Infection of mice by Salmonella enterica serovar enteritidis involves additional genes that are absent in the genome of serovar typhimurium

Cecilia A. Silva, Carlos J. Blondel, Carolina P. Quezada, Steffen Porwollik, Helene L. Andrews-Polymenis, Cecilia S. Toro, Mercedes Zaldívar, Inés Contreras, Michael Mcclelland, Carlos A. Santiviago

Resultado de la investigación: Article

44 Citas (Scopus)

Resumen

Salmonella enterica serovar Enteritidis causes a systemic, typhoid-like infection in newly hatched poultry and mice. In the present study, a library of 54,000 transposon mutants of S. Enteritidis phage type 4 (PT4) strain P125109 was screened for mutants deficient in the in vivo colonization of the BALB/c mouse model using a microarray-based negative-selection screening. Mutants in genes known to contribute to systemic infection (e.g., Salmonella pathogenicity island 2 [SPI-2], aro, rfa, rfb, phoP, and phoQ) and enteric infection (e.g., SPI-1 and SPI-5) in this and other Salmonella serovars displayed colonization defects in our assay. In addition, a strong attenuation was observed for mutants in genes and genomic islands that are not present in S. Typhimurium or in most other Salmonella serovars. These genes include a type I restriction/modification system (SEN4290 to SEN4292), the peg fimbrial operon (SEN2144A to SEN2145B), a putative pathogenicity island (SEN1970 to SEN1999), and a type VI secretion system remnant SEN1001, encoding a hypothetical protein containing a lysin motif (LysM) domain associated with peptidoglycan binding. Proliferation defects for mutants in these individual genes and in exemplar genes for each of these clusters were confirmed in competitive infections with wild-type S. Enteritidis. A ΔSEN1001 mutant was defective for survival within RAW264.7 murine macrophages in vitro. Complementation assays directly linked the SEN1001 gene to phenotypes observed in vivo and in vitro. The genes identified here may perform novel virulence functions not characterized in previous Salmonella models.

Idioma originalEnglish
Páginas (desde-hasta)839-849
Número de páginas11
PublicaciónInfection and Immunity
Volumen80
N.º2
DOI
EstadoPublished - feb 2012

Huella dactilar

Salmonella enteritidis
Genome
Genomic Islands
Infection
Salmonella
Genes
DNA Restriction-Modification Enzymes
Peptidoglycan
Salmonella Infections
Typhoid Fever
Poultry
Operon
Multigene Family
Bacteriophages
Libraries
Virulence
Serogroup
Macrophages
Phenotype
Proteins

ASJC Scopus subject areas

  • Immunology
  • Microbiology
  • Parasitology
  • Infectious Diseases

Citar esto

Silva, Cecilia A. ; Blondel, Carlos J. ; Quezada, Carolina P. ; Porwollik, Steffen ; Andrews-Polymenis, Helene L. ; Toro, Cecilia S. ; Zaldívar, Mercedes ; Contreras, Inés ; Mcclelland, Michael ; Santiviago, Carlos A. / Infection of mice by Salmonella enterica serovar enteritidis involves additional genes that are absent in the genome of serovar typhimurium. En: Infection and Immunity. 2012 ; Vol. 80, N.º 2. pp. 839-849.
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title = "Infection of mice by Salmonella enterica serovar enteritidis involves additional genes that are absent in the genome of serovar typhimurium",
abstract = "Salmonella enterica serovar Enteritidis causes a systemic, typhoid-like infection in newly hatched poultry and mice. In the present study, a library of 54,000 transposon mutants of S. Enteritidis phage type 4 (PT4) strain P125109 was screened for mutants deficient in the in vivo colonization of the BALB/c mouse model using a microarray-based negative-selection screening. Mutants in genes known to contribute to systemic infection (e.g., Salmonella pathogenicity island 2 [SPI-2], aro, rfa, rfb, phoP, and phoQ) and enteric infection (e.g., SPI-1 and SPI-5) in this and other Salmonella serovars displayed colonization defects in our assay. In addition, a strong attenuation was observed for mutants in genes and genomic islands that are not present in S. Typhimurium or in most other Salmonella serovars. These genes include a type I restriction/modification system (SEN4290 to SEN4292), the peg fimbrial operon (SEN2144A to SEN2145B), a putative pathogenicity island (SEN1970 to SEN1999), and a type VI secretion system remnant SEN1001, encoding a hypothetical protein containing a lysin motif (LysM) domain associated with peptidoglycan binding. Proliferation defects for mutants in these individual genes and in exemplar genes for each of these clusters were confirmed in competitive infections with wild-type S. Enteritidis. A ΔSEN1001 mutant was defective for survival within RAW264.7 murine macrophages in vitro. Complementation assays directly linked the SEN1001 gene to phenotypes observed in vivo and in vitro. The genes identified here may perform novel virulence functions not characterized in previous Salmonella models.",
author = "Silva, {Cecilia A.} and Blondel, {Carlos J.} and Quezada, {Carolina P.} and Steffen Porwollik and Andrews-Polymenis, {Helene L.} and Toro, {Cecilia S.} and Mercedes Zald{\'i}var and In{\'e}s Contreras and Michael Mcclelland and Santiviago, {Carlos A.}",
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Silva, CA, Blondel, CJ, Quezada, CP, Porwollik, S, Andrews-Polymenis, HL, Toro, CS, Zaldívar, M, Contreras, I, Mcclelland, M & Santiviago, CA 2012, 'Infection of mice by Salmonella enterica serovar enteritidis involves additional genes that are absent in the genome of serovar typhimurium', Infection and Immunity, vol. 80, n.º 2, pp. 839-849. https://doi.org/10.1128/IAI.05497-11

Infection of mice by Salmonella enterica serovar enteritidis involves additional genes that are absent in the genome of serovar typhimurium. / Silva, Cecilia A.; Blondel, Carlos J.; Quezada, Carolina P.; Porwollik, Steffen; Andrews-Polymenis, Helene L.; Toro, Cecilia S.; Zaldívar, Mercedes; Contreras, Inés; Mcclelland, Michael; Santiviago, Carlos A.

En: Infection and Immunity, Vol. 80, N.º 2, 02.2012, p. 839-849.

Resultado de la investigación: Article

TY - JOUR

T1 - Infection of mice by Salmonella enterica serovar enteritidis involves additional genes that are absent in the genome of serovar typhimurium

AU - Silva, Cecilia A.

AU - Blondel, Carlos J.

AU - Quezada, Carolina P.

AU - Porwollik, Steffen

AU - Andrews-Polymenis, Helene L.

AU - Toro, Cecilia S.

AU - Zaldívar, Mercedes

AU - Contreras, Inés

AU - Mcclelland, Michael

AU - Santiviago, Carlos A.

PY - 2012/2

Y1 - 2012/2

N2 - Salmonella enterica serovar Enteritidis causes a systemic, typhoid-like infection in newly hatched poultry and mice. In the present study, a library of 54,000 transposon mutants of S. Enteritidis phage type 4 (PT4) strain P125109 was screened for mutants deficient in the in vivo colonization of the BALB/c mouse model using a microarray-based negative-selection screening. Mutants in genes known to contribute to systemic infection (e.g., Salmonella pathogenicity island 2 [SPI-2], aro, rfa, rfb, phoP, and phoQ) and enteric infection (e.g., SPI-1 and SPI-5) in this and other Salmonella serovars displayed colonization defects in our assay. In addition, a strong attenuation was observed for mutants in genes and genomic islands that are not present in S. Typhimurium or in most other Salmonella serovars. These genes include a type I restriction/modification system (SEN4290 to SEN4292), the peg fimbrial operon (SEN2144A to SEN2145B), a putative pathogenicity island (SEN1970 to SEN1999), and a type VI secretion system remnant SEN1001, encoding a hypothetical protein containing a lysin motif (LysM) domain associated with peptidoglycan binding. Proliferation defects for mutants in these individual genes and in exemplar genes for each of these clusters were confirmed in competitive infections with wild-type S. Enteritidis. A ΔSEN1001 mutant was defective for survival within RAW264.7 murine macrophages in vitro. Complementation assays directly linked the SEN1001 gene to phenotypes observed in vivo and in vitro. The genes identified here may perform novel virulence functions not characterized in previous Salmonella models.

AB - Salmonella enterica serovar Enteritidis causes a systemic, typhoid-like infection in newly hatched poultry and mice. In the present study, a library of 54,000 transposon mutants of S. Enteritidis phage type 4 (PT4) strain P125109 was screened for mutants deficient in the in vivo colonization of the BALB/c mouse model using a microarray-based negative-selection screening. Mutants in genes known to contribute to systemic infection (e.g., Salmonella pathogenicity island 2 [SPI-2], aro, rfa, rfb, phoP, and phoQ) and enteric infection (e.g., SPI-1 and SPI-5) in this and other Salmonella serovars displayed colonization defects in our assay. In addition, a strong attenuation was observed for mutants in genes and genomic islands that are not present in S. Typhimurium or in most other Salmonella serovars. These genes include a type I restriction/modification system (SEN4290 to SEN4292), the peg fimbrial operon (SEN2144A to SEN2145B), a putative pathogenicity island (SEN1970 to SEN1999), and a type VI secretion system remnant SEN1001, encoding a hypothetical protein containing a lysin motif (LysM) domain associated with peptidoglycan binding. Proliferation defects for mutants in these individual genes and in exemplar genes for each of these clusters were confirmed in competitive infections with wild-type S. Enteritidis. A ΔSEN1001 mutant was defective for survival within RAW264.7 murine macrophages in vitro. Complementation assays directly linked the SEN1001 gene to phenotypes observed in vivo and in vitro. The genes identified here may perform novel virulence functions not characterized in previous Salmonella models.

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