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.

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. Research Abstract Details 

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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. Abstract Text:

Christopher C Silliman,Brian R Curtis,Patricia M Kopko,Samina Y Khan,Marguerite R Kelher,Randy M Schuller,Baindu Sannoh,Daniel R Ambruso,

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.

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. Publishing Authors By Initials

CC Silliman,BR Curtis,PM Kopko,SY Khan,MR Kelher,RM Schuller,B Sannoh,DR Ambruso,

For similar respiratory tract diseases: lung diseases: respiratory distress syndrome, adult research abstracts see: respiratory tract diseases: lung diseases: respiratory distress syndrome, adult research

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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. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Blood

VOLUME: 109

Page Numbers: 1752-5

Journal Abbreviation: Blood

ISSN: 0006-4971

DAY: 12

MONTH: 10

YEAR: 2006

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. Information

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LANGUAGE: eng

NlmUniqueID: 7603509

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. Keywords Mesh Terms:

KEYWORDS: Respiratory Distress Syndrome, Adult

MESH TERMS: immunology

Chemical & Substance for Abstract: 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. Information

Substance Name: Isoantigens

Registry Number: 0

Grant and Affiliation Information for 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.

AFFILIATION: Bonfils Blood Center and the Department of Pediatrics, University of Colorado at Denver School of Medicine 80230, USA. christopher.silliman@uchsc.edu

Country: United States

AGENCY: United States NIGMS

GRANT: P50 GM49222-12

ACRONYM: GM

MEDLINETA: Blood

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