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Role of anti‐Nak a antibody, monocytes and platelets in the development of transfusion‐related acute lung injury
Author(s) -
Nakajima F.,
Nishimura M.,
Hashimoto S.,
Okazaki H.,
Tadokoro K.
Publication year - 2008
Publication title -
vox sanguinis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.68
H-Index - 83
eISSN - 1423-0410
pISSN - 0042-9007
DOI - 10.1111/j.1423-0410.2008.01095.x
Subject(s) - platelet , nak , immunology , antibody , medicine , monocyte , cd36 , transfusion related acute lung injury , lung , receptor , telecommunications link , computer network , computer science , pulmonary edema
Background and Objectives Transfusion‐related acute lung injury (TRALI) is one of the most serious side‐effects of transfusion. We report here the first two cases of TRALI caused by anti‐Nak a (anti‐CD36) antibody from a single blood donor. The aim of this study was to clarify the role of the anti‐Nak a antibody in TRALI development. Materials and Methods Human lung microvascular endothelial cells were co‐cultured with Nak a ‐positive monocytes and Nak a ‐positive platelets together with serum prepared from blood products of a TRALI‐caused anti‐Nak a antibody‐carrying donor. Expressions of leukotriene B 4 (LTB 4 ) and tumour necrosis factor α (TNF‐α) in the co‐culture supernatants were determined. Results The expressions of LTB 4 and TNF‐α were found to be markedly increased, particularly in the presence of both Nak a ‐positive monocytes and platelets. The expressions of these mediators were almost completed within 4 h after the initiation of co‐culture. Monocyte contribution seemed to be stronger than that of platelets. In the absence of human lung microvascular endothelial, no significant LTB 4 or TNF‐α release was observed. Conclusion Anti‐Nak a antibody may be strongly implicated in lung microvascular endothelial dysfunctions that lead to TRALI in a monocyte‐ and platelet‐dependent manner.