Endothelial cell activation induced by tumor necrosis factor and lymphotoxin.
Endothelial cell activation induced by tumor necrosis factor and lymphotoxin.
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发表时间：
1989-03
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通讯作者：
Druie E. Cavender;D. Edelbaum;Morris Ziff
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作者：
Druie E. Cavender;D. Edelbaum;Morris Ziff
在慢性炎症和免疫反应部位反复观察到血管内皮细胞（EC）形态和组织化学的变化。这些变化在有大量淋巴细胞浸润的区域中存在的 EC 毛细血管后微静脉中最为突出，包括柱状或立方形形态的获得、核糖核酸酶敏感异染性的发展以及细胞内细胞器的增加。因此，炎症部位的 EC 似乎被激活并表现出代谢活性增加。这项研究报告称，肿瘤坏死因子-α (TNF) 和淋巴毒素 (LT) 均可激活培养的人脐静脉 EC，具体表现如下：1) 淋巴细胞粘附性增加；2) 细胞代谢增加（通过 RNA 和蛋白质合成测量）；3) 细胞体积增加。虽然γ干扰素（IFN-γ）和白细胞介素-1（IL-1）先前已被证明可以刺激淋巴细胞的EC粘附性，但这两种细胞因子对EC RNA和蛋白质合成仅产生边际影响，并且均导致EC体积减少。这些发现表明，TNF 和 LT 在体内 EC 激活类型中发挥作用，从而导致高内皮细胞的发育和淋巴细胞迁移的增加。
Alterations in the morphology and histochemistry of vascular endothelial cells (EC) have been repeatedly observed at sites of chronic inflammation and immune reactions. These changes, which are most prominent in the EC postcapillary venules present in areas with large lymphocytic infiltrates, include the acquisition of a columnar or cuboidal morphology, the development of ribonuclease-sensitive metachromasia, and an increase in intracellular organelles. Thus, EC at sites of inflammation appear to be activated and to demonstrate increased metabolic activity. This study reports that both tumor necrosis factor-alpha (TNF) and lymphotoxin (LT) can activate cultured human umbilical vein EC, as measured by: 1) increased adhesiveness for lymphocytes, 2) increased cell metabolism, as measured by RNA and protein synthesis, and 3) increased cell volume. Although gamma interferon (IFN-gamma) and interleukin-1 (IL-1) have been shown previously to stimulate EC adhesiveness for lymphocytes, these two cytokines had only marginal effects on EC RNA and protein synthesis, and both caused a decrease in EC volume. These findings suggest that TNF and LT play a role in the type of activation of EC in vivo that leads to the development of tall endothelium and increased lymphocyte emigration.