血栓素A2在脂多糖诱导未成熟胸腺细胞凋亡中的作用。

Paulo N Rocha, Troy J Plumb, Lisa A Robinson, Robert Spurney, David Pisetsky, Beverly H Koller, Thomas M Coffman
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引用次数: 13

摘要

脂多糖(LPS)引起CD4(+) CD8(+)胸腺细胞的凋亡缺失,这一现象与败血症期间的免疫功能障碍和生存率低下有关。鉴于CD4(+) CD8(+)胸腺细胞中有丰富的血栓素-前列腺素(TP)受体,并且体外有证据表明血栓素A(2) (TXA(2))会导致这些细胞凋亡,我们测试了增强的TXA(2)的产生是否在lps诱导的胸腺细胞凋亡中起作用。腹腔注射50微LPS的小鼠胸腺内TXA(2)和前列腺素E(2)的生成明显增加,CD4(+)和CD8(+)胸腺细胞凋亡缺失。吲哚美辛或罗非昔布可抑制前列腺素合成,但不影响胸腺细胞死亡。相比之下,tp缺陷小鼠的胸腺细胞凋亡对LPS的反应明显减弱。这些研究表明,TXA(2)介导了部分LPS引起的胸腺细胞凋亡。缺乏对前列腺素合成的整体抑制作用表明前列腺素在该模型中具有复杂的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of thromboxane A2 in the induction of apoptosis of immature thymocytes by lipopolysaccharide.

Lipopolysaccharide (LPS) causes apoptotic deletion of CD4(+) CD8(+) thymocytes, a phenomenon that has been linked to immune dysfunction and poor survival during sepsis. Given the abundance of thromboxane-prostanoid (TP) receptors in CD4(+) CD8(+) thymocytes and in vitro evidence that thromboxane A(2) (TXA(2)) causes apoptosis of these cells, we tested whether enhanced generation of TXA(2) plays a role in LPS-induced thymocyte apoptosis. Mice injected with 50 micro LPS intraperitoneally displayed a marked increase in generation of TXA(2) and prostaglandin E(2) in the thymus as well as apoptotic deletion of CD4(+) CD8(+) thymocytes. Administration of indomethacin or rofecoxib inhibited prostanoid synthesis but did not affect thymocyte death. In contrast, thymocyte apoptosis in response to LPS was significantly attenuated in TP-deficient mice. These studies indicate that TXA(2) mediates a portion of apoptotic thymocyte death caused by LPS. The absence of an effect of global inhibition of prostanoid synthesis suggests a complex role for prostanoids in this model.

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