The Homolog of the Gene bstA of the BTP1 Phage from Salmonella enterica Serovar Typhimurium ST313 Is an Antivirulence Gene in Salmonella enterica Serovar Dublin
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The Homolog of the Gene bstA of the BTP1 Phage from Salmonella enterica Serovar Typhimurium ST313 Is an Antivirulence Gene in Salmonella enterica Serovar Dublin. / Herrero-Fresno, Ana; Espinel, Irene Cartas; Spiegelhauer, Malene Roed; Guerra, Priscila Regina; Andersen, Karsten Wiber; Olsen, John Elmerdahl.
I: Infection and Immunity, Bind 86, Nr. 1, e00784-17, 01.2018.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - The Homolog of the Gene bstA of the BTP1 Phage from Salmonella enterica Serovar Typhimurium ST313 Is an Antivirulence Gene in Salmonella enterica Serovar Dublin
AU - Herrero-Fresno, Ana
AU - Espinel, Irene Cartas
AU - Spiegelhauer, Malene Roed
AU - Guerra, Priscila Regina
AU - Andersen, Karsten Wiber
AU - Olsen, John Elmerdahl
PY - 2018/1
Y1 - 2018/1
N2 - In a previous study, a novel virulence gene, bstA, identified in a Salmonella enterica serovar Typhimurium sequence type 313 (ST313) strain was found to be conserved in all published Salmonella enterica serovar Dublin genomes. In order to analyze the role of this gene in the host-pathogen interaction in S. Dublin, a mutant where this gene was deleted (S. Dublin ΔbstA) and a mutant which was further genetically complemented with bstA (S. Dublin 3246-C) were constructed and tested in models of in vitro and in vivo infection as well as during growth competition assays in M9 medium, Luria-Bertani broth, and cattle blood. In contrast to the results obtained for a strain of S. Typhimurium ST313, the lack of bstA was found to be associated with increased virulence in S. Dublin. Thus, S. Dublin ΔbstA showed higher levels of uptake than the wild-type strain during infection of mouse and cattle macrophages and higher net replication within human THP-1 cells. Furthermore, during mouse infections, S. Dublin ΔbstA was more virulent than the wild type following a single intraperitoneal infection and showed an increased competitive index during competitive infection assays. Deletion of bstA did not affect either the amount of cytokines released by THP-1 macrophages or the cytotoxicity toward these cells. The histology of the livers and spleens of mice infected with the wild-type strain and the S. Dublin ΔbstA mutant revealed similar levels of inflammation between the two groups. The gene was not important for adherence to or invasion of human epithelial cells and did not influence bacterial growth in rich medium, minimal medium, or cattle blood. In conclusion, a lack of bstA affects the pathogenicity of S. Dublin by decreasing its virulence. Therefore, it might be regarded as an antivirulence gene in this serovar.
AB - In a previous study, a novel virulence gene, bstA, identified in a Salmonella enterica serovar Typhimurium sequence type 313 (ST313) strain was found to be conserved in all published Salmonella enterica serovar Dublin genomes. In order to analyze the role of this gene in the host-pathogen interaction in S. Dublin, a mutant where this gene was deleted (S. Dublin ΔbstA) and a mutant which was further genetically complemented with bstA (S. Dublin 3246-C) were constructed and tested in models of in vitro and in vivo infection as well as during growth competition assays in M9 medium, Luria-Bertani broth, and cattle blood. In contrast to the results obtained for a strain of S. Typhimurium ST313, the lack of bstA was found to be associated with increased virulence in S. Dublin. Thus, S. Dublin ΔbstA showed higher levels of uptake than the wild-type strain during infection of mouse and cattle macrophages and higher net replication within human THP-1 cells. Furthermore, during mouse infections, S. Dublin ΔbstA was more virulent than the wild type following a single intraperitoneal infection and showed an increased competitive index during competitive infection assays. Deletion of bstA did not affect either the amount of cytokines released by THP-1 macrophages or the cytotoxicity toward these cells. The histology of the livers and spleens of mice infected with the wild-type strain and the S. Dublin ΔbstA mutant revealed similar levels of inflammation between the two groups. The gene was not important for adherence to or invasion of human epithelial cells and did not influence bacterial growth in rich medium, minimal medium, or cattle blood. In conclusion, a lack of bstA affects the pathogenicity of S. Dublin by decreasing its virulence. Therefore, it might be regarded as an antivirulence gene in this serovar.
KW - Salmonella enterica serovar Dublin
KW - bstA
KW - antivirulence
KW - infection
KW - cell lines
KW - cattle blood
KW - mouse
U2 - 10.1128/IAI.00784-17
DO - 10.1128/IAI.00784-17
M3 - Journal article
C2 - 29109173
VL - 86
JO - Infection and Immunity
JF - Infection and Immunity
SN - 0019-9567
IS - 1
M1 - e00784-17
ER -
ID: 187583298