The effect of platelet‐derived microparticles in stored apheresis platelet concentrates on polymorphonuclear leucocyte respiratory burst

Abstract

Platelet-derived microparticles (PMPs) and other proinflammatory mediators, which are accumulated during the storage process, might induce transfusion adverse events. We hypothesized that the PMP primed polymorphonuclear neutrophil (PMN) respiratory burst after the transfusion, which could be linked to the transfusion-related acute lung injury (TRALI). The PMPs were isolated by centrifugation of the platelet-free plasma from 10 apheresis platelet concentrates (A-PLTs) at 20,000×g for 1 h. The PMPs were counted by flow cytometric analysis, followed by Western blotting, that were performed on isolated PMPs. The soluble CD40 ligand (sCD40L, sCD154) was assayed with ELISA. The priming of the formyl-Met-Leu-Phe (fMLP)-activated PMN respiratory burst was measured with the hydrogen peroxide production. The PMP counts increased by 1·7-folds after 3 days of storage. Meanwhile, sCD40L also significantly increased in PMP fraction isolated from the 3-day stored A-PLTs. Furthermore, Western blotting indicated that sCD40L was involved and concentrated in PMP. The PMPs were able to effectively prime the fMLP-activated PMN respiratory burst, which was partly inhibited by CD154 monoclonal antibody or by filtration with 0·1 μM membrane. Significant relativity was existed between the PMP counts, sCD40L and priming activity during the A-PLT storage. The platelet-derived microparticles, which carried the sCD40L, accumulated in the apheresis platelet concentrates during the 5 days of storage. They primed the fMLP-activated PMN respiration burst, which might be relative to TRALI.