Conte M P, Longhi C, Marchetti M, Valenti P, Seganti L
Institute of Microbiology, University La Sapienza, Rome, Italy.
Acta Microbiol Hung. 1992;39(3-4):281-7.
We investigated the effect of some eucaryotic cytoplasmic structure and function inhibitors on the entry into HeLa cells of the Escherichia coli HB101 K12 strain, harbouring the recombinant plasmid pRI203, in which is cloned a 3.2 Kb chromosomal fragment of Yersinia pseudotuberculosis. Substances impairing microfilament structures and functions (cytochalasin B and trifluoroperazine) significantly reduced invasion ability whereas microtubule organization inhibitors (colchicine and vinblastine) were ineffective. Data obtained with a lipophilic weak base (methylamine), which raises the pH of intracellular vesicles, demonstrated that, in entry pathway of E. coli HB101 (pRI203), endosome acidification is not required. Host cell energy has been shown to contribute to bacterial internalization since the presence of oxidative phosphorylation and glycolysis inhibitors (sodium azide, 2-dinitrophenol and 2-deoxy-D-glucose) during the invasion process, affected bacterial entry.
我们研究了一些真核细胞质结构和功能抑制剂对携带重组质粒pRI203的大肠杆菌HB101 K12菌株进入HeLa细胞的影响,该重组质粒中克隆了假结核耶尔森菌的一个3.2 Kb染色体片段。损害微丝结构和功能的物质(细胞松弛素B和三氟拉嗪)显著降低了侵袭能力,而微管组织抑制剂(秋水仙碱和长春碱)则无效。用一种能提高细胞内囊泡pH值的亲脂性弱碱(甲胺)获得的数据表明,在大肠杆菌HB101(pRI203)的进入途径中,内体酸化并非必需。由于在侵袭过程中存在氧化磷酸化和糖酵解抑制剂(叠氮化钠、2-二硝基苯酚和2-脱氧-D-葡萄糖)影响细菌进入,已证明宿主细胞能量有助于细菌内化。