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Blood, 1 February 2006, Vol. 107, No. 3, pp. 1217-1219.
Prepublished online as a Blood First Edition Paper on October 6, 2005; DOI 10.1182/blood-2005-04-1744.
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Submitted April 28, 2005
Accepted September 23, 2005
Antibody-induced neutrophil activation as a trigger for transfusion-related acute lung injury in an ex vivo rat lung model
Ulrich J Sachs*, Katja Hattar, Norbert Weissmann, Rainer M Bohle, Timo Weiss, Ulf Sibelius, and Juergen Bux
Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany; Rudolf Virchow Center for Experimental Biomedicine, Wuerzburg, Germany
Department of Internal Medicine, Justus Liebig University, Giessen, Germany
Department of Pathology, Justus Liebig University, Giessen, Germany
Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany
German Red Cross Blood Service West, Hagen, Germany
* Corresponding author; email: ulrich.sachs{at}med.uni-giessen.de.
Transfusion-related acute lung injury (TRALI) is a hazardous complication of transfusion and has become the leading cause of transfusion-related death in the United States and the United Kingdom. Although leukoagglutinating antibodies have been frequently shown to be associated with the syndrome, the mechanism by which they induce TRALI is poorly understood. Therefore, we reproduced TRALI in an ex vivo rat lung model. Our data demonstrate that TRALI induction by antileukocyte antibodies is dependent on the density of the cognate antigen, but does not necessarily require leukoagglutinating properties of the antibody or presence of complement proteins. Rather, antibody-mediated activation of neutrophils seems to initiate TRALI, a process that could be triggered by neutrophil stimulation with fMLP. Antibody-mediated neutrophil activation and subsequent release of reactive oxygen species may thus represent key events in the pathophysiological cascade that leads to immunogenic TRALI.
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