Neutrophil-reactive autoantibodies in blood donors: Can we expect TRALI?

献血者体内中性粒细胞反应性自身抗体:我们是否可能出现输血相关性急性肺损伤?

阅读:2

Abstract

BACKGROUND: Transfusion-related acute lung injury (TRALI) is a clinical condition characterized by acute non-cardiogenic pulmonary edema during or after transfusion. Despite several mitigation strategies, TRALI remains a leading cause of transfusion-related deaths. Tests on blood donors involved in TRALI, apart from leukocyte/endothelial reactive alloantibodies, can also reveal the presence of neutrophil autoantibodies. Here, we ask the question whether these autoantibodies could play a role in the development of TRALI. MATERIALS AND METHODS: Sera (n = 15) from donors involved in TRALI and not containing alloantibodies against human neutrophil antigens (HNAs) and human leukocyte antigens (HLAs) were collected if their serological characterization was suggestive for the presence of neutrophil-reactive autoantibodies. Sera (n = 12) were suitable for the study. Their ability to bind complement, to activate neutrophils, and to disrupt the endothelial barrier using albumin influx through an endothelial monolayer in a transwell chamber in the presence and absence of neutrophils was investigated. RESULTS: None of the AIN sera, but 2/12 TRALI sera, induced reactive oxygen species (ROS) in neutrophils. Both of these TRALI sera induced endothelial barrier permeability in the presence, but not in the absence, of neutrophils. These two sera did not activate complement. CONCLUSION: Autoantibodies against neutrophils present in transfused blood components appear to be capable of contributing to TRALI in selected but not in all investigated cases, based on their ability to activate neutrophil ROS and induce endothelial cell permeability in vitro. Further analysis is required to understand the potential functional effects of neutrophil autoantibodies in TRALI.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。