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首页> 外文期刊>Infection and immunity >Identification of Macrophage-Specific Infectivity Loci (mil) of Legionella pneumophila That Are Not Required for Infectivity of Protozoa
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Identification of Macrophage-Specific Infectivity Loci (mil) of Legionella pneumophila That Are Not Required for Infectivity of Protozoa

机译：原生动物的感染力不需要的嗜肺军团菌的巨噬细胞特异性感染位点（mil）的鉴定

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We have recently shown that many mutants of Legionella pneumophila exhibit similar defective phenotypes within both U937 human-derived macrophages and the protozoan hostAcanthamoeba (L.-Y. Gao, O. S. Harb, and Y. Abu Kwaik, Infect. Immun. 65:4738–4746, 1997). These observations have suggested that many of the mechanisms utilized by L. pneumophila to parasitize mammalian and protozoan cells are similar, but our data have not excluded the possibility that there are unique mechanisms utilized by L. pneumophila to survive and replicate within macrophages but not protozoa. To examine this possibility, we screened a bank of 5,280 miniTn10::kan transposon insertion mutants of L. pneumophila for potential mutants that exhibited defective phenotypes of cytopathogenicity and intracellular replication within macrophage-like U937 cells but not within Acanthamoeba polyphaga. We identified 32 mutants with various degrees of defects in cytopathogenicity, intracellular survival, and replication within human macrophages, and most of the mutants exhibited wild-type phenotypes within protozoa. Six of the mutants exhibited mild defects in protozoa. The defective loci were designated mil (for macrophage-specific infectivity loci). Based on their intracellular growth defects within macrophages, the mil mutants were grouped into five phenotypic groups. Groups I to III included the mutants that were severely defective in macrophages, while members of the other two groups exhibited a modestly defective phenotype within macrophages. The growth kinetics of many mutants belonging to groups I to III were also examined, and these were shown to have a similar defective phenotype in peripheral blood monocytes and a wild-type phenotype within another protozoan host, Hartmannella vermiformis. Transmission electron microscopy of A. polyphaga infected by three of the mil mutants belonging to groups I and II showed that they were similar to the parent strain in their capacity to recruit the rough endoplasmic reticulum (RER) around the phagosome. In contrast, infection of macrophages showed that the three mutants failed to recruit the RER around the phagosome during early stages of the infection. None of themil mutants was resistant to NaCl, and the dotor icm NaClr mutants are severely defective within mammalian and protozoan cells. Our data indicated that in addition to differences in mechanisms of uptake of L. pneumophila by macrophages and protozoa, there were also genetic loci required for L. pneumophila to parasitize mammalian but not protozoan cells. We hypothesize that L. pneumophilahas evolved as a protozoan parasite in the environment but has acquired loci specific for intracellular replication within macrophages. Alternatively, ecological coevolution with protozoa has allowedL. pneumophila to possess multiple redundant mechanisms to parasitize protozoa and that some of these mechanisms do not function within macrophages.
机译：我们最近发现，许多 Legionella pneumophila 突变体在人类U937巨噬细胞和原生动物宿主 Acanthamoeba 中都表现出相似的缺陷表型（L.-Y. Gao，OS Harb） ，和Y. Abu Kwaik，Infect。Immun。65：4738-4746，1997）。这些观察结果表明， L利用了许多机制。寄生于哺乳动物和原生动物细胞的嗜肺菌相似，但我们的数据并未排除 L利用独特机制的可能性。嗜肺菌能够在巨噬细胞中生存并复制，但不能在原生动物中复制。为了检验这种可能性，我们筛选了5280个 L的miniTn 10 :: kan转座子插入突变体。肺炎：潜在的突变体在巨噬细胞样U937细胞中表现出细胞致病性和细胞内复制的缺陷表型，而在棘阿米巴多噬菌体中却没有。我们鉴定出32种突变体，它们在细胞致病性，细胞内存活和人类巨噬细胞内复制方面均具有不同程度的缺陷，并且大多数突变体在原生动物内均表现出野生型表型。六个突变体在原生动物中表现出轻度缺陷。有缺陷的基因座被指定为 mil （用于巨噬细胞特异性感染性基因座）。根据它们在巨噬细胞内的细胞内生长缺陷，将 mil 突变体分为五个表型组。 I至III组包括在巨噬细胞中严重缺陷的突变体，而其他两组的成员在巨噬细胞中表现出中等缺陷的表型。还检查了许多属于I至III组的突变体的生长动力学，这些突变体在外周血单核细胞中具有相似的缺陷表型，在另一种原生动物宿主 Hartmannella vermiformis 中具有野生型表型。 。 A的透射电子显微镜。被第I和第II组的三个 mil 突变体感染的多噬菌体显示，它们与亲本菌株在吞噬体周围募集粗糙内质网（RER）的能力相似。相反，巨噬细胞的感染表明，在感染的早期阶段，这三个突变体未能在吞噬体周围募集RER。 mil 突变体均未对NaCl产生抗性，而 dot 或 icm NaCl r 突变体在NaCl中均存在严重缺陷哺乳动物和原生动物细胞。我们的数据表明，除了摄取 L的机制不同外。巨噬细胞和原生动物的嗜肺性， L也需要遗传位点。肺炎可以寄生哺乳动物而不是原生动物细胞。我们假设 L。肺炎支原体已经在环境中进化为原生动物寄生虫，但是已经获得了巨噬细胞内细胞内复制特异的基因座。可替代地，与原生动物的生态共进化允许L。肺炎具有多种寄生虫原虫的冗余机制，其中某些机制在巨噬细胞中不起作用。

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