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dc.contributor.authorCollins, Madison M.
dc.contributor.authorBehera, Ranjan K.
dc.contributor.authorPallister, Kyler B.
dc.contributor.authorEvans, Tyler J.
dc.contributor.authorBurroughs, Owen
dc.contributor.authorFlack, Caralyn
dc.contributor.authorGuerra, Fermin E.
dc.contributor.authorPullman, Willis
dc.contributor.authorCone, Brock
dc.contributor.authorDankoff, Jennifer G.
dc.contributor.authorNygaard, Tyler K.
dc.contributor.authorBrinsmade, Shaun R.
dc.contributor.authorVoyich, Jovanka M.
dc.date.accessioned2021-09-17T18:40:02Z
dc.date.available2021-09-17T18:40:02Z
dc.date.issued2020-04
dc.identifier.citationCollins, Madison M., Ranjan K. Behera, Kyler B. Pallister, Tyler J. Evans, Owen Burroughs, Caralyn Flack, Fermin E. Guerra, et al. “The Accessory Gene saeP of the SaeR/S Two-Component Gene Regulatory System Impacts Staphylococcus Aureus Virulence During Neutrophil Interaction.” Frontiers in Microbiology 11 (April 22, 2020). doi:10.3389/fmicb.2020.00561.en_US
dc.identifier.issn1664-302X
dc.identifier.urihttps://scholarworks.montana.edu/xmlui/handle/1/16451
dc.description.abstractStaphylococcus aureus (S. aureus) causes a range of diseases ranging from superficial skin and soft-tissue infections to invasive and life-threatening conditions (Klevens et al., 2007; Kobayashi et al., 2015). S. aureus utilizes the Sae sensory system to adapt to neutrophil challenge. Although the roles of the SaeR response regulator and its cognate sensor kinase SaeS have been demonstrated to be critical for surviving neutrophil interaction and for causing infection, the roles for the accessory proteins SaeP and SaeQ remain incompletely defined. To characterize the functional role of these proteins during innate immune interaction, we generated isogenic deletion mutants lacking these accessory genes in USA300 (USA300ΔsaeP and USA300ΔsaeQ). S. aureus survival was increased following phagocytosis of USA300ΔsaeP compared to USA300 by neutrophils. Additionally, secreted extracellular proteins produced by USA300ΔsaeP cells caused significantly more plasma membrane damage to human neutrophils than extracellular proteins produced by USA300 cells. Deletion of saeQ resulted in a similar phenotype, but effects did not reach significance during neutrophil interaction. The enhanced cytotoxicity of USA300ΔsaeP cells toward human neutrophils correlated with an increased expression of bi-component leukocidins known to target these immune cells. A saeP and saeQ double mutant (USA300ΔsaePQ) showed a significant increase in survival following neutrophil phagocytosis that was comparable to the USA300ΔsaeP single mutant and increased the virulence of USA300 during murine bacteremia. These data provide evidence that SaeP modulates the Sae-mediated response of S. aureus against human neutrophils and suggest that saeP and saeQ together impact pathogenesis in vivo.en_US
dc.language.isoen_USen_US
dc.titleThe Accessory Gene saeP of the SaeR/S Two-Component Gene Regulatory System Impacts Staphylococcus aureus Virulence During Neutrophil Interactionen_US
dc.typeArticleen_US
mus.citation.journaltitleFrontiers in Microbiologyen_US
mus.citation.volume11en_US
mus.identifier.doi10.3389/fmicb.2020.00561en_US
mus.relation.collegeCollege of Agricultureen_US
mus.relation.collegeCollege of Letters & Scienceen_US
mus.relation.departmentMicrobiology & Immunology.en_US
mus.relation.universityMontana State University - Bozemanen_US
mus.data.thumbpage3en_US


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