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Possible involvement of heparin‐binding protein in transfusion‐related acute lung injury
Author(s) -
Yasui Kazuta,
Furuta Rika A.,
Matsuyama Nobuki,
Fukumori Yasuo,
Kimura Takafumi,
Tani Yoshihiko,
Shibata Hirotoshi,
Hirayama Fumiya
Publication year - 2008
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1111/j.1537-2995.2007.01632.x-i2
Subject(s) - antibody , transfusion related acute lung injury , immunology , flow cytometry , heparin , immune system , medicine , cell , cd16 , tumor necrosis factor alpha , in vitro , blocking antibody , lung , chemistry , biochemistry , cd3 , cd8 , pulmonary edema
BACKGROUND: In antibody‐mediated nonhemolytic transfusion reactions, transfusion‐related acute lung injury (TRALI) tends to occur typically within 2 hours after a blood transfusion. White cell antibodies or immune complexes have been frequently shown to be associated with the syndrome, although the mechanisms by which they induce TRALI are poorly understood. The aim of this study was to characterize soluble mediators that are released from cells at an early stage after immune stimulation. STUDY DESIGN AND METHODS: To explore the mechanism of TRALI, an in vitro whole‐blood cell culture assay was established in which cells were stimulated by human antibodies and the activation of neutrophils was monitored by a cell surface marker (Mac‐1) with flow cytometry and by measurement of the release of soluble factors, including perforin, interleukin‐6, tumor necrosis factor‐α, and heparin‐binding protein (HBP) with enzyme‐linked immunosorbent assays. In addition, the involvement of two neutrophil FcγRs (FcγRIIIb and FcγRIIa, also known as CD16 and CD32, respectively) was examined during antibody‐induced cell activation with anti‐FcγR blocking antibodies. RESULTS: Substantial amounts of HBP were released within 30 minutes of stimulation by human antibodies, although other soluble mediators were not released within the same period. Furthermore, the release of HBP was mediated via signals through both FcγRIIIb and FcγRIIa. CONCLUSION: HBP appears to be one of the primary effector molecules of antibody‐mediated nonhemolytic transfusion reactions including TRALI.