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The SaeR/S gene regulatory system is essential for innate immune evasion by Staphylococcus aureus.


ABSTRACT: Methicillin-resistant Staphylococcus aureus is problematic both in hospitals and in the community. Currently, we have limited understanding of mechanisms of innate immune evasion used by S. aureus. To that end, we created an isogenic deletion mutant in strain MW2 (USA400) of the saeR/S 2-component gene regulatory system and studied its role in mouse models of pathogenesis and during human neutrophil interaction. In this study, we demonstrate that saeR/S plays a distinct role in S. aureus pathogenesis and is vital for virulence of MW2 in a mouse model of sepsis. Moreover, deletion of saeR/S significantly impaired survival of MW2 in human blood and after neutrophil phagocytosis. Microarray analysis revealed that SaeR/S of MW2 influences expression of a wide variety of genes with diverse biological functions. These data provide new insight into how virulence is regulated in S. aureus and associates a specific staphylococcal gene-regulatory system with invasive staphylococcal disease.

SUBMITTER: Voyich JM 

PROVIDER: S-EPMC2799113 | biostudies-literature | 2009 Jun

REPOSITORIES: biostudies-literature

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The SaeR/S gene regulatory system is essential for innate immune evasion by Staphylococcus aureus.

Voyich Jovanka M JM   Vuong Cuong C   DeWald Mark M   Nygaard Tyler K TK   Kocianova Stanislava S   Griffith Shannon S   Jones Jennifer J   Iverson Courtney C   Sturdevant Daniel E DE   Braughton Kevin R KR   Whitney Adeline R AR   Otto Michael M   DeLeo Frank R FR  

The Journal of infectious diseases 20090601 11


Methicillin-resistant Staphylococcus aureus is problematic both in hospitals and in the community. Currently, we have limited understanding of mechanisms of innate immune evasion used by S. aureus. To that end, we created an isogenic deletion mutant in strain MW2 (USA400) of the saeR/S 2-component gene regulatory system and studied its role in mouse models of pathogenesis and during human neutrophil interaction. In this study, we demonstrate that saeR/S plays a distinct role in S. aureus pathoge  ...[more]

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