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Legionella pneumophila multiplication is enhanced by chronic AMPK signalling in mitochondrially diseased dictyostelium cells

Francione, Lisa, Smith, Paige K., Accari, Sandra L., Taylor, Philip E., Bokko, Paul B., Bozzaro, Salvatore, Beech, Peter L. and Fisher, Paul R. 2009, Legionella pneumophila multiplication is enhanced by chronic AMPK signalling in mitochondrially diseased dictyostelium cells, Disease models and mechanisms, vol. 2, no. 9-10, September/October, pp. 479-489, doi: 10.1242/dmm.003319.

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Title Legionella pneumophila multiplication is enhanced by chronic AMPK signalling in mitochondrially diseased dictyostelium cells
Formatted title Legionella pneumophila multiplication is enhanced by chronic AMPK signalling in mitochondrially diseased dictyostelium cells
Author(s) Francione, Lisa
Smith, Paige K.
Accari, Sandra L.
Taylor, Philip E.ORCID iD for Taylor, Philip E. orcid.org/0000-0002-4204-1893
Bokko, Paul B.
Bozzaro, Salvatore
Beech, Peter L.
Fisher, Paul R.
Journal name Disease models and mechanisms
Volume number 2
Issue number 9-10
Season September/October
Start page 479
End page 489
Total pages 11
Publisher Company of Biologists
Place of publication Cambridge, England
Publication date 2009-09
ISSN 1754-8403
1754-8411
Keyword(s) mitochondrial diseases
dictyostelium
legionella
Summary Human patients with mitochondrial diseases are more susceptible to bacterial infections, particularly of the respiratory tract. To investigate the susceptibility of mitochondrially diseased cells to an intracellular bacterial respiratory pathogen, we exploited the advantages of Dictyostelium discoideum as an established model for mitochondrial disease and for Legionella pneumophila pathogenesis. Legionella infection of macrophages involves recruitment of mitochondria to the Legionella-containing phagosome. We confirm here that this also occurs in Dictyostelium and investigate the effect of mitochondrial dysfunction on host cell susceptibility to Legionella. In mitochondrially diseased Dictyostelium strains, the pathogen was taken up at normal rates, but it grew faster and reached counts that were twofold higher than in the wild-type host. We reported previously that other mitochondrial disease phenotypes for Dictyostelium are the result of the activity of an energy-sensing cellular alarm protein, AMP-activated protein kinase (AMPK). Here, we show that the increased ability of mitochondrially diseased cells to support Legionella proliferation is suppressed by antisense-inhibiting expression of the catalytic AMPKα subunit. Conversely, mitochondrial dysfunction is phenocopied, and intracellular Legionella growth is enhanced, by overexpressing an active form of AMPKα in otherwise normal cells. These results indicate that AMPK signalling in response to mitochondrial dysfunction enhances Legionella proliferation in host cells.
Language eng
DOI 10.1242/dmm.003319
Field of Research 110801 Medical Bacteriology
Socio Economic Objective 920109 Infectious Diseases
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2009, Company of Biologists
Persistent URL http://hdl.handle.net/10536/DRO/DU:30028426

Document type: Journal Article
Collections: School of Life and Environmental Sciences
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.