Yoshida T, Fukada M, Koide N, Ikeda H, Sugiyama T, Kato Y, Ishikawa N, Yokochi T
Department of Microbiology, Research Center for Infectious Diseases, Aichi Medical University, Yazako, Nagakute, Japan.
J Infect Dis. 1999 Dec;180(6):2048-52. doi: 10.1086/315116.
Various endothelial cells, with the exception of those from human microvasculatures, have been known to resist Shiga toxins (Stxs) in vitro. However, freshly prepared primary cultures of human endothelial cells from the umbilical vein and artery and the saphenous vein were shown to be killed by a very low dose of Stxs. This cytotoxicity of Stxs involves apoptosis, which seems to be caused by a mechanism distinct from the well-known action of Stxs to inhibit protein synthesis, since the blockade of protein synthesis by cycloheximide could not induce apoptosis or enhance the effect of Stxs. Passaged human endothelial cells have been found to be highly resistant to Stxs, which is consistent with previous reports, and not to show any evidence of apoptosis even when they are killed by a high dose of Stxs.
除了来自人微血管的内皮细胞外，已知各种内皮细胞在体外对志贺毒素（Stxs）具有抗性。然而，新鲜制备的来自人脐静脉、动脉和大隐静脉的原代内皮细胞培养物经低剂量的Stxs处理后被证明会死亡。Stxs的这种细胞毒性涉及细胞凋亡，这似乎是由一种不同于Stxs抑制蛋白质合成的著名作用机制引起的，因为环己酰亚胺对蛋白质合成的阻断不能诱导细胞凋亡或增强Stxs的作用。已发现传代的人内皮细胞对Stxs具有高度抗性，这与先前的报道一致，并且即使在高剂量Stxs处理下死亡也没有显示出任何细胞凋亡的迹象。
