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Updated: May 27, 2026
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Improved Enzyme Protection Assay to Study Staphylococcus aureus Internalization and Intracellular Efficacy of Antimicrobial Compounds
Published on: September 8, 2021
Internalization by osteoblasts of two Staphylococcus aureus clinical isolates differing in their adhesin gene pattern
Francesca Testoni1, Lucio Montanaro, Alessandro Poggi
1Research Unit on Implant Infections, Rizzoli Orthopaedic Institute, Bologna, Italy.
The International Journal of Artificial Organs
|November 19, 2011
Summary
Staphylococcus aureus invades host cells during orthopedic implant infections. Fibronectin-binding protein A (FnBPA) is crucial for this internalization, with other adhesins aiding initial bacterial adhesion.
Area of Science:
- Microbiology
- Infectious Diseases
- Biomedical Engineering
Background:
- Staphylococcus aureus is a primary cause of orthopedic implant infections.
- S. aureus, once thought extracellular, can invade host cells.
- Bacterial adhesion to implants initiates infection and host cell invasion.
Purpose of the Study:
- To investigate the role of specific adhesins in Staphylococcus aureus internalization into host cells.
- To elucidate the mechanisms of S. aureus adhesion and invasion in orthopedic infections.
Main Methods:
- Comparative analysis of two epidemic S. aureus clinical strains with distinct adhesin profiles.
- Experimental observation of bacterial-host cell interactions.
Main Results:
- Fibronectin-binding protein A (FnBPA) plays a critical role in S. aureus internalization.
- CNA and Bbp adhesins contribute synergistically to initial bacterial adhesion to osteoblasts.
- Adhesion mediated by CNA and Bbp facilitates subsequent FnBPA-dependent internalization.
Conclusions:
- FnBPA is essential for Staphylococcus aureus internalization into host cells.
- CNA and Bbp adhesins promote S. aureus adhesion, enhancing subsequent invasion.
- Understanding these adhesin roles can inform strategies against implant-associated S. aureus infections.
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