Effect of rickettsial toxin VapC on its eukaryotic host.

Rickettsia are intracellular bacteria typically associated with arthropods that can be transmitted to humans by infected vectors. Rickettsia spp. can cause mild to severe human disease with a possible protection effect of corticosteroids when antibiotic treatments are initiated. We identified latera...

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Autores principales:	Gilles Audoly, Renaud Vincentelli, Sophie Edouard, Kalliopi Georgiades, Oleg Mediannikov, Grégory Gimenez, Cristina Socolovschi, Jean-Louis Mège, Christian Cambillau, Didier Raoult
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e158d56e02124a93b21719b46d27e8f2
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spelling	oai:doaj.org-article:e158d56e02124a93b21719b46d27e8f22021-11-18T07:35:36ZEffect of rickettsial toxin VapC on its eukaryotic host.1932-620310.1371/journal.pone.0026528https://doaj.org/article/e158d56e02124a93b21719b46d27e8f22011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22046301/?tool=EBIhttps://doaj.org/toc/1932-6203Rickettsia are intracellular bacteria typically associated with arthropods that can be transmitted to humans by infected vectors. Rickettsia spp. can cause mild to severe human disease with a possible protection effect of corticosteroids when antibiotic treatments are initiated. We identified laterally transferred toxin-antitoxin (TA) genetic elements, including vapB/C, in several Rickettsia genomes and showed that they are functional in bacteria and eukaryotic cells. We also generated a plaque assay to monitor the formation of lytic plaques over time and demonstrated that chloramphenicol accelerates host cell lysis of vapB/C-containing Rickettsia. Whole-genome expression, TUNEL and FISH assays on the infected cells following exposure to the antibiotic revealed early apoptosis of host cells, which was linked to over-transcription of bacterial vapB/C operons and subsequent cytoplasmic VapC toxin release. VapC that is expressed in Escherichia coli and Saccharomyces cerevisiae or microinjected into mammalian cells is toxic through RNase activity and is prevented by dexamethasone. This study provides the first biological evidence that toxin-antitoxin elements act as pathogenic factors in bacterial host cells, confirming comparative genomic evidence of their role in bacterial pathogenicity. Our results suggest that early mortality following antibiotic treatment of some bacterial infections can be prevented by administration of dexamethasone.Gilles AudolyRenaud VincentelliSophie EdouardKalliopi GeorgiadesOleg MediannikovGrégory GimenezCristina SocolovschiJean-Louis MègeChristian CambillauDidier RaoultPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 10, p e26528 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Gilles Audoly Renaud Vincentelli Sophie Edouard Kalliopi Georgiades Oleg Mediannikov Grégory Gimenez Cristina Socolovschi Jean-Louis Mège Christian Cambillau Didier Raoult Effect of rickettsial toxin VapC on its eukaryotic host.
description	Rickettsia are intracellular bacteria typically associated with arthropods that can be transmitted to humans by infected vectors. Rickettsia spp. can cause mild to severe human disease with a possible protection effect of corticosteroids when antibiotic treatments are initiated. We identified laterally transferred toxin-antitoxin (TA) genetic elements, including vapB/C, in several Rickettsia genomes and showed that they are functional in bacteria and eukaryotic cells. We also generated a plaque assay to monitor the formation of lytic plaques over time and demonstrated that chloramphenicol accelerates host cell lysis of vapB/C-containing Rickettsia. Whole-genome expression, TUNEL and FISH assays on the infected cells following exposure to the antibiotic revealed early apoptosis of host cells, which was linked to over-transcription of bacterial vapB/C operons and subsequent cytoplasmic VapC toxin release. VapC that is expressed in Escherichia coli and Saccharomyces cerevisiae or microinjected into mammalian cells is toxic through RNase activity and is prevented by dexamethasone. This study provides the first biological evidence that toxin-antitoxin elements act as pathogenic factors in bacterial host cells, confirming comparative genomic evidence of their role in bacterial pathogenicity. Our results suggest that early mortality following antibiotic treatment of some bacterial infections can be prevented by administration of dexamethasone.
format	article
author	Gilles Audoly Renaud Vincentelli Sophie Edouard Kalliopi Georgiades Oleg Mediannikov Grégory Gimenez Cristina Socolovschi Jean-Louis Mège Christian Cambillau Didier Raoult
author_facet	Gilles Audoly Renaud Vincentelli Sophie Edouard Kalliopi Georgiades Oleg Mediannikov Grégory Gimenez Cristina Socolovschi Jean-Louis Mège Christian Cambillau Didier Raoult
author_sort	Gilles Audoly
title	Effect of rickettsial toxin VapC on its eukaryotic host.
title_short	Effect of rickettsial toxin VapC on its eukaryotic host.
title_full	Effect of rickettsial toxin VapC on its eukaryotic host.
title_fullStr	Effect of rickettsial toxin VapC on its eukaryotic host.
title_full_unstemmed	Effect of rickettsial toxin VapC on its eukaryotic host.
title_sort	effect of rickettsial toxin vapc on its eukaryotic host.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/e158d56e02124a93b21719b46d27e8f2
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Effect of rickettsial toxin VapC on its eukaryotic host.

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