Role of the accessory gene regulator (agr) in pathogenesis of staphylococcal osteomyelitis
By A. Gillaspy, S. G. Hickmon, R. Skinner, J. R. Thomas, C. Nelson, M. Smeltzer. 1995
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- M. Otto
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- Gordon Y C Cheung
- S. Gill
- Justin S. Bae
- D. Bartels
Citations in the corpus
- Quorum Sensing in Staphylococcus aureus Biofilms (2004, methodology): “The agr system contributes to virulence in model biofilm-associated infections, including endocarditis (7, 50) and osteomyelitis (3, 15), although the precise role of the agr system varies with the type of infection model used (16, 17, 54).”
- Staphylococcus aureus Leukocidin A/B (LukAB) Kills Human Monocytes via Host NLRP3 and ASC when Extracellular, but Not Intracellular (2015, unknown): “59 USA 200 WT USA 200 [63]”
- Pathogenicity and virulence of Staphylococcus aureus (2021, background): “tissue infections [225,234], pneumonia [235,236], septic arthritis [237], osteomyelitis [238], and atopic dermati-”
- Quorum sensing in staphylococci. (2008, background): “endocarditis (24), septic arthritis (1), and osteomyelitis (43).”
- SarT, a Repressor of α-Hemolysin inStaphylococcus aureus (2001, background): “While mutations in sarA and agr have been shown to reduce virulence in several animal model studies, these mutations did not render the bacteria avirulent (1, 8, 22, 24), suggesting that other regulatory factors may be at work.”