Sachs Ulrich J H, Hattar Katja, Weissmann Norbert, Bohle Rainer M, Weiss Timo, Sibelius Ulf, Bux Juergen
Department of Internal Medicine, Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Germany.
Blood. 2006 Feb 1;107(3):1217-9. doi: 10.1182/blood-2005-04-1744. Epub 2005 Oct 6.
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 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 the 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 pathophysiologic cascade that leads to immune TRALI.
输血相关急性肺损伤（TRALI）是一种危险的输血并发症，已成为美国和英国输血相关死亡的主要原因。尽管白细胞凝集抗体经常被证明与该综合征有关，但其诱发TRALI的机制仍知之甚少。因此，我们在体外大鼠肺模型中重现了TRALI。我们的数据表明，抗白细胞抗体诱导TRALI取决于同源抗原的密度，但不一定需要抗体的白细胞凝集特性或补体蛋白的存在。相反，抗体介导的中性粒细胞激活似乎启动了TRALI，这一过程可能由fMLP刺激中性粒细胞触发。因此，抗体介导的中性粒细胞激活和随后活性氧的释放可能是导致免疫性TRALI的病理生理级联反应中的关键事件。
