期刊
CELLULAR MICROBIOLOGY
卷 17, 期 7, 页码 935-950出版社
WILEY
DOI: 10.1111/cmi.12450
关键词
-
资金
- Swiss National Science Foundation (SNF) [31003A_153200]
- German Research Foundation (DFG) [HI 1511/1-1, SPP1580]
- 'Bundesministerium fur Bildung und Forschung (BMBF)' through the 'Medical Infection Genomics' initiative [0315834C]
- 'Bundesministerium fur Bildung und Forschung (BMBF)' through the ERA-NET Infect-ERA of the EUGENPATH network [031A401A]
Legionella species are ubiquitous, waterborne bacteria that thrive in numerous ecological niches. Yet, in contrast to many other environmental bacteria, Legionella spp. are also able to grow intracellularly in predatory protozoa. This feature mainly accounts for the pathogenicity of Legionella pneumophila, which causes the majority of clinical cases of a severe pneumonia termed Legionnaires' disease. The pathomechanism underlying L.pneumophila infection is based on macrophage resistance, which in turn is largely defined by the opportunistic pathogen's resistance towards amoebae. L.pneumophila replicates in macrophages or amoebae in a unique membrane-bound compartment, the Legionella-containing vacuole (LCV). LCV formation requires the bacterial intracellular multiplication/defective for organelle trafficking (Icm/Dot) type IV secretion system and involves a plethora of translocated effector proteins, which subvert pivotal processes in the host cell. Of the ca.300 different experimentally validated Icm/Dot substrates, about 50 have been studied and attributed a cellular function to date. The versatility and ingenuity of these effectors' mode of actions is striking. In this review, we summarize insight into the cellular functions and biochemical activities of well-characterized L.pneumophila effector proteins and the host pathways they target. Recent studies not only substantially increased our knowledge about pathogen-host interactions, but also shed light on novel biological mechanisms.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据