Polyamines are required for virulence in Salmonella enterica serovar Typhimurium.

Sensing and responding to environmental cues is a fundamental characteristic of bacterial physiology and virulence. Here we identify polyamines as novel environmental signals essential for virulence of Salmonella enterica serovar Typhimurium, a major intracellular pathogen and a model organism for s...

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Autores principales: Lotte Jelsbak, Line Elnif Thomsen, Inke Wallrodt, Peter Ruhdal Jensen, John Elmerdahl Olsen
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Publicado: Public Library of Science (PLoS) 2012
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spelling oai:doaj.org-article:85bc1855eb6c4cde8501403a2418b3902021-11-18T07:20:11ZPolyamines are required for virulence in Salmonella enterica serovar Typhimurium.1932-620310.1371/journal.pone.0036149https://doaj.org/article/85bc1855eb6c4cde8501403a2418b3902012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22558361/?tool=EBIhttps://doaj.org/toc/1932-6203Sensing and responding to environmental cues is a fundamental characteristic of bacterial physiology and virulence. Here we identify polyamines as novel environmental signals essential for virulence of Salmonella enterica serovar Typhimurium, a major intracellular pathogen and a model organism for studying typhoid fever. Central to its virulence are two major virulence loci Salmonella Pathogenicity Island 1 and 2 (SPI1 and SPI2). SPI1 promotes invasion of epithelial cells, whereas SPI2 enables S. Typhimurium to survive and proliferate within specialized compartments inside host cells. In this study, we show that an S. Typhimurium polyamine mutant is defective for invasion, intracellular survival, killing of the nematode Caenorhabditis elegans and systemic infection of the mouse model of typhoid fever. Virulence of the mutant could be restored by genetic complementation, and invasion and intracellular survival could, as well, be complemented by the addition of exogenous putrescine and spermidine to the bacterial cultures prior to infection. Interestingly, intracellular survival of the polyamine mutant was significantly enhanced above the wild type level by the addition of exogenous putrescine and spermidine to the bacterial cultures prior to infection, indicating that these polyamines function as an environmental signal that primes S. Typhimurium for intracellular survival. Accordingly, experiments addressed at elucidating the roles of these polyamines in infection revealed that expression of genes from both of the major virulence loci SPI1 and SPI2 responded to exogenous polyamines and was reduced in the polyamine mutant. Together our data demonstrate that putrescine and spermidine play a critical role in controlling virulence in S. Typhimurium most likely through stimulation of expression of essential virulence loci. Moreover, our data implicate these polyamines as key signals in S. Typhimurium virulence.Lotte JelsbakLine Elnif ThomsenInke WallrodtPeter Ruhdal JensenJohn Elmerdahl OlsenPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 4, p e36149 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Lotte Jelsbak
Line Elnif Thomsen
Inke Wallrodt
Peter Ruhdal Jensen
John Elmerdahl Olsen
Polyamines are required for virulence in Salmonella enterica serovar Typhimurium.
description Sensing and responding to environmental cues is a fundamental characteristic of bacterial physiology and virulence. Here we identify polyamines as novel environmental signals essential for virulence of Salmonella enterica serovar Typhimurium, a major intracellular pathogen and a model organism for studying typhoid fever. Central to its virulence are two major virulence loci Salmonella Pathogenicity Island 1 and 2 (SPI1 and SPI2). SPI1 promotes invasion of epithelial cells, whereas SPI2 enables S. Typhimurium to survive and proliferate within specialized compartments inside host cells. In this study, we show that an S. Typhimurium polyamine mutant is defective for invasion, intracellular survival, killing of the nematode Caenorhabditis elegans and systemic infection of the mouse model of typhoid fever. Virulence of the mutant could be restored by genetic complementation, and invasion and intracellular survival could, as well, be complemented by the addition of exogenous putrescine and spermidine to the bacterial cultures prior to infection. Interestingly, intracellular survival of the polyamine mutant was significantly enhanced above the wild type level by the addition of exogenous putrescine and spermidine to the bacterial cultures prior to infection, indicating that these polyamines function as an environmental signal that primes S. Typhimurium for intracellular survival. Accordingly, experiments addressed at elucidating the roles of these polyamines in infection revealed that expression of genes from both of the major virulence loci SPI1 and SPI2 responded to exogenous polyamines and was reduced in the polyamine mutant. Together our data demonstrate that putrescine and spermidine play a critical role in controlling virulence in S. Typhimurium most likely through stimulation of expression of essential virulence loci. Moreover, our data implicate these polyamines as key signals in S. Typhimurium virulence.
format article
author Lotte Jelsbak
Line Elnif Thomsen
Inke Wallrodt
Peter Ruhdal Jensen
John Elmerdahl Olsen
author_facet Lotte Jelsbak
Line Elnif Thomsen
Inke Wallrodt
Peter Ruhdal Jensen
John Elmerdahl Olsen
author_sort Lotte Jelsbak
title Polyamines are required for virulence in Salmonella enterica serovar Typhimurium.
title_short Polyamines are required for virulence in Salmonella enterica serovar Typhimurium.
title_full Polyamines are required for virulence in Salmonella enterica serovar Typhimurium.
title_fullStr Polyamines are required for virulence in Salmonella enterica serovar Typhimurium.
title_full_unstemmed Polyamines are required for virulence in Salmonella enterica serovar Typhimurium.
title_sort polyamines are required for virulence in salmonella enterica serovar typhimurium.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/85bc1855eb6c4cde8501403a2418b390
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AT lineelnifthomsen polyaminesarerequiredforvirulenceinsalmonellaentericaserovartyphimurium
AT inkewallrodt polyaminesarerequiredforvirulenceinsalmonellaentericaserovartyphimurium
AT peterruhdaljensen polyaminesarerequiredforvirulenceinsalmonellaentericaserovartyphimurium
AT johnelmerdahlolsen polyaminesarerequiredforvirulenceinsalmonellaentericaserovartyphimurium
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