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The Staphylococcus aureus ArlRS two-component system is a novel regulator of agglutination and pathogenesis
Journal article   Open access   Peer reviewed

The Staphylococcus aureus ArlRS two-component system is a novel regulator of agglutination and pathogenesis

Jennifer N Walker, Heidi A Crosby, Adam R Spaulding, Wilmara Salgado-Pabón, Cheryl L Malone, Carolyn B Rosenthal, Patrick M Schlievert, Jeffrey M Boyd and Alexander R Horswill
PLoS pathogens, Vol.9(12), pp.e1003819-17
2013
DOI: 10.1371/journal.ppat.1003819
PMCID: PMC3868527
PMID: 24367264
url
https://doi.org/10.1371/journal.ppat.1003819View
Published (Version of record) Open Access

Abstract

Staphylococcus aureus is a prominent bacterial pathogen that is known to agglutinate in the presence of human plasma to form stable clumps. There is increasing evidence that agglutination aids S. aureus pathogenesis, but the mechanisms of this process remain to be fully elucidated. To better define this process, we developed both tube based and flow cytometry methods to monitor clumping in the presence of extracellular matrix proteins. We discovered that the ArlRS two-component system regulates the agglutination mechanism during exposure to human plasma or fibrinogen. Using divergent S. aureus strains, we demonstrated that arlRS mutants are unable to agglutinate, and this phenotype can be complemented. We found that the ebh gene, encoding the Giant Staphylococcal Surface Protein (GSSP), was up-regulated in an arlRS mutant. By introducing an ebh complete deletion into an arlRS mutant, agglutination was restored. To assess whether GSSP is the primary effector, a constitutive promoter was inserted upstream of the ebh gene on the chromosome in a wildtype strain, which prevented clump formation and demonstrated that GSSP has a negative impact on the agglutination mechanism. Due to the parallels of agglutination with infective endocarditis development, we assessed the phenotype of an arlRS mutant in a rabbit combined model of sepsis and endocarditis. In this model the arlRS mutant displayed a large defect in vegetation formation and pathogenesis, and this phenotype was partially restored by removing GSSP. Altogether, we have discovered that the ArlRS system controls a novel mechanism through which S. aureus regulates agglutination and pathogenesis.
Staphylococcus aureus - genetics Rabbits Fibrinogen - physiology Staphylococcal Infections - genetics Staphylococcus aureus - physiology Humans Bacterial Proteins - genetics Male Bacterial Proteins - physiology Staphylococcus aureus - pathogenicity Carrier Proteins - genetics Animals Agglutination - genetics Endocarditis, Bacterial - genetics Endocarditis, Bacterial - microbiology Female Staphylococcal Infections - microbiology Organisms, Genetically Modified Gene Expression Regulation, Bacterial

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