Journal
INFECTION AND IMMUNITY
Volume 79, Issue 7, Pages 2839-2846Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.01243-10
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Funding
- INSERM
- INRA
- Pasteur Institute
- ERC [233348]
- European Research Council (ERC) [233348] Funding Source: European Research Council (ERC)
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Chromatin modification triggered by bacteria is a newly described mechanism by which pathogens impact host transcription. Listeria monocytogenes dephosphorylates histone H3 through the action of listeriolysin O (LLO); however, the underlying mechanism is unknown. Here we show that an unrelated pore-forming toxin, Aeromonas aerolysin, also provokes H3 dephosphorylation (dePH3). As reported for aerolysin, we show that LLO and related toxins induce a pore-dependent K+ efflux and that this efflux is the signal required for dePH3. In addition, LLO-induced K+ efflux activates caspase-1. However, we demonstrate that dePH3 is unlinked to this activation. Therefore, our study unveils K+ efflux as an important signal leading to two independent events critical for infection, inflammasome activation and histone modification.
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