Micro-managing the executioner: pathogen targeting of mitochondria

Blanke, Steven R.

doi:10.1016/j.tim.2004.12.007

Cited by 48 publications

(49 citation statements)

References 59 publications

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“…Of interest, VacA-dependent mitochondrial dysfunction is also dependent on the toxin's channel activity. 44,45 The consequences of VacA-mediated induction of autophagic processes within H. pylori infected cells may be complex. Autophagy is one mechanism used by host cells to clear intracellular infectious microbes.…”

Section: Discussionmentioning

confidence: 99%

Effect ofHelicobacter pylori’s vacuolating cytotoxin on the autophagy pathway in gastric epithelial cells

et al. 2009

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Section: Discussionmentioning

confidence: 99%

Effect ofHelicobacter pylori’s vacuolating cytotoxin on the autophagy pathway in gastric epithelial cells

et al. 2009

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“…The targeting of mitochondrial membranes by bacterial toxins is becoming a powerful strategy to control cell viability (3). In fact, the list of toxins that might translocate to host cell mitochondria and cause apoptosis is exponentially increasing.…”

Section: Discussionmentioning

confidence: 99%

“…For all of the experiments, we have then chosen the concentration of 3 ng/ml toxin B (corresponding to 10 Ϫ11 M) that induced cell retraction in the whole population within 30 min. HEp-2 cells were treated with 3 ng/ml wild-type (WT) TcdB or rec TcdB for different time lengths (1,3,6,18, and 32 h). Isolated mitochondria (see below for the preparation) were challenged with (i) WT TcdB (1.5, 3, or 6 ng/ml), (ii) rec TcdB (3 ng/ml), (iii) NterTcdB (1.5, 3, 4.5, or 6 ng/ml), and (iv) VacA (5 g/ml).…”

Section: Methodsmentioning

confidence: 99%

“…In recent years, the targeting of mitochondrial membranes is emerging as a widespread strategy employed by bacterial pathogens in controlling the host cell destiny (reviewed in Ref. 3). The direct targeting of mitochondria, in fact, can allow bacteria to bypass upstream checkpoints of cell death, thus straightforwardly handling one of the central executioners of apoptosis.…”

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confidence: 99%

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Clostridium difficile Toxin B Causes Apoptosis in Epithelial Cells by Thrilling Mitochondria

Matarrese

Falzano

Fabbri

et al. 2007

Journal of Biological Chemistry

105

109

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Targeting to mitochondria is emerging as a common strategy that bacteria utilize to interact with these central executioners of apoptosis. Several lines of evidence have in fact indicated mitochondria as specific targets for bacterial protein toxins, regarded as the principal virulence factors of pathogenic bacteria. This work shows, for the first time, the ability of the Clostridium difficile toxin B (TcdB), a glucosyltransferase that inhibits the Rho GTPases, to impact mitochondria. In living cells, TcdB provokes an early hyperpolarization of mitochondria that follows a calcium-associated signaling pathway and precedes the final execution step of apoptosis (i.e. mitochondria depolarization). Importantly, in isolated mitochondria, the toxin can induce a calcium-dependent mitochondrial swelling, accompanied by the release of the proapoptogenic factor cytochrome c. This is consistent with a mitochondrial targeting that does not require the Rho-inhibiting activity of the toxin. Of interest, the mitochondrial ATP-sensitive potassium channels are also involved in the apoptotic response to TcdB and appear to be crucial for the cell death execution phase, as demonstrated by using specific modulators of these channels. To our knowledge, the involvement of these mitochondrial channels in the ability of a bacterial toxin to control cell fate is a hitherto unreported finding.

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“…Several pathogens including both viruses and bacteria directly or indirectly target mitochondria to interfere with the host apoptotic machinery (20)(21)(22)(23)(24). Depending on the pathogen and host-cell type, this interference can inhibit cell death to preserve the pathogen's replication niche or induce cell death to promote infection spreading (25).…”

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confidence: 99%

Listeria monocytogenes transiently alters mitochondrial dynamics during infection

Stavru

Bouillaud

Sartori

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

207

214

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Mitochondria are essential and highly dynamic organelles, constantly undergoing fusion and fission. We analyzed mitochondrial dynamics during infection with the human bacterial pathogen Listeria monocytogenes and show that this infection profoundly alters mitochondrial dynamics by causing transient mitochondrial network fragmentation. Mitochondrial fragmentation is specific to pathogenic Listeria monocytogenes, and it is not observed with the nonpathogenic Listeria innocua species or several other intracellular pathogens. Strikingly, the efficiency of Listeria infection is affected in cells where either mitochondrial fusion or fission has been altered by siRNA treatment, highlighting the relevance of mitochondrial dynamics for Listeria infection. We identified the secreted pore-forming toxin listeriolysin O as the bacterial factor mainly responsible for mitochondrial network disruption and mitochondrial function modulation. Together, our results suggest that the transient shutdown of mitochondrial function and dynamics represents a strategy used by Listeria at the onset of infection to interfere with cellular physiology.bacterial infection | calcium influx | bioenergetics

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Micro-managing the executioner: pathogen targeting of mitochondria

Cited by 48 publications

References 59 publications

Effect ofHelicobacter pylori’s vacuolating cytotoxin on the autophagy pathway in gastric epithelial cells

Effect ofHelicobacter pylori’s vacuolating cytotoxin on the autophagy pathway in gastric epithelial cells

Clostridium difficile Toxin B Causes Apoptosis in Epithelial Cells by Thrilling Mitochondria

Listeria monocytogenes transiently alters mitochondrial dynamics during infection

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