Staphylococcus epidermidis recovered from indwelling catheters exhibit enhanced biofilm dispersal and “self-renewal” through downregulation of agr
1 Key Laboratory of Arrhythmias, Ministry of Education, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China
2 Departments of Medicine, Louisiana State University Health Sciences Center, Stanley S. Scott Cancer Center, 533 Bolivar St., New Orleans, LA, 70112, USA
3 Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, Stanley S. Scott Cancer Center, 533 Bolivar St., New Orleans, LA, 70112, USA
4 Infection Microbiology Group, Centre for Systems Biology, Technical University of Denmark, DK-2800, Lyngby, Denmark
5 Departments of Pathology and Laboratory Medicine, Medical University of South Carolina, 86 Jonathan Lucas St., Charleston, SC, 29425, USA
BMC Microbiology 2012, 12:102 doi:10.1186/1471-2180-12-102Published: 8 June 2012
In recent years, Staphylococcus epidermidis ( Se) has become a major nosocomial pathogen and the most common cause of infections of implanted prostheses and other indwelling devices. This is due in part to avid biofilm formation by Se on device surfaces. However, it still remains unknown that how the process of Se biofilm development is associated with relapsed infection in such patients.
We have identified clinical Se isolates displaying enhanced biofilm dispersal and self-renewal relative to reference strain. These isolates also exhibit enhanced initial cell attachment, extracellular DNA release, cell autolysis and thicker microcolonies during biofilm development relative to reference strain. Our genetic analyses suggest that these clinical isolates exhibit significant downregulation of RNAIII, the effector molecule of the agr quorum sensing system, and upregulation of the autolysin gene atlE. Isogenic deletion of the agr system in Se 1457 confirmed that agr negatively regulating atlE resulted in enhanced initial cell attachment, extracellular DNA release, cell autolysis and biofilm formation abilities. In contrast, double deletion of agr and atlE significantly abolished these features.
Collectively, these data reveal the role of agr system in long-term biofilm development and pathogenesis during Se caused indwelling devices-related relapsed infection.