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Int J Med Microbiol. 2017 Aug 16. pii: S1438-4221(17)30291-6. doi: 10.1016/j.ijmm.2017.08.004. [Epub ahead of print]

Formation of the Legionella-containing vacuole: phosphoinositide conversion, GTPase modulation and ER dynamics.

Author information

1
Institute of Medical Microbiology, University of Zürich, Gloriastrasse 30, 8006 Zürich, Switzerland.
2
Institute of Medical Microbiology, University of Zürich, Gloriastrasse 30, 8006 Zürich, Switzerland. Electronic address: hilbi@imm.uzh.ch.

Abstract

The environmental bacterium Legionella pneumophila replicates in free-living amoeba as well as in alveolar macrophages upon inhalation of bacteria-laden aerosols. Resistance of the opportunistic pathogen to macrophages is a prerequisite to cause a severe pneumonia called Legionnaires' disease. L. pneumophila grows intracellularly in a unique, ER-associated compartment, the Legionella-containing vacuole (LCV). The bacterial Icm/Dot type IV secretion system represents an essential virulence factor, which translocates approximately 300 "effector proteins" into protozoan or mammalian host cells. Some of these effectors contribute to the formation of the LCV by targeting conserved host factors implicated in membrane dynamics, such as phosphoinositide lipids and small GTPases. Here we review recent findings on the role of phosphoinositides, small and large GTPases as well as ER dynamics for pathogen vacuole formation and intracellular replication of L. pneumophila.

KEYWORDS:

Amoeba; Dictyostelium discoideum; Effector protein; Endoplasmic reticulum; GTPase; Host-pathogen interaction; Intracellular bacteria; Legionella; Macrophage; Pathogen vacuole; Phosphoinositide lipid; Type IV secretion; Vesicle trafficking

PMID:
28865995
DOI:
10.1016/j.ijmm.2017.08.004

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