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Virulence of iron transport mutants of Shigella flexneri and utilization of host iron compounds.

机译:弗氏志贺氏菌铁转运突变体的毒力和宿主铁化合物的利用。

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Mutants of Shigella flexneri defective in aerobactin-mediated iron transport were assayed for virulence in several model systems. A Tn5 insertion mutant was invasive in HeLa cells, lethal in the chicken embryo, and produced keratoconjunctivitis in the guinea pig, indicating little or no loss of ability to invade and multiply intracellularly. Although the mutant failed to grow in low-iron medium in vitro, growth equivalent to that of the wild type was observed in HeLa cell lysates. Thus, there appears to be sufficient available iron inside the HeLa cell to allow growth in the absence of siderophore synthesis. Possible host iron sources were tested, and both the mutant and wild type utilized hemin or hematin as a sole source of iron. Only the wild-type, aerobactin-producing strain could remove iron from transferrin or lactoferrin. Two deletion mutants were also assayed for virulence and were found to be avirulent for the chicken embryo. These deletions encompass flanking sequences as well as the aerobactin genes; therefore, adjacent genes may be required for virulence.
机译:在几种模型系统中分析了在航空杆菌素介导的铁运输中有缺陷的志贺氏志贺菌的突变体的毒力。 Tn5插入突变体侵袭HeLa细胞,在鸡胚中致死,并在豚鼠中产生角膜结膜炎,表明侵袭能力和细胞内繁殖能力几乎没有或没有丧失。尽管该突变体无法在低铁培养基中体外生长,但在HeLa细胞裂解物中观察到了与野生型相同的生长。因此,似乎在HeLa细胞内部有足够的可用铁以允许在没有铁载体合成的情况下生长。测试了可能的宿主铁源,并且突变型和野生型均利用血红素或血红素作为唯一的铁源。只有野生型产气杆菌素的菌株才能从转铁蛋白或乳铁蛋白中除去铁。还检测了两个缺失突变体的毒力,发现它们对鸡胚无毒。这些缺失包括侧翼序列以及气杆菌素基因;因此,毒力可能需要邻近的基因。

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