A toxin-antitoxin module of Salmonella promotes virulence in mice.

Toxin-antitoxin (TA) modules are widely prevalent in both bacteria and archaea. Originally described as stabilizing elements of plasmids, TA modules are also widespread on bacterial chromosomes. These modules promote bacterial persistence in response to specific environmental stresses. So far, the p...

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Autores principales:	Miguel A De la Cruz, Weidong Zhao, Carine Farenc, Grégory Gimenez, Didier Raoult, Christian Cambillau, Jean-Pierre Gorvel, Stéphane Méresse
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/e65d83f5ec874c14b804e140f07ae8b7
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spelling	oai:doaj.org-article:e65d83f5ec874c14b804e140f07ae8b72021-11-18T06:07:12ZA toxin-antitoxin module of Salmonella promotes virulence in mice.1553-73661553-737410.1371/journal.ppat.1003827https://doaj.org/article/e65d83f5ec874c14b804e140f07ae8b72013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24385907/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Toxin-antitoxin (TA) modules are widely prevalent in both bacteria and archaea. Originally described as stabilizing elements of plasmids, TA modules are also widespread on bacterial chromosomes. These modules promote bacterial persistence in response to specific environmental stresses. So far, the possibility that TA modules could be involved in bacterial virulence has been largely neglected, but recent comparative genomic studies have shown that the presence of TA modules is significantly associated with the pathogenicity of bacteria. Using Salmonella as a model, we investigated whether TA modules help bacteria to overcome the stress conditions encountered during colonization, thereby supporting virulence in the host. By bioinformatics analyses, we found that the genome of the pathogenic bacterium Salmonella Typhimurium encodes at least 11 type II TA modules. Several of these are conserved in other pathogenic strains but absent from non-pathogenic species indicating that certain TA modules might play a role in Salmonella pathogenicity. We show that one TA module, hereafter referred to as sehAB, plays a transient role in virulence in perorally inoculated mice. The use of a transcriptional reporter demonstrated that bacteria in which sehAB is strongly activated are predominantly localized in the mesenteric lymph nodes. In addition, sehAB was shown to be important for the survival of Salmonella in these peripheral lymphoid organs. These data indicate that the transient activation of a type II TA module can bring a selective advantage favouring virulence and demonstrate that TA modules are engaged in Salmonella pathogenesis.Miguel A De la CruzWeidong ZhaoCarine FarencGrégory GimenezDidier RaoultChristian CambillauJean-Pierre GorvelStéphane MéressePublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 9, Iss 12, p e1003827 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Miguel A De la Cruz Weidong Zhao Carine Farenc Grégory Gimenez Didier Raoult Christian Cambillau Jean-Pierre Gorvel Stéphane Méresse A toxin-antitoxin module of Salmonella promotes virulence in mice.
description	Toxin-antitoxin (TA) modules are widely prevalent in both bacteria and archaea. Originally described as stabilizing elements of plasmids, TA modules are also widespread on bacterial chromosomes. These modules promote bacterial persistence in response to specific environmental stresses. So far, the possibility that TA modules could be involved in bacterial virulence has been largely neglected, but recent comparative genomic studies have shown that the presence of TA modules is significantly associated with the pathogenicity of bacteria. Using Salmonella as a model, we investigated whether TA modules help bacteria to overcome the stress conditions encountered during colonization, thereby supporting virulence in the host. By bioinformatics analyses, we found that the genome of the pathogenic bacterium Salmonella Typhimurium encodes at least 11 type II TA modules. Several of these are conserved in other pathogenic strains but absent from non-pathogenic species indicating that certain TA modules might play a role in Salmonella pathogenicity. We show that one TA module, hereafter referred to as sehAB, plays a transient role in virulence in perorally inoculated mice. The use of a transcriptional reporter demonstrated that bacteria in which sehAB is strongly activated are predominantly localized in the mesenteric lymph nodes. In addition, sehAB was shown to be important for the survival of Salmonella in these peripheral lymphoid organs. These data indicate that the transient activation of a type II TA module can bring a selective advantage favouring virulence and demonstrate that TA modules are engaged in Salmonella pathogenesis.
format	article
author	Miguel A De la Cruz Weidong Zhao Carine Farenc Grégory Gimenez Didier Raoult Christian Cambillau Jean-Pierre Gorvel Stéphane Méresse
author_facet	Miguel A De la Cruz Weidong Zhao Carine Farenc Grégory Gimenez Didier Raoult Christian Cambillau Jean-Pierre Gorvel Stéphane Méresse
author_sort	Miguel A De la Cruz
title	A toxin-antitoxin module of Salmonella promotes virulence in mice.
title_short	A toxin-antitoxin module of Salmonella promotes virulence in mice.
title_full	A toxin-antitoxin module of Salmonella promotes virulence in mice.
title_fullStr	A toxin-antitoxin module of Salmonella promotes virulence in mice.
title_full_unstemmed	A toxin-antitoxin module of Salmonella promotes virulence in mice.
title_sort	toxin-antitoxin module of salmonella promotes virulence in mice.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/e65d83f5ec874c14b804e140f07ae8b7
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A toxin-antitoxin module of Salmonella promotes virulence in mice.

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