Cianciotto N P, Fields B S
Department of Microbiology and Immunology, Northwestern University, Chicago, IL 60611.
Proc Natl Acad Sci U S A. 1992 Jun 1;89(11):5188-91. doi: 10.1073/pnas.89.11.5188.
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, approximately 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.
嗜肺军团菌是淡水原生动物和人类巨噬细胞的胞内寄生虫。最近的研究表明,巨噬细胞感染增强因子(Mip)表面蛋白,一种FK506结合蛋白的原核同源物,是巨噬细胞最佳感染所必需的。为了确定Mip是否也参与嗜肺军团菌对原生动物的感染,我们检测了一株缺失Mip的菌株寄生哈氏变形虫和草履虫的能力。孵育3天后,与感染同基因Mip+菌株的原生动物共培养物相比,从感染Mip-菌株的原生动物共培养物中回收的细菌数量减少了约1000倍。然而,mip突变体与变形虫细胞表面结合的能力并未受损,这表明Mip参与了细菌对细胞内杀伤和/或细胞内增殖的抗性。这些数据表明,嗜肺军团菌利用相似的基因和机制感染人类细胞和原生动物。此外,它们支持这样一种假设,即嗜肺军团菌寄生巨噬细胞并因此导致人类疾病的能力是其先前适应原生动物细胞内生长的结果。