Listeria infection modulates mitochondrial dynamics

Abstract

Mitochondria are highly dynamic organelles that are central to several cellular processes, the most prominent being energy production. Several reports have shown that pathogens target mitochondria in various ways to interfere with apoptosis, but to our knowledge only one study has specifically addressed the effects of infection on mitochondrial dynamics. We focused on this aspect during infection with the intracellular pathogen L. monocytogenes and could recently show that this bacterium profoundly alters mitochondrial dynamics, causing transient fragmentation of the mitochondrial network. This mitochondrial fragmentation occurs early during infection and is specific to pathogenic L. monocytogenes, as it is not observed with other intracellular pathogens. The relevance of mitochondrial dynamics for L. monocytogenes infection is highlighted by the finding that siRNA-mediated inhibition of mitochondrial fusion or fission decreases or increases the efficiency of L. monocytogenes infection, respectively. The main bacterial factor responsible for mitochondrial network disruption was identified as the secreted pore-forming toxin listeriolysin O, which also appeared to impair mitochondrial function. Our work suggests that in order to establish an efficient infection, L. monocytogenes interferes with cellular physiology at early timepoints by transient disruption of mitochondrial dynamics and function

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Figures and Tables

Figure 1 Model depicting the effect of Listeria infection on host cells. Early during Listeria infection, secreted LLO inserts into the plasma membrane of host cells (which can also be bystander cells), causing fragmentation of the mitochondrial network along with a decrease in mitochondrial membrane potential and intracellular ATP levels. Cellular signaling pathways that remain to be identified may sense changes in mitochondrial dynamics and bioenergetics to impact on infection efficiency.

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