injury. In xenotransplantation, inflammation associated with donor factors will be reduced and, as the patients will receive a pig graft at a much earlier stage of their chronic organ failure, the contribution of recipient factors should also be reduced. However, there is a well-documented systemic inflammatory response to the presence of a pig xenograft (probably associated with species molecular differences) that plays a role in activating the innate immune response. Indeed, there is a complex interaction between inflammation, coagulation dysfunction, and the innate and adaptive immune responses. Suppression of the inflammatory response, for example, by interleukin-6 receptor blockade, would appear to be beneficial after xenotransplantation. Several biomarkers of inflammation have been identified that may be valuable in assessing the response to therapy.

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