Intracellular invasion of Staphylococcus aureus against human gingival fibroblasts

Staphylococcus aureus (S. aureus) is one of the most common bacterial pathogens, causing approximately 80% of all cases of osteomyelitis with a broad host range in coagulase-positive staphylococci and is one of the leading causes of infections in oral and maxillofacial regions1, 2. Moreover, the rapidly increasing frequency of antibiotic-resistant bacteria has caused considerable alarm within the dental and medical community3, 4. Infections associated with this organism are extremely common and often life threatening; therefore, there is serious potential for S. aureus to cause increased morbidity and mortality in oral and maxillofacial regions3-6. To cause the infection, the bacteria do the followings: adhere and enter the host, multiply on or in the host tissues, resist host defences, and damage the host. All four processes must be accomplished in order to produce an infectious disease, and each is complex, involving several determinants. Bacterial attachment and penetration into underlying tissues play an important role in the initiation of infection. Some bacteria may penetrate tissue surfaces by producing lytic substances that break down the tissue surface, easing penetration to the deeper tissues, and other bacteria can penetrate through epithelial cells. It is likely that a variety of mechanisms are used by different organisms to penetrate the various tissue surfaces that they use as their portal of entry7. However lately, many authors have demonstrated the capability of the bacteria to attach on and invade the internal space of non-phagocytic eukaryotes8-13. On the other hand, it has been suggested that the continuous process of actin filament elongation provides the driving force for bacterial propulsion in infected cells or cytoplasmic extracts14-16. Several unrelated intracellular bacterial pathogens, including Listeria monocytogenes (L. monocytogenes), Shigella flexneri, Rickettsiae and Vaccinia virus, are known to share the ability to use actin polymerization as a driving force for intracellular movement, cell-to-cell spread and dissemination within infected tissues. While S. aureus has not traditionally been considered to be an intracellular pathogen, previous studies have revealed that S. aureus may be actively internalized by phagocytosis and are capable of intracellular survival in epithelial and endothelial cells17, 18. It has also been suggested that S. aureus interact with or binds to the cell surface of bovine