These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Role of anti-Nak(a) antibody, monocytes and platelets in the development of transfusion-related acute lung injury. Author: Nakajima F, Nishimura M, Hashimoto S, Okazaki H, Tadokoro K. Journal: Vox Sang; 2008 Nov; 95(4):318-23. PubMed ID: 19138262. Abstract: 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.[Abstract] [Full Text] [Related] [New Search]