Helicobacter pylori targets mitochondrial import and components of mitochondrial DNA replication machinery through an alternative VacA-dependent and a VacA-independent mechanisms View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-11-21

AUTHORS

Laurent Chatre, Julien Fernandes, Valérie Michel, Laurence Fiette, Patrick Avé, Giuseppe Arena, Utkarsh Jain, Rainer Haas, Timothy C. Wang, Miria Ricchetti, Eliette Touati

ABSTRACT

Targeting mitochondria is a powerful strategy for pathogens to subvert cell physiology and establish infection. Helicobacter pylori is a bacterial pathogen associated with gastric cancer development that is known to target mitochondria directly and exclusively through its pro-apoptotic and vacuolating cytotoxin VacA. By in vitro infection of gastric epithelial cells with wild-type and VacA-deficient H. pylori strains, treatment of cells with purified VacA proteins and infection of a mouse model, we show that H. pylori deregulates mitochondria by two novel mechanisms, both rather associated with host cell survival. First, early upon infection VacA induces transient increase of mitochondrial translocases and a dramatic accumulation of the mitochondrial DNA replication and maintenance factors POLG and TFAM. These events occur when VacA is not detected intracellularly, therefore do not require the direct interaction of the cytotoxin with the organelle, and are independent of the toxin vacuolating activity. In vivo, these alterations coincide with the evolution of gastric lesions towards severity. Second, H. pylori also induces VacA-independent alteration of mitochondrial replication and import components, suggesting the involvement of additional H. pylori activities in mitochondria-mediated effects. These data unveil two novel mitochondrial effectors in H. pylori-host interaction with links on gastric pathogenesis. More... »

PAGES

15901

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-017-15567-3

DOI

http://dx.doi.org/10.1038/s41598-017-15567-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1092714970

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29162845


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35 schema:description Targeting mitochondria is a powerful strategy for pathogens to subvert cell physiology and establish infection. Helicobacter pylori is a bacterial pathogen associated with gastric cancer development that is known to target mitochondria directly and exclusively through its pro-apoptotic and vacuolating cytotoxin VacA. By in vitro infection of gastric epithelial cells with wild-type and VacA-deficient H. pylori strains, treatment of cells with purified VacA proteins and infection of a mouse model, we show that H. pylori deregulates mitochondria by two novel mechanisms, both rather associated with host cell survival. First, early upon infection VacA induces transient increase of mitochondrial translocases and a dramatic accumulation of the mitochondrial DNA replication and maintenance factors POLG and TFAM. These events occur when VacA is not detected intracellularly, therefore do not require the direct interaction of the cytotoxin with the organelle, and are independent of the toxin vacuolating activity. In vivo, these alterations coincide with the evolution of gastric lesions towards severity. Second, H. pylori also induces VacA-independent alteration of mitochondrial replication and import components, suggesting the involvement of additional H. pylori activities in mitochondria-mediated effects. These data unveil two novel mitochondrial effectors in H. pylori-host interaction with links on gastric pathogenesis.
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42 DNA replication machinery
43 H. pylori
44 H. pylori activity
45 H. pylori strains
46 H. pylori-host interactions
47 Helicobacter pylori
48 POLG
49 TFAM
50 VacA
51 VacA proteins
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56 bacterial pathogens
57 cancer development
58 cell physiology
59 cell survival
60 cells
61 components
62 cytotoxin
63 cytotoxin VacA.
64 data
65 development
66 direct interaction
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68 effect
69 effectors
70 epithelial cells
71 events
72 evolution
73 gastric cancer development
74 gastric epithelial cells
75 gastric lesions
76 gastric pathogenesis
77 host cell survival
78 import
79 import components
80 increase
81 infection
82 interaction
83 involvement
84 lesions
85 link
86 machinery
87 mechanism
88 mitochondria
89 mitochondrial DNA replication
90 mitochondrial DNA replication machinery
91 mitochondrial effectors
92 mitochondrial import
93 mitochondrial replication
94 mitochondrial translocases
95 model
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98 organelles
99 pathogenesis
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101 physiology
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