research into preservation methods that target molecular mechanisms of organ injury is being actively pursued.Newer preservation methods, including targeted perfusion solutions and advanced machine perfusion methods may provide opportunities to treat, maintain, and assess marginal organs and ultimately improve transplant outcomes. This review summarizes recent advancements in preservation solutions and machine perfusion methods, including hypothermic, normothermic, and subnormotherimic machine perfusion applicable to kidney, liver, pancreas, intestine, heart, and lung transplantation. MethodsThe comprehensive review of the literature was performed by systematic analysis of published literature to February, 2019. The PubMed database (https:// www.ncbi.nlm.nih.gov/pubmed/) was searched for variations of keywords: hypothermic machine reperfusion; normothermic machine reperfusion; subnormothermic machine reperfusion; kidney transplant perfusion; liver transplant perfusion; pancreas transplant perfusion; intestine transplant perfusion; heart transplant perfusion; lung transplant perfusion; and perfusion solution additions. Publication review included deceased and live donor types, cellular, animal and human studies. Prospective and retrospective clinical studies including center studies, meta-analyses and review articles were included. Waitlist and transplantation data was included from the Organ Procurement and Transplantation Network (OPTN; https://optn.transplant.hrsa.gov/data/organ-datasource/).

Pattern recognition receptors (PRRs) are potent triggers of tissue injury following renal ischemia/ reperfusion injury (IRI). Specific PRRs, such as the toll-like receptor 2 (TLR2) and the nucleotidebinding oligomerization domain-like receptors (NLRs) NOD1 and NOD2 are promising targets to abrogate inflammatory injury associated with renal IRI. Several recent reports have shown there is crosstalk between TLRs and NODs, which might boost inflammatory responses to tissue injury. This study examined the relative roles of TLR2 and NODs 1 and 2 in activation of myeloid cells that contribute to inflammation after renal IRI. We found that TLR2 and NOD1 and 2 signaling induces neutrophil, macrophage and dendritic cell migration in vitro, however their blockade only decreases neutrophil infiltration into ischemic kidneys. The results of this study suggest that future therapies targeted to innate immune blockade should consider that either TLR2 or NOD1/2 blockade could decrease neutrophil inflammation following an ischemic insult to the kidney, however blockade of these PRRs would not likely impact infiltration of dendritic cells or macrophages. Developing rational approaches that target innate immunity in IRI-induced acute kidney injury requires an understanding of the relative role of PRRs in directing inflammation in the kidney.