Abstract
Transfusion-related acute lung injury (TRALI) is a severe form of pulmonary insufficiency induced by transfusion. TRALI is the leading cause of transfusion-related death, and is caused by the infusion of either anti-leukocyte antibodies in plasma containing blood products or neutrophil priming substances that accumulate during storage of cellular blood products. Among these neutrophil priming substances are bioactive lipids, such as lyso-phosphatidylcholines (lysoPCs) and arachidonic acid, soluble CD40L (sCD40L) and possibly other, as yet unidentified substances. The accumulation of these substances during cellular blood product storage and their role in the induction of “non-immune mediated” TRALI pathogenesis are highly relevant for the current debate of the use of longer vs. shorter stored blood products. In this review, the accumulation of these different substances during storage, as well as their mode of action in inducing TRALI are discussed. In addition, different improvements in current blood banking procedures to prevent TRALI due to these non-immune mediators will be proposed.
Keywords: Transfusion, TRALI, Storage lesion, Bioactive lipids, sCD40L, LysoPC, Non-immune, anti-leukocyte antibodies, blood products, blood banking procedures
Current Pharmaceutical Design
Title:Prevention of Non-immune Mediated Transfusion-related Acute Lung Injury; from Blood Bank to Patient
Volume: 18 Issue: 22
Author(s): Robin van Bruggen and Dirk de Korte
Affiliation:
Keywords: Transfusion, TRALI, Storage lesion, Bioactive lipids, sCD40L, LysoPC, Non-immune, anti-leukocyte antibodies, blood products, blood banking procedures
Abstract: Transfusion-related acute lung injury (TRALI) is a severe form of pulmonary insufficiency induced by transfusion. TRALI is the leading cause of transfusion-related death, and is caused by the infusion of either anti-leukocyte antibodies in plasma containing blood products or neutrophil priming substances that accumulate during storage of cellular blood products. Among these neutrophil priming substances are bioactive lipids, such as lyso-phosphatidylcholines (lysoPCs) and arachidonic acid, soluble CD40L (sCD40L) and possibly other, as yet unidentified substances. The accumulation of these substances during cellular blood product storage and their role in the induction of “non-immune mediated” TRALI pathogenesis are highly relevant for the current debate of the use of longer vs. shorter stored blood products. In this review, the accumulation of these different substances during storage, as well as their mode of action in inducing TRALI are discussed. In addition, different improvements in current blood banking procedures to prevent TRALI due to these non-immune mediators will be proposed.
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Cite this article as:
van Bruggen Robin and de Korte Dirk, Prevention of Non-immune Mediated Transfusion-related Acute Lung Injury; from Blood Bank to Patient, Current Pharmaceutical Design 2012; 18 (22) . https://dx.doi.org/10.2174/1381612811209023249
DOI https://dx.doi.org/10.2174/1381612811209023249 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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