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血小板耗竭可减轻,但不能预防实验性输血相关性急性肺损伤的发生。

Platelet depletion limits the severity but does not prevent the occurrence of experimental transfusion-related acute lung injury.

机构信息

Université de Lyon, GIMAP-EA3064, Saint-Etienne, France.

Établissement Français du Sang Auvergne-Rhône-Alpes, Saint-Étienne, France.

出版信息

Transfusion. 2020 Apr;60(4):713-723. doi: 10.1111/trf.15738. Epub 2020 Feb 28.

Abstract

BACKGROUND

Transfusion-related acute lung injury (TRALI) is a severe pulmonary reaction due to blood transfusions. The pathophysiology of this complication is still not widely elucidated by the scientific community, especially regarding the direct role of blood platelets within the cellular mechanism responsible for the development of TRALI.

STUDY DESIGN AND METHODS

In this study, a mouse model was used to induce the development of antibody-mediated acute lung injury through injections of lipopolysaccharide and an anti-major histocompatibility complex Class I antibody. BALB/c mice were pretreated with an anti-GPIbα antibody, which induces platelet depletion, or ML354, a protease receptor 4 pathway inhibitor, 30 minutes before TRALI induction.

RESULTS

Depletion of platelets before TRALI induction appeared to reduce the severity of TRALI without completely inhibiting its development. Also, inhibition of platelet activation by ML354 did not prevent the onset of TRALI. Finally, the stimuli used for TRALI induction also triggered specific platelet activation upon ex vivo stimulation.

CONCLUSIONS

This study suggests that blood platelets are not critically required for TRALI induction, although they are to some extent involved in its pathophysiology.

摘要

背景

输血相关的急性肺损伤(TRALI)是一种严重的肺部反应,由输血引起。该并发症的病理生理学尚未被科学界广泛阐明,特别是在负责 TRALI 发展的细胞机制中血小板的直接作用方面。

研究设计和方法

在这项研究中,使用小鼠模型通过注射脂多糖和抗主要组织相容性复合体 I 抗体来诱导抗体介导的急性肺损伤的发展。在 TRALI 诱导前 30 分钟,用抗 GPIbα 抗体(诱导血小板耗竭)或 ML354(蛋白酶受体 4 途径抑制剂)预处理 BALB/c 小鼠。

结果

TRALI 诱导前血小板耗竭似乎减轻了 TRALI 的严重程度,但并未完全抑制其发展。此外,ML354 抑制血小板激活并不能预防 TRALI 的发生。最后,用于 TRALI 诱导的刺激物在体外刺激时也会引发特定的血小板激活。

结论

本研究表明,尽管血小板在 TRALI 的发病机制中起一定作用,但在诱导 TRALI 中并非至关重要。

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