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Acanthamoeba and Dictyostelium as Cellular Models for Legionella Infection.

Affiliation/Institute
Institute of Medical Microbiology, Medical Faculty, University of Zurich
Swart, A Leoni;
Affiliation/Institute
Max von Pettenkofer Institute, Medical Faculty, Ludwig-Maximilians University Munich, Munich, Germany.
Harrison, Christopher F;
Affiliation/Institute
Institute for Biochemistry I, Medical Faculty, University Hospital Cologne, Cologne, Germany.
Eichinger, Ludwig;
GND
1139863819
Affiliation/Institute
Department of Life Sciences, Institute of Microbiology, Technical University of Braunschweig, Braunschweig, Germany.
Steinert, Michael;
ORCID
0000-0002-5462-9301
Affiliation/Institute
Institute of Medical Microbiology, Medical Faculty, University of Zurich, Zurich, Switzerland.
Hilbi, Hubert

Environmental bacteria of the genus Legionella naturally parasitize free-living amoebae. Upon inhalation of bacteria-laden aerosols, the opportunistic pathogens grow intracellularly in alveolar macrophages and can cause a life-threatening pneumonia termed Legionnaires' disease. Intracellular replication in amoebae and macrophages takes place in a unique membrane-bound compartment, the Legionella-containing vacuole (LCV). LCV formation requires the bacterial Icm/Dot type IV secretion system, which translocates literally hundreds of "effector" proteins into host cells, where they modulate crucial cellular processes for the pathogen's benefit. The mechanism of LCV formation appears to be evolutionarily conserved, and therefore, amoebae are not only ecologically significant niches for Legionella spp., but also useful cellular models for eukaryotic phagocytes. In particular, Acanthamoeba castellanii and Dictyostelium discoideum emerged over the last years as versatile and powerful models. Using genetic, biochemical and cell biological approaches, molecular interactions between amoebae and Legionella pneumophila have recently been investigated in detail with a focus on the role of phosphoinositide lipids, small and large GTPases, autophagy components and the retromer complex, as well as on bacterial effectors targeting these host factors.

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