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Post-phagocytosis activation of NLRP3 inflammasome by two novel T6SS effectors

Hadar Cohen, Noam Baram, Chaya M. Fridman, Liat Edry-Botzer, View ORCID ProfileDor Salomon, View ORCID ProfileMotti Gerlic
doi: https://doi.org/10.1101/2022.08.11.503615
Hadar Cohen
1Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel
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Noam Baram
1Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel
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Chaya M. Fridman
1Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel
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Liat Edry-Botzer
1Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel
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Dor Salomon
1Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel
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  • For correspondence: dorsalomon@mail.tau.ac.il mgerlic@tauex.tau.ac.il
Motti Gerlic
1Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel
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  • For correspondence: dorsalomon@mail.tau.ac.il mgerlic@tauex.tau.ac.il
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Summary

The type VI secretion system (T6SS) is used by bacteria to deliver toxic effectors directly into target cells. Most T6SSs mediate antibacterial activities, whereas the potential anti-eukaryotic role of T6SS remains understudied. Here, we found a Vibrio T6SS that delivers two novel effectors into mammalian host immune cells. We showed that these effectors induce a pyroptotic cell death in a phagocytosis-dependent manner; we identified the NLRP3 inflammasome as being the underlying mechanism leading to the T6SS-induced pyroptosis. Moreover, we identified a compensatory T6SS-induced pathway that is activated upon inhibition of the canonical pyroptosis pathway. Genetic analyses revealed possible horizontal spread of this T6SS and its anti-eukaryotic effectors into emerging pathogens in the marine environment. Our findings reveal novel T6SS effectors that activate the host inflammasome and possibly contribute to virulence and to the emergence of bacterial pathogens.

Footnotes

  • Lead Contact: Motti Gerlic PhD, Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. Tel. (Office): +972-3-640-9400, Fax: +972-3-640-9160, e-mail: mgerlic{at}tauex.tau.ac.il

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted August 12, 2022.
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Post-phagocytosis activation of NLRP3 inflammasome by two novel T6SS effectors
Hadar Cohen, Noam Baram, Chaya M. Fridman, Liat Edry-Botzer, Dor Salomon, Motti Gerlic
bioRxiv 2022.08.11.503615; doi: https://doi.org/10.1101/2022.08.11.503615
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Post-phagocytosis activation of NLRP3 inflammasome by two novel T6SS effectors
Hadar Cohen, Noam Baram, Chaya M. Fridman, Liat Edry-Botzer, Dor Salomon, Motti Gerlic
bioRxiv 2022.08.11.503615; doi: https://doi.org/10.1101/2022.08.11.503615

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