Phospholipase C and perfringolysin O from Clostridium perfringens upregulate endothelial cell-leukocyte adherence molecule 1 and intercellular leukocyte adherence molecule 1 expression and induce interleukin-8 synthesis in cultured human umbilical vein endothelial cells
Phospholipase C and perfringolysin O from Clostridium perfringens upregulate endothelial cell-leukocyte adherence molecule 1 and intercellular leukocyte adherence molecule 1 expression and induce interleukin-8 synthesis in cultured human umbilical vein endothelial cells
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DOI：
10.1128/iai.64.1.358-362.1996
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发表时间：
1996-01-01
影响因子：
3.1
通讯作者：
Stevens, DL
中科院分区：
文献类型：
--
作者：
Bryant, AE;Stevens, DL
产气荚膜梭菌磷脂酶C(PLC)和产气荚膜溶血素O(PFO)分别诱导人脐静脉内皮细胞表达和合成内皮细胞-白细胞黏附分子-1(ELAM-1)、细胞间白细胞黏附分子-1(ICAM-1)和白介素8(1L-8)。PLC强烈诱导ELAM-1、ICAM-1和IL-8的表达，而PFO刺激早期ICAM-1的表达，但不促进ELAM-1的表达或IL-8的合成。PLC使人脐静脉内皮细胞呈现成纤维细胞样形态，而PFO，在高浓度或长期低剂量毒素暴露后，导致细胞死亡。毒素诱导的前黏附蛋白和活化蛋白的表达以及直接的细胞病变作用可能是导致产气荚膜梭菌气性坏疽的白细胞停滞、血管损害和毛细血管渗漏特征的原因之一。
Clostridium perfringens phospholipase C (PLC) and perfringolysin O (PFO) differentially induced human umbilical vein endothelial cell expression and synthesis of endothelial cell-leukocyte adherence molecule-1 (ELAM-1), intercellular leukocyte adherence molecule-1 (ICAM-1), and interleukin-8 (1L-8). PLC strongly induced expression of ELAM-1, ICAM-1, and IL-8, while PFO stimulated early ICAM-1 expression but did not promote ELAM-1 expression or IL-8 synthesis. PLC caused human umbilical vein endothelial cells to assume a fibroblastoid morphology, whereas PFO, in high concentrations or after prolonged low-dose toxin exposure, caused cell death. The toxin-induced expression of proadhesive and activational proteins and direct cytopathic effects may contribute to the leukostasis, vascular compromise, and capillary leak characteristics of C. perfringens gas gangrene.