Vox sanguinis · 2008
Role of anti-Nak(a) antibody, monocytes and platelets in the development of transfusion-related acute lung injury.
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Nakajima F, Nishimura M, Hashimoto S, Okazaki H, Tadokoro K
Аннотация
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 alpha (TNF-alpha) in the co-culture supernatants were determined.
RESULTS: The expressions of LTB(4) and TNF-alpha 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-alpha 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.
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 alpha (TNF-alpha) in the co-culture supernatants were determined.
RESULTS: The expressions of LTB(4) and TNF-alpha 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-alpha 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.