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Infect Immun. 2019 Jun 17. pii: IAI.00231-19. doi: 10.1128/IAI.00231-19. [Epub ahead of print]

Contribution of hla regulation by SaeR to Staphylococcus aureus USA300 Pathogenesis.

Author information

1
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205.
2
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 clee2@uams.edu.

Abstract

The SaeRS two-component system in Staphylococcus aureus is critical for regulation of many virulence genes including hla that encodes α-toxin. However, the impact of regulation of α-toxin by Sae on S. aureus pathogenesis has not been directly addressed. Here, we mutated the SaeR-binding sequences in the hla regulatory region and determined the contribution of this mutation on hla expression and pathogenesis in strain USA300 JE2. Western blot analyses revealed drastic reduction of α-toxin in the culture supernatants of SaeR-binding mutant in contrast to marked α-toxin production in the wild type. The SaeR-binding mutation had no significant effect on α-toxin regulation by Agr, MgrA and CcpA. In animal studies, we found that the SaeR-binding mutation did not contribute to USA300 JE2 pathogeneses using a rat infective endocarditis model. However, in a rat skin and soft tissue infection model, the sizes of abscesses on rats infected with the mutant were significantly smaller than those infected with the wild type but similar to those infected with a saeR mutant. These studies indicate that there is a direct effect of hla regulation by SaeR on pathogenesis but the effect depends on animal model used.

PMID:
31209148
DOI:
10.1128/IAI.00231-19

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