Abstract
Bone implants infected with
Staphylococcus epidermidis often require surgical intervention because of the failure of antibiotic treatment. The reasons why such infections are resistant to therapy are poorly understood. We have previously reported that another bacterium,
Staphylococcus aureus, can invade bone cells and thereby evade antimicrobial therapy. In this study we have investigated the hypothesis that
S. epidermidis can also invade bone cells and may therefore explain the difficulties of treating infections with this organism. We found that
S. epidermidis was capable of invading bone cells but that there were significant strain dependent differences in this capacity. A recombinant protein encompassing the D1–D4 repeat region of
S. aureus fibronectin-binding protein B completely inhibited internalization of
S. aureus but failed to block internalization of
S. epidermidis. Similarly a blocking antibody to α5β1 integrin inhibited internalization of
S. aureus by bone cells but had no effect on the uptake of
S. epidermidis. Therefore unlike
S. aureus,
S. epidermidis does not gain entrance into bone cells through a fibronectin bridge between the α5β1 integrin and a bacterial adhesin.