Lysophosphatidylcholines: Bioactive Lipids Generated During Storage of Blood Components

Abstract

Transfusion-related acute lung injury (TRALI) is suggested to be a "two hit" event, resulting from priming and activation of pulmonary neutrophils. It is known that neutrophil activation may result from infusion of lysophosphatidylcholines (LysoPCs) accumulated during storage of blood components. The aim of our study was to verify whether the LysoPCs are released into the storage medium of blood components. We measured the LysoPCs concentration in the supernatants from stored apheresis platelet concentrates (PLTs), packed non-leukoreduced red blood cell concentrates (RBCs), leukoreduced red blood cell concentrates (L-RBCs), fresh frozen plasma (FFP) and donor plasma (control). Lipids were separated on high-performance thin-layer chromatography, detected by primulin spray and quantified by photodensitometric scanning. The LysoPCs concentration in donor plasma was similar to that in FFP. During storage the LysoPCs content in PLTs increased almost two-fold as compared to the fresh isolated platelets. In RBCs and L-RBCs the LysoPC level was very low or below detection limit and did not increase throughout the storage period. According to our observations bioactive LysoPCs may be considered a neutrophil-activating factor only following PLT transfusions but not RBCs transfusions.

Pathogenesis of non-antibody mediated transfusion-related acute lung injury from bench to bedside

“…In these models LPS was also used as "first hit" followed by either aged RBCs or aged PLTs. LysoPCs did not accumulate in both murine and human aged RBCs and were only slightly elevated in aged PLTs [47,48] which was also confirmed by two other groups [54,55]. Clinical studies also report conflicting results on the role of lysoPCs [56,57].…”

“…Moreover, in vitro priming studies showed that accumulation of LysoPCs is not cell derived, but plasma derived and storage temperature dependent as opposed to storage time related. Neutrophil priming in these reports was LysoPCs independent [54,57]. These different results are possibly explained by different storage procedures.…”

“…Non-polar lipids can be isolated in RBCs but not in PLTs. Therefore, LysoPCs, the polar lipids, are thought to be platelet derived and arachidonic acid, 5-HETE, 12-HETE and 15-HETE, the nonpolar lipids, to be RBC derived [53,54]. The role of both LysoPCs and non-polar lipids in TRALI is still debated.…”

“…These different results are possibly explained by different storage procedures. Studies in which LysoPCs were implicated in TRALI originate from the United States whereas the studies where no role was found for LysoPCs come from either Europe or Asia [8,11,12,14,47,48,54,57]. The role of nonpolar lipids arachidonic acid, 5-HETE, 12-HETE and 15-HETE has been investigated in an in vivo rat model.…”

Transfusion-related acute lung injury: A dangerous and underdiagnosed noncardiogenic pulmonary edema

“…-non-immune-mediated TRALI, which may be attributed to transfusion of biologically active compounds accumulated in stored blood components such as bioactive lipids, proinfl ammatory cytokines or platelet microparticles with high procoagulant activity. A high potassium level is considered an additional risk factor [4,[13][14][15][16][17][18][19][20]. Leukocyte antibodies are currently believed to be crucial for TRALI development.…”