HeLa细胞结构和功能抑制剂对大肠杆菌HB101 (PRI203)进入过程的影响

Acta microbiologica Hungarica Pub Date : 1992-01-01
M P Conte, C Longhi, M Marchetti, P Valenti, L Seganti
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引用次数: 0

摘要

我们研究了一些真核细胞质结构和功能抑制剂对大肠杆菌HB101 K12菌株进入HeLa细胞的影响,重组质粒pRI203克隆了一个3.2 Kb的假结核耶尔森菌染色体片段。损害微丝结构和功能的物质(细胞松弛素B和三氟拉嗪)显著降低了侵入能力,而微管组织抑制剂(秋水仙碱和长春花碱)则无效。通过提高细胞内囊泡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,内体不需要酸化。由于在入侵过程中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)的存在影响了细菌的进入,宿主细胞能量已被证明有助于细菌的内化。
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Effect of inhibitors of HeLa cell structures and functions on Escherichia coli HB101 (PRI203) entry process.

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.

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