Only one of the two type VI secretion systems encoded in the Salmonella enterica serotype Dublin genome is involved in colonization of the avian and murine hosts
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2014Metadata
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Pezoa, David
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Only one of the two type VI secretion systems encoded in the Salmonella enterica serotype Dublin genome is involved in colonization of the avian and murine hosts
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Abstract
The type VI secretion system (T6SS) is a virulence factor for many Gram-negative bacteria. Salmonella genus harbors
five phylogenetically distinct T6SS loci encoded in Salmonella Pathogenicity Islands (SPIs) SPI-6, SPI-19, SPI-20, SPI-21
and SPI-22, which are differentially distributed among serotypes. The T6SSs encoded in SPI-6 and SPI-19 contribute
to pathogenesis of serotypes Typhimurium and Gallinarum in mice and chickens, respectively. Salmonella Dublin is
a pathogen restricted to cattle where it causes a systemic disease. Also, it can colonize other hosts such as chickens
and mice, which can act as reservoirs of this serotype. Salmonella Dublin harbors the genes for both T6SSSPI-6 and
T6SSSPI-19. This study has determined the contribution of T6SSSPI-6 and T6SSSPI-19 to host-colonization by Salmonella
Dublin using avian and murine models of infection. Competitive index experiments showed that, a mutant strain
lacking both T6SSs (ΔT6SSSPI-6/ΔT6SSSPI-19) presents a strong colonization defect in cecum of chickens, similar to the
defect observed for the ΔT6SSSPI-6 mutant, suggesting that this serotype requires a functional T6SSSPI-6 for efficient
colonization of the avian gastrointestinal tract. Colonization of mice was also defective, although to a lesser extent
than in chickens. In contrast, the T6SSSPI-19 was not necessary for colonization of either chickens or mice. Transfer of
T6SSSPI-6, but not T6SSSPI-19, restored the ability of the double mutant to colonize both animal hosts. Our data
indicate that Salmonella Dublin requires only the T6SSSPI-6 for efficient colonization of mice and chickens, and that
the T6SSSPI-6 and T6SSSPI-19 are not functionally redundant.
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This work was supported by grant 1100092 from Fondo Nacional de
Desarrollo Científico y Tecnológico (FONDECYT), Chile. CJB was supported by
Postdoctoral Fellowship 3120175 from FONDECYT. David Pezoa was
supported by fellowships from FULBRIGHT, CONICYT (N°21090041,
AT-24121297, 75110062 BCH-3), CAS was supported by grant 1110172 from
FONDECYT. HAP was supported by grants NIH/NIAID R01AI083646,
R56AI077645, R21AI083964 and USDA 2009–03579.
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Veterinary Research 2014, 45:2
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