The pro-inflammatory effects of platelet contamination in plasma and mitigation strategies for avoidance

Vox Sang. 2012 May;102(4):345-53. doi: 10.1111/j.1423-0410.2011.01559.x. Epub 2011 Nov 18.

Abstract

Background and objectives: Plasma and platelet concentrates are disproportionately implicated in transfusion-related acute lung injury (TRALI). Platelet-derived pro-inflammatory mediators, including soluble CD40 ligand (sCD40L), accumulate during storage. We hypothesized that platelet contamination induces sCD40L generation that causes neutrophil [polymorphonuclear leucocyte (PMN)] priming and PMN-mediated cytotoxicity.

Materials and methods: Plasma was untreated, centrifuged (12,500 g) or separated from leucoreduced whole blood (WBLR) prior to freezing. Platelet counts and sCD40L concentrations were measured 1-5 days post-thaw. The plasma was assayed for PMN priming activity and was used in a two-event in vitro model of PMN-mediated human pulmonary microvascular endothelial cell (HMVEC) cytotoxicity.

Results: Untreated plasma contained 42±4·2×10(3)/μl platelets, which generated sCD40L accumulation (1·6-eight-fold vs. controls). Priming activity and HMVEC cytotoxicity were directly proportional to sCD40L concentration. WBLR and centrifugation reduced platelet and sCD40L contamination, abrogating the pro-inflammatory potential.

Conclusion: Platelet contamination causes sCD40L accumulation in stored plasma that may contribute to TRALI. Platelet reduction is potentially the first TRALI mitigation effort in plasma manufacturing.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / etiology*
  • Blood Platelets / microbiology
  • Blood Platelets / pathology*
  • CD40 Ligand / blood
  • Humans
  • Inflammation / etiology*
  • Neutrophil Activation
  • Neutrophils
  • Transfusion Reaction*

Substances

  • CD40 Ligand