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Blood, 15 February 2007, Vol. 109, No. 4, pp. 1752-1755. Prepublished online as a Blood First Edition Paper on October 12, 2006; DOI 10.1182/blood-2006-05-025106. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-05-025106v1 109/4/1752    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Silliman, C. C. Articles by Ambruso, D. R. Search for Related Content PubMed PubMed Citation Articles by Silliman, C. C. Articles by Ambruso, D. R. Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Phagocytes Transfusion Medicine Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Brief Report Donor antibodies to HNA-3a implicated in TRALI reactions prime neutrophils and cause PMN-mediated damage to human pulmonary microvascular endothelial cells in a two-event in vitro model Christopher C. Silliman1,3, Brian R. Curtis4, Patricia M. Kopko5, Samina Y. Khan2, Marguerite R. Kelher3, Randy M. Schuller6, Baindu Sannoh2, and Daniel R. Ambruso1,2 1 Bonfils Blood Center and the 2 Departments of Pediatrics and 3 Surgery, University of Colorado at Denver School of Medicine; 4 Blood Center of Southeastern Wisconsin, Milwaukee; 5 BloodSource, Sacramento, CA; 6 American Red Cross–North Central Blood Services, St Paul, MN Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related mortality. Antibodies to HNA-3a are commonly implicated in TRALI. We hypothesized that HNA-3a antibodies prime neutrophils (PMNs) and cause PMN-mediated cytotoxicity through a two-event pathogenesis. Isolated HNA-3a+ or HNA-3a– PMNs were incubated with plasma containing HNA-3a antibodies implicated in TRALI, and their ability to prime the oxidase was measured. Human pulmonary microvascular endothelial cells (HMVECs) were activated with endotoxin or buffer, HNA-3a+ or HNA-3a– PMNs were added, and the coculture was incubated with plasma ± antibodies to HNA-3a. PMN-mediated damage was measured by counting viable HMVECs/mm2. Plasma containing HNA-3a antibodies primed the fMLP-activated respiratory burst of HNA-3a+, but not HNA-3a–, PMNs and elicited PMN-mediated damage of LPS-activated HMVECs when HNA-3a+, but not HNA-3a–, PMNs were used. Thus, antibodies to HNA-3a primed PMNs and caused PMN-mediated HMVEC cytotoxicity in a two-event model identical to biologic response modifiers implicated in TRALI. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. J. Triulzi Transfusion-Related Acute Lung Injury: Current Concepts for the Clinician Anesth. Analg., March 1, 2009; 108(3): 770 - 776. [Abstract] [Full Text] [PDF] M. R. Kelher, T. Masuno, E. E. Moore, S. Damle, X. Meng, Y. Song, X. Liang, J. Niedzinski, S. S. Geier, S. Y. Khan, et al. Plasma from stored packed red blood cells and MHC class I antibodies causes acute lung injury in a 2-event in vivo rat model Blood, February 26, 2009; 113(9): 2079 - 2087. [Abstract] [Full Text] [PDF]

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