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位点特异性改变的Mip蛋白对嗜肺军团菌在真核细胞内生存的影响。

Influence of site specifically altered Mip proteins on intracellular survival of Legionella pneumophila in eukaryotic cells.

作者信息

Wintermeyer E, Ludwig B, Steinert M, Schmidt B, Fischer G, Hacker J

机构信息

Institut für Molekulare Infektionsbiologie, Universität Würzburg, Germany.

出版信息

Infect Immun. 1995 Dec;63(12):4576-83. doi: 10.1128/iai.63.12.4576-4583.1995.

Abstract

Legionella pneumophila, the causative agent of Legionnaires' disease, is able to survive intracellularly in eukaryotic cells such as monocytes, macrophages, and protozoan organisms. The Mip (macrophage infectivity potentiator) protein represents a factor of L. pneumophila necessary for optimal intracellular survival. Interestingly, Mip belongs to the substance class of FK 506-binding proteins and exhibits peptidyl-prolyl cis/trans isomerase (PPIase) activity that can be inhibited by the immunosuppressant FK506. In order to identify amino acids most likely to be involved in the enzymatic activity of Mip, site-directed mutagenized Mip proteins were constructed and characterized. It was shown that an Asp-142 to Leu-142 mutation and a Tyr-185 to Ala-185 substitution resulted in strongly reduced PPIase activity of the recombinant Mip proteins (5.3 and 0.6% of the activity of the wild-type Mip, respectively). Genes coding for the wild-type and for site-directed-mutagenized Mip proteins were used to complement three different Mip-negative mutants of the L. pneumophila Corby, Philadelphia I, and Wadsworth. While Mip protein expression could be restored in the corresponding complementants, significant Mip-specific PPIase activity could be detected only in Mip mutants complemented with wild-type mip genes. To investigate the influence of the PPIase activity of Mip on intracellular survival of L. pneumophila, invasion assays were performed using the macrophage-like cell line U937, human blood monocytes, and Acanthamoeba castellanii. The Mip-negative mutants were approximately 50- to 100-fold less infective for A. castellanii and for human mononuclear phagocytes in vitro compared with their isogenic Mip-positive parental strains. The wild-type invasion rate could be restored by introducing an intact copy of the mip gene into Mip-negative strains. In addition, no differences in intracellular survival were observed between the wild-type isolates and the Legionella strains exhibiting strongly reduced PPIase activity. These data indicated that the enzymatic activity of Mip does not contribute to intracellular survival of L. pneumophila.

摘要

嗜肺军团菌是军团病的病原体,能够在真核细胞(如单核细胞、巨噬细胞和原生动物)内生存。巨噬细胞感染增强因子(Mip)蛋白是嗜肺军团菌在细胞内实现最佳生存所必需的一个因子。有趣的是,Mip属于FK506结合蛋白物质类别,并表现出肽基脯氨酰顺/反异构酶(PPIase)活性,该活性可被免疫抑制剂FK506抑制。为了确定最有可能参与Mip酶活性的氨基酸,构建并表征了定点诱变的Mip蛋白。结果表明,天冬氨酸142突变为亮氨酸142以及酪氨酸185突变为丙氨酸185会导致重组Mip蛋白的PPIase活性大幅降低(分别为野生型Mip活性的5.3%和0.6%)。编码野生型和定点诱变Mip蛋白的基因被用于补充嗜肺军团菌科比株、费城1株和沃兹沃思株的三种不同的Mip阴性突变体。虽然在相应的互补菌株中可以恢复Mip蛋白表达,但仅在与野生型mip基因互补的Mip突变体中能检测到显著的Mip特异性PPIase活性。为了研究Mip的PPIase活性对嗜肺军团菌细胞内存活的影响,使用巨噬细胞样细胞系U937、人血单核细胞和卡氏棘阿米巴进行了侵袭试验。与同基因的Mip阳性亲本菌株相比,Mip阴性突变体对卡氏棘阿米巴和人单核吞噬细胞的体外感染性降低了约50至100倍。通过将完整的mip基因拷贝引入Mip阴性菌株,可以恢复野生型侵袭率。此外,在野生型分离株和PPIase活性大幅降低的军团菌菌株之间,未观察到细胞内存活的差异。这些数据表明,Mip的酶活性对嗜肺军团菌的细胞内存活没有贡献。

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