Interaction of Staphylococcus epidermidis with abiotic and biotic surfaces : a role in bone and wound infections
Staphylococcus epidermidis has become one of the most important causes of nosocomial and foreign device-related infections. It causes osteomyelitis around orthopaedic implants and secrets surface associated proteins which have osteolytic activity. Adherence of S. epidermidis to biomaterials is a key factor in the development of a device-related infection. Colonisation of surgical sutures with bacteria has been suggested to increase the risk of wound infection and consequent complications. Recent studies have shown that S. epidermidis can persist inside macrophages. The data presented in this thesis show that S. epidermidis is internalised by bone cells and epithelial cells and that the capacity of different strains to be internalised varied considerably. Use of a panel of inhibitors that block mammalian cell endocytic pathways showed that the process of internalisation of S. epidermidis by host cells was via a receptor mediated pathway. However there were differences in the pathways utilised by epithelial cells and bone cells to internalise S. epidermidis. The SdrG protein of S. epidermidis played a significant role in the internalisation of strain HB by bone cells and, to a lesser extent, by epithelial cells. Investigation of the effect of S. epidermidis internalisation by bone cells on cytokine secretion showed that the uptake process did not induce higher levels of the secretion of four different cytokines (IL-6, IL-8, IL-ip and TNF-a). Additionally uptake of S. epidermidis did not induce apoptosis of bone cells, in contrast to what has been reported for S. aureus. The capacity of S. epidermidis to adhere to surgical sutures constructed from different materials was strain dependent. Coating the sutures with human plasma increased the numbers of bacteria adhering to the sutures. A number of putative S. epidermidis virulence factors, including the GehD lipase, SdrG, the fibronectin binding protein Embp and the autolysin AtlE were found to be involved in the adhesion of this bacterium to sutures. The findings presented in this thesis contribute to our understanding of the interactions of S. epidermidis with abiotic surfaces and host cells.