Identification of Burkholderia cenocepacia strain H111 virulence factors using nonmammalian infection hosts
Research output: Contribution to journal › Journal article › Research › peer-review
Standard
Identification of Burkholderia cenocepacia strain H111 virulence factors using nonmammalian infection hosts. / Schwager, Stephan; Agnoli, Kirsty; Köthe, Manuela; Feldmann, Friederike; Givskov, Michael; Carlier, Aurelien; Eberl, Leo.
In: Infection and Immunity, Vol. 81, No. 1, 2013, p. 143-53.Research output: Contribution to journal › Journal article › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Identification of Burkholderia cenocepacia strain H111 virulence factors using nonmammalian infection hosts
AU - Schwager, Stephan
AU - Agnoli, Kirsty
AU - Köthe, Manuela
AU - Feldmann, Friederike
AU - Givskov, Michael
AU - Carlier, Aurelien
AU - Eberl, Leo
PY - 2013
Y1 - 2013
N2 - Burkholderia cenocepacia H111, a strain isolated from a cystic fibrosis patient, has been shown to effectively kill the nematode Caenorhabditis elegans. We used the C. elegans model of infection to screen a mini-Tn5 mutant library of B. cenocepacia H111 for attenuated virulence. Of the approximately 5,500 B. cenocepacia H111 random mini-Tn5 insertion mutants that were screened, 22 showed attenuated virulence in C. elegans. Except for the quorum-sensing regulator cepR, none of the mutated genes coded for the biosynthesis of classical virulence factors such as extracellular proteases or siderophores. Instead, the mutants contained insertions in metabolic and regulatory genes. Mutants attenuated in virulence in the C. elegans infection model were also tested in the Drosophila melanogaster pricking model, and those also attenuated in this model were further tested in Galleria mellonella. Six of the 22 mutants were attenuated in D. melanogaster, and five of these were less pathogenic in the G. mellonella model. We show that genes encoding enzymes of the purine, pyrimidine, and shikimate biosynthesis pathways are critical for virulence in multiple host models of infection.
AB - Burkholderia cenocepacia H111, a strain isolated from a cystic fibrosis patient, has been shown to effectively kill the nematode Caenorhabditis elegans. We used the C. elegans model of infection to screen a mini-Tn5 mutant library of B. cenocepacia H111 for attenuated virulence. Of the approximately 5,500 B. cenocepacia H111 random mini-Tn5 insertion mutants that were screened, 22 showed attenuated virulence in C. elegans. Except for the quorum-sensing regulator cepR, none of the mutated genes coded for the biosynthesis of classical virulence factors such as extracellular proteases or siderophores. Instead, the mutants contained insertions in metabolic and regulatory genes. Mutants attenuated in virulence in the C. elegans infection model were also tested in the Drosophila melanogaster pricking model, and those also attenuated in this model were further tested in Galleria mellonella. Six of the 22 mutants were attenuated in D. melanogaster, and five of these were less pathogenic in the G. mellonella model. We show that genes encoding enzymes of the purine, pyrimidine, and shikimate biosynthesis pathways are critical for virulence in multiple host models of infection.
U2 - 10.1128/IAI.00768-12
DO - 10.1128/IAI.00768-12
M3 - Journal article
C2 - 23090963
VL - 81
SP - 143
EP - 153
JO - Infection and Immunity
JF - Infection and Immunity
SN - 0019-9567
IS - 1
ER -
ID: 44311148