Pandey Jaya, Warburton David
Developmental Biology Program, Saban Research Institute, Childrens Hospital of Los Angeles, 4650, Sunset Blvd., Los Angeles, CA 90027, USA.
Microbes Infect. 2004 Jul;6(9):835-43. doi: 10.1016/j.micinf.2004.04.013.
Herein we report the knock-on cytotoxic effect of lethal toxin (LeTx) on human umbilical vascular endothelial cells (HUVECs). HUVECs were treated either directly with LeTx or indirectly with LeTx conditioned medium (LeTxCM) prepared from RAW264.7 macrophage cells. Cytotoxicity assays were done on HUVECs and A549 cells using LeTx. HUVECs were more susceptible to LeTx (61-74% survivals) as compared to A549 cells (83-94% survivals, P < 0.005). However, LeTxCM from RAW264.7 further potentiated killing of HUVECs (37% survival) compared to the LeTxCM from A549 cells (up to 70-100% survivals). LeTxCM challenge induced an apoptotic cell death in HUVECs, and this was confirmed by reduction of BCL-2 levels to 54%. Protective antigen (PA) binding to macrophage cell line RAW264.7 > HUVECs >> A549 cells. Thus, we postulate that after the initial prodormal phase of pulmonary entry, LeTx causes not only significant direct damage to macrophages and endothelial cells, but also mediates additional indirect damage to endothelial cells mediated by a knock-on effect of LeTx on macrophages that causes apoptotic cell death in endothelial cells.
在此,我们报告致死毒素(LeTx)对人脐静脉血管内皮细胞(HUVECs)的连锁细胞毒性作用。HUVECs要么直接用LeTx处理,要么间接用从RAW264.7巨噬细胞制备的LeTx条件培养基(LeTxCM)处理。使用LeTx对HUVECs和A549细胞进行细胞毒性测定。与A549细胞(存活率83 - 94%,P < 0.005)相比,HUVECs对LeTx更敏感(存活率61 - 74%)。然而,与来自A549细胞的LeTxCM(存活率高达70 - 100%)相比,来自RAW264.7的LeTxCM进一步增强了对HUVECs的杀伤作用(存活率37%)。LeTxCM刺激诱导HUVECs发生凋亡性细胞死亡,这通过将BCL - 2水平降低至54%得到证实。保护性抗原(PA)与巨噬细胞系RAW264.7的结合 > HUVECs >> A549细胞。因此,我们推测在肺部进入的初始前驱期之后,LeTx不仅对巨噬细胞和内皮细胞造成显著的直接损伤,还通过LeTx对巨噬细胞的连锁效应介导对内皮细胞的额外间接损伤,从而导致内皮细胞发生凋亡性细胞死亡。