LEGIONELLA-PNEUMOPHILA-MIP GENE POTENTIATES INTRACELLULAR INFECTION OF PROTOZOA AND HUMAN MACROPHAGES
LEGIONELLA-PNEUMOPHILA-MIP GENE POTENTIATES INTRACELLULAR INFECTION OF PROTOZOA AND HUMAN MACROPHAGES
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DOI：
10.1073/pnas.89.11.5188
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发表时间：
1992-06-01
影响因子：
11.1
通讯作者：
FIELDS, BS
中科院分区：
文献类型：
--
作者：
CIANCIOTTO, NP;FIELDS, BS
嗜肺军团菌是淡水原虫和人巨噬细胞的胞内寄生虫。最近的研究表明，巨噬细胞感染性增强因子(MIP)表面蛋白是巨噬细胞最佳感染所必需的，它是FK506结合蛋白的原核同源物。为了确定MIP是否也与嗜肺乳杆菌感染原生动物有关，我们检测了一株缺乏MIP的菌株寄生哈特曼氏阿米巴和纤毛虫的能力。培养3天后，从感染MIP-菌株的原生动物共培养物中回收的细菌数量几乎相当于感染同基因MIP+菌株的共培养物中的细菌数量的1000倍。然而，MIP突变体与阿米巴细胞表面的结合能力并未受到损害，这表明MIP参与了细菌对细胞内杀伤和/或细胞内增殖的抵抗。这些数据表明，嗜肺乳杆菌使用相似的基因和机制感染人类细胞和原生动物。此外，他们支持这样的假设，即嗜肺乳杆菌寄生巨噬细胞从而导致人类疾病的能力是其先前适应原生动物内细胞内生长的结果。
Legionella pneumophila is an intracellular parasite of freshwater protozoa and human macrophages. Recent studies determined that the macrophage infectivity potentiator (Mip) surface protein, a prokaryotic homolog of the FK506-binding proteins, is required for optimal infection of macrophages. To determine whether Mip is also involved in L. pneumophila infection of protozoa, we examined the ability of a strain lacking Mip to parasitize Hartmannella amoebae and Tetrahymena ciliates. After 3 days of incubation, almost-equal-to 1000-fold fewer bacteria were recovered from protozoan cocultures infected with the Mip- strain than from those cocultures infected with an isogenic Mip+ strain. The mip mutant was, however, not impaired in its ability to bind to amoebae cell surfaces, indicating that Mip is involved in bacterial resistance to intracellular killing and/or intracellular multiplication. These data suggest that L. pneumophila employs similar genes and mechanisms to infect human cells and protozoa. Furthermore, they support the hypothesis that the ability of L. pneumophila to parasitize macrophages and hence to cause human disease is a consequence of its prior adaptation to intracellular growth within protozoa.