BACKGROUND: Staphylococcus aureus is an important human pathogen of endovascular diseases that can take an acute destructive course and/or develop into a chronic infection with a high rate of relapse. Despite good activity of the appropriate antimicrobial substances in vitro, these infections are often difficult to treat, perhaps because of the complex infection process of endovascular tissue. METHODS: We used the microarray technique to analyze the response of endothelial cells to different S. aureus strains, including highly virulent isolates (6850 and ST239); the Cowan I strain, which has a nonfunctioning accessory gene regulator (agr) quorum-sensing system; and various clinical isolates. RESULTS: All tested strains were equally invasive in endothelial cells and were found intracellularly, but they differed greatly in their ability to induce inflammation. Wild-type isolates (6850 and ST239) up-regulated a huge number of genes, including many genes involved in innate immunity. By contrast, Cowan I, which failed to express important virulence factors related to the agr system (eg, alpha-toxin and proteases), did not induce these dramatic changes in endothelial gene expression. Similar results were obtained with clinical isolates. CONCLUSION: Given that agr-defective strains are commonly recovered during colonization and infection, agr deficiency might represent a strategy of S. aureus to hide intracellularly without provoking the host immune system and causing relapsing infections.
BACKGROUND:Staphylococcus aureus is an important human pathogen of endovascular diseases that can take an acute destructive course and/or develop into a chronic infection with a high rate of relapse. Despite good activity of the appropriate antimicrobial substances in vitro, these infections are often difficult to treat, perhaps because of the complex infection process of endovascular tissue. METHODS: We used the microarray technique to analyze the response of endothelial cells to different S. aureus strains, including highly virulent isolates (6850 and ST239); the Cowan I strain, which has a nonfunctioning accessory gene regulator (agr) quorum-sensing system; and various clinical isolates. RESULTS: All tested strains were equally invasive in endothelial cells and were found intracellularly, but they differed greatly in their ability to induce inflammation. Wild-type isolates (6850 and ST239) up-regulated a huge number of genes, including many genes involved in innate immunity. By contrast, Cowan I, which failed to express important virulence factors related to the agr system (eg, alpha-toxin and proteases), did not induce these dramatic changes in endothelial gene expression. Similar results were obtained with clinical isolates. CONCLUSION: Given that agr-defective strains are commonly recovered during colonization and infection, agr deficiency might represent a strategy of S. aureus to hide intracellularly without provoking the host immune system and causing relapsing infections.
Authors: Emma Jane Smith; Livia Visai; Steven W Kerrigan; Pietro Speziale; Timothy J Foster Journal: Infect Immun Date: 2011-06-27 Impact factor: 3.441
Authors: Kati Seidl; Arnold S Bayer; James A McKinnell; Steven Ellison; Scott G Filler; Yan Q Xiong Journal: Cell Microbiol Date: 2011-07-21 Impact factor: 3.715
Authors: Gregory S Canfield; Johanna M Schwingel; Matthew H Foley; Kelly L Vore; Kanitsak Boonanantanasarn; Ann L Gill; Mark D Sutton; Steven R Gill Journal: J Bacteriol Date: 2012-11-30 Impact factor: 3.490
Authors: Kati Seidl; Norma V Solis; Arnold S Bayer; Wessam Abdel Hady; Steven Ellison; Meredith C Klashman; Yan Q Xiong; Scott G Filler Journal: PLoS One Date: 2012-06-22 Impact factor: 3.240