Thomsen, Line E.

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orcid::0000-0001-5460-9178
  • Thomsen, Line E. (1)
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Removal of the phage-shock protein PspB causes reduction of virulence in Salmonella enterica serovar Typhimurium independently of NRAMP1

Wallrodt, Inke; Jelsbak, Lotte; Thomsen, Line E.; Brix, Lena; Lemire, Sebastien; Gautier, Laurent; Nielsen, Dennis S.; Jovanović, Goran; Buck, Martin; Olsen, John E.

(Soc General Microbiology, Reading, 2014)

TY  - JOUR
AU  - Wallrodt, Inke
AU  - Jelsbak, Lotte
AU  - Thomsen, Line E.
AU  - Brix, Lena
AU  - Lemire, Sebastien
AU  - Gautier, Laurent
AU  - Nielsen, Dennis S.
AU  - Jovanović, Goran
AU  - Buck, Martin
AU  - Olsen, John E.
PY  - 2014
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/704
AB  - The phage-shock protein (Psp) system is believed to manage membrane stress in all Enterobacteriaceae and has recently emerged as being important for virulence in several pathogenic species of this phylum. The core of the Psp system consists of the pspA-D operon and the distantly located pspG gene. In Salmonella enterica serovar Typhimurium (S. Typhimurium), it has recently been reported that PspA is essential for systemic infection of mice, but only in NRAMP1(+) mice, signifying that attenuation is related to coping with divalent cation starvation in the intracellular environment. In the present study, we investigated the contribution of individual psp genes to virulence of S. Typhimurium. Interestingly, deletion of the whole pspA-D set of genes caused attenuation in both NRAMP1(+) and NRAMP1(-) mice, indicating that one or more of the psp genes contribute to virulence independently of NRAMP1 expression in the host. Investigations of single gene mutants showed that knock out of pspB reduced virulence in both types of mice, while deletion of pspA only caused attenuation in NRAMP1(+) mice, and deletion of pspD had a minor effect in NRAMP1(-) mice, while deletions of either pspC or pspG did not affect virulence. Experiments addressed at elucidating the role of PspB in virulence revealed that PspB is dispensable for uptake to and intracellular replication in cultured macrophages and resistance to complement-induced killing. Furthermore, the Psp system of S. Typhimurium was dispensable during pIV-induced secretin stress. In conclusion, our results demonstrate that removal of PspB reduces virulence in S. Typhimurium independently of host NRAMP1 expression, demonstrating that PspB has roles in intra-host survival distinct from the reported contributions of PspA.
PB  - Soc General Microbiology, Reading
T2  - Journal of Medical Microbiology
T1  - Removal of the phage-shock protein PspB causes reduction of virulence in Salmonella enterica serovar Typhimurium independently of NRAMP1
EP  - 795
SP  - 788
VL  - 63
DO  - 10.1099/jmm.0.072223-0
ER  - 
@article{
author = "Wallrodt, Inke and Jelsbak, Lotte and Thomsen, Line E. and Brix, Lena and Lemire, Sebastien and Gautier, Laurent and Nielsen, Dennis S. and Jovanović, Goran and Buck, Martin and Olsen, John E.",
year = "2014",
abstract = "The phage-shock protein (Psp) system is believed to manage membrane stress in all Enterobacteriaceae and has recently emerged as being important for virulence in several pathogenic species of this phylum. The core of the Psp system consists of the pspA-D operon and the distantly located pspG gene. In Salmonella enterica serovar Typhimurium (S. Typhimurium), it has recently been reported that PspA is essential for systemic infection of mice, but only in NRAMP1(+) mice, signifying that attenuation is related to coping with divalent cation starvation in the intracellular environment. In the present study, we investigated the contribution of individual psp genes to virulence of S. Typhimurium. Interestingly, deletion of the whole pspA-D set of genes caused attenuation in both NRAMP1(+) and NRAMP1(-) mice, indicating that one or more of the psp genes contribute to virulence independently of NRAMP1 expression in the host. Investigations of single gene mutants showed that knock out of pspB reduced virulence in both types of mice, while deletion of pspA only caused attenuation in NRAMP1(+) mice, and deletion of pspD had a minor effect in NRAMP1(-) mice, while deletions of either pspC or pspG did not affect virulence. Experiments addressed at elucidating the role of PspB in virulence revealed that PspB is dispensable for uptake to and intracellular replication in cultured macrophages and resistance to complement-induced killing. Furthermore, the Psp system of S. Typhimurium was dispensable during pIV-induced secretin stress. In conclusion, our results demonstrate that removal of PspB reduces virulence in S. Typhimurium independently of host NRAMP1 expression, demonstrating that PspB has roles in intra-host survival distinct from the reported contributions of PspA.",
publisher = "Soc General Microbiology, Reading",
journal = "Journal of Medical Microbiology",
title = "Removal of the phage-shock protein PspB causes reduction of virulence in Salmonella enterica serovar Typhimurium independently of NRAMP1",
pages = "795-788",
volume = "63",
doi = "10.1099/jmm.0.072223-0"
}
Wallrodt, I., Jelsbak, L., Thomsen, L. E., Brix, L., Lemire, S., Gautier, L., Nielsen, D. S., Jovanović, G., Buck, M.,& Olsen, J. E.. (2014). Removal of the phage-shock protein PspB causes reduction of virulence in Salmonella enterica serovar Typhimurium independently of NRAMP1. in Journal of Medical Microbiology
Soc General Microbiology, Reading., 63, 788-795.
https://doi.org/10.1099/jmm.0.072223-0
Wallrodt I, Jelsbak L, Thomsen LE, Brix L, Lemire S, Gautier L, Nielsen DS, Jovanović G, Buck M, Olsen JE. Removal of the phage-shock protein PspB causes reduction of virulence in Salmonella enterica serovar Typhimurium independently of NRAMP1. in Journal of Medical Microbiology. 2014;63:788-795.
doi:10.1099/jmm.0.072223-0 .
Wallrodt, Inke, Jelsbak, Lotte, Thomsen, Line E., Brix, Lena, Lemire, Sebastien, Gautier, Laurent, Nielsen, Dennis S., Jovanović, Goran, Buck, Martin, Olsen, John E., "Removal of the phage-shock protein PspB causes reduction of virulence in Salmonella enterica serovar Typhimurium independently of NRAMP1" in Journal of Medical Microbiology, 63 (2014):788-795,
https://doi.org/10.1099/jmm.0.072223-0 . .
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