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Front. Cell. Infect. Microbiol. | doi: 10.3389/fcimb.2018.00061

Acanthamoeba and Dictyostelium as cellular models for Legionella infection

  • 1University of Zurich, Switzerland
  • 2Ludwig-Maximilians-Universität München, Germany
  • 3Universitätsklinikum köln, Germany
  • 4Technische Universitat Braunschweig, Germany

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, protein kinases and the retromer complex, as well as on bacterial effectors targeting these host factors.

Keywords: Amoebae, Dictyostelium discoideum, Effector protein, Endoplasmic Reticulum, endosome, GTPase, host-pathogen interaction, Legionella, macrophage, pathogen vacuole, phosphoinositide lipid, retrograde transport, Secretory Pathway, Type IV secretion, vesicle trafficking, Autophagy

Received: 23 Nov 2017; Accepted: 13 Feb 2018.

Edited by:

Matthew S. Francis, Umeå University, Sweden

Reviewed by:

Eric D. Cambronne, Oregon Health & Science University, United States
Hayley J. Newton, University of Melbourne, Australia
Jason King, University of Sheffield, United Kingdom  

Copyright: © 2018 Swart, Harrison, Eichinger, Steinert and Hilbi. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Hubert Hilbi, University of Zurich, Zürich, Switzerland,