Contribution of the SitABCD, MntH, and FeoB metal transporters to the virulence of avian pathogenic Escherichia coli O78 strain χ7122

Mourad Sabri, Mélissa Caza, Julie Proulx, Maria H. Lymberopoulos, Annie Brée, Maryvonne Moulin-Schouleur, Roy Curtiss, Charles M. Dozois

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Abstract

The roles of SitABCD, MntH, and FeoB metal transporters in the virulence of avian pathogenic Escherichia coli (APEC) O78 strain χ7122 were assessed using isogenic mutants in chicken infection models. In a single-strain infection model, compared to χ7122, the Δsit strain demonstrated reduced colonization of the lungs, liver, and spleen. Complementation of the Δsit strain restored virulence. In a coinfection model, compared to the virulent APEC strain, the Δsit strain demonstrated mean 50-fold, 126-fold, and 25-fold decreases in colonization of the lungs, liver, and spleen, respectively. A ΔmntH Δsit strain was further attenuated, demonstrating reduced persistence in blood and mean 1,400-fold, 954-fold, and 83-fold reduced colonization in the lungs, liver, and spleen, respectively. In coinfections, the ΔfeoB Δsit strain demonstrated reduced persistence in blood but increased colonization of the liver. The ΔmntH, ΔfeoB, and ΔfeoB ΔmntH strains were as virulent as the wild type in either of the infection models. Strains were also tested for sensitivity to oxidative stress-generating agents. The ΔmntH Δsit strain was the most sensitive strain and was significantly more sensitive than the other strains to hydrogen peroxide, plumbagin, and paraquat. sit sequences were highly associated with APEC and human extraintestinal pathogenic E. coli compared to commensal isolates and diarrheagenic E. coli. Comparative genomic analyses also demonstrated that sit sequences are carried on conjugative plasmids or associated with phage elements and were likely acquired by distinct genetic events among pathogenic E. coli and Shigella sp. strains. Overall, the results demonstrate that SitABCD contributes to virulence and, together with MntH, to increased resistance to oxidative stress.

Original languageEnglish (US)
Pages (from-to)601-611
Number of pages11
JournalInfection and Immunity
Volume76
Issue number2
DOIs
StatePublished - Feb 2008

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Virulence
Metals
Escherichia coli
Spleen
Liver
Coinfection
Lung
Oxidative Stress
Infection
Paraquat
Shigella
Bacteriophages
Hydrogen Peroxide
Chickens
Plasmids

ASJC Scopus subject areas

  • Immunology

Cite this

Sabri, M., Caza, M., Proulx, J., Lymberopoulos, M. H., Brée, A., Moulin-Schouleur, M., ... Dozois, C. M. (2008). Contribution of the SitABCD, MntH, and FeoB metal transporters to the virulence of avian pathogenic Escherichia coli O78 strain χ7122. Infection and Immunity, 76(2), 601-611. https://doi.org/10.1128/IAI.00789-07

Contribution of the SitABCD, MntH, and FeoB metal transporters to the virulence of avian pathogenic Escherichia coli O78 strain χ7122. / Sabri, Mourad; Caza, Mélissa; Proulx, Julie; Lymberopoulos, Maria H.; Brée, Annie; Moulin-Schouleur, Maryvonne; Curtiss, Roy; Dozois, Charles M.

In: Infection and Immunity, Vol. 76, No. 2, 02.2008, p. 601-611.

Research output: Contribution to journalArticle

Sabri, M, Caza, M, Proulx, J, Lymberopoulos, MH, Brée, A, Moulin-Schouleur, M, Curtiss, R & Dozois, CM 2008, 'Contribution of the SitABCD, MntH, and FeoB metal transporters to the virulence of avian pathogenic Escherichia coli O78 strain χ7122', Infection and Immunity, vol. 76, no. 2, pp. 601-611. https://doi.org/10.1128/IAI.00789-07
Sabri, Mourad ; Caza, Mélissa ; Proulx, Julie ; Lymberopoulos, Maria H. ; Brée, Annie ; Moulin-Schouleur, Maryvonne ; Curtiss, Roy ; Dozois, Charles M. / Contribution of the SitABCD, MntH, and FeoB metal transporters to the virulence of avian pathogenic Escherichia coli O78 strain χ7122. In: Infection and Immunity. 2008 ; Vol. 76, No. 2. pp. 601-611.
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abstract = "The roles of SitABCD, MntH, and FeoB metal transporters in the virulence of avian pathogenic Escherichia coli (APEC) O78 strain χ7122 were assessed using isogenic mutants in chicken infection models. In a single-strain infection model, compared to χ7122, the Δsit strain demonstrated reduced colonization of the lungs, liver, and spleen. Complementation of the Δsit strain restored virulence. In a coinfection model, compared to the virulent APEC strain, the Δsit strain demonstrated mean 50-fold, 126-fold, and 25-fold decreases in colonization of the lungs, liver, and spleen, respectively. A ΔmntH Δsit strain was further attenuated, demonstrating reduced persistence in blood and mean 1,400-fold, 954-fold, and 83-fold reduced colonization in the lungs, liver, and spleen, respectively. In coinfections, the ΔfeoB Δsit strain demonstrated reduced persistence in blood but increased colonization of the liver. The ΔmntH, ΔfeoB, and ΔfeoB ΔmntH strains were as virulent as the wild type in either of the infection models. Strains were also tested for sensitivity to oxidative stress-generating agents. The ΔmntH Δsit strain was the most sensitive strain and was significantly more sensitive than the other strains to hydrogen peroxide, plumbagin, and paraquat. sit sequences were highly associated with APEC and human extraintestinal pathogenic E. coli compared to commensal isolates and diarrheagenic E. coli. Comparative genomic analyses also demonstrated that sit sequences are carried on conjugative plasmids or associated with phage elements and were likely acquired by distinct genetic events among pathogenic E. coli and Shigella sp. strains. Overall, the results demonstrate that SitABCD contributes to virulence and, together with MntH, to increased resistance to oxidative stress.",
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