Hertle R, Hilger M, Weingardt-Kocher S, Walev I
Microbiology II, University of Tübingen, 72076 Tübingen, Germany.
Infect Immun. 1999 Feb;67(2):817-25. doi: 10.1128/IAI.67.2.817-825.1999.
Incubation of human epithelial cells with nanomolar concentrations of chromatographically purified Serratia marcescens hemolysin (ShlA) caused irreversible vacuolation and subsequent lysis of the cells. Vacuolation differed from vacuole formation by Helicobacter pylori VacA. Sublytic doses of ShlA led to a reversible depletion of intracellular ATP. Restoration to the initial ATP level was presumably due to the repair of the toxin damage and was inhibited by cycloheximide. Pores formed in epithelial cells and fibroblasts without disruption of the plasma membrane, and the pores appeared to be considerably smaller than those observed in artificial lipid membranes and in erythrocytes and did not allow the influx of propidium iodide or trypan blue. All cytotoxic effects induced by isolated recombinant ShlA were also obtained with exponentially growing S. marcescens cells. The previously suggested role of the hemolysin in the pathogenicity of S. marcescens is supported by these data.
用纳摩尔浓度经色谱纯化的粘质沙雷氏菌溶血素(ShlA)孵育人上皮细胞,会导致细胞出现不可逆的空泡化并随后裂解。空泡化与幽门螺杆菌VacA形成的液泡不同。亚裂解剂量的ShlA导致细胞内ATP可逆性耗竭。ATP水平恢复到初始水平可能是由于毒素损伤的修复,且受环己酰亚胺抑制。上皮细胞和成纤维细胞中形成的孔未破坏质膜,且这些孔似乎比在人工脂质膜、红细胞中观察到的孔小得多,并且不允许碘化丙啶或台盼蓝流入。分离的重组ShlA诱导的所有细胞毒性作用也在指数生长的粘质沙雷氏菌细胞中观察到。这些数据支持了先前提出的溶血素在粘质沙雷氏菌致病性中的作用。