Complement Activation in Liver Transplantation: Role of Donor Macrosteatosis and Implications in Delayed Graft Function

The complement system anchors the innate inflammatory response by triggering both cell-mediated and antibody-mediated immune responses against pathogens. The complement system also plays a critical role in sterile tissue injury by responding to damage-associated molecular patterns. The degree and du...

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Bibliographic Details
Published in:International journal of molecular sciences 2018-06, Vol.19 (6), p.1750
Main Authors: Núñez, Kelley, Thevenot, Paul, Alfadhli, Abeer, Cohen, Ari
Format: Article
Language:English
Subjects:
Anaphylatoxins
Animal models
Complement
Complement activation
Complement component C5a
Damage patterns
extended criteria donor
Graft rejection
Grafting
Immune response (cell-mediated)
Inflammation
Inflammatory response
Injury prevention
Ischemia
Liver
liver transplantation
Liver transplants
Reperfusion
Review
Steatosis
Thrombolysis
Transplantation
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Summary:The complement system anchors the innate inflammatory response by triggering both cell-mediated and antibody-mediated immune responses against pathogens. The complement system also plays a critical role in sterile tissue injury by responding to damage-associated molecular patterns. The degree and duration of complement activation may be a critical variable controlling the balance between regenerative and destructive inflammation following sterile injury. Recent studies in kidney transplantation suggest that aberrant complement activation may play a significant role in delayed graft function following transplantation, confirming results obtained from rodent models of renal ischemia/reperfusion (I/R) injury. Deactivating the complement cascade through targeting anaphylatoxins (C3a/C5a) might be an effective clinical strategy to dampen reperfusion injury and reduce delayed graft function in liver transplantation. Targeting the complement cascade may be critical in donor livers with mild to moderate steatosis, where elevated lipid burden amplifies stress responses and increases hepatocyte turnover. Steatosis-driven complement activation in the donor liver may also have implications in rejection and thrombolytic complications following transplantation. This review focuses on the roles of complement activation in liver I/R injury, strategies to target complement activation in liver I/R, and potential opportunities to translate these strategies to transplanting donor livers with mild to moderate steatosis.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms19061750