Rochford, E. T. J. (Edward Thomas James)

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2016 - 20182

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    Infection burden and immunological responses are equivalent for polymeric and metallic implant materials in vitro and in a murine model of fracture-related infection
    (Wiley, 2018) Zeiter, S. (Stephan); Richards, R. G. (R. Geoff); Rochford, E. T. J. (Edward Thomas James); Sabaté-Brescó, M. (Marina); Moriarty, T. F. (T. Fintan); O'Mahony, L. (Liam); Ziegler, M. (Mario); Kluge, K. (Katharina); Poulsson, A. (Alexandra)
    The development of an infection is a major complication for some patients with implanted biomaterials. Whether the material or surface composition of the used biomaterial influences infection has not been directly compared for key biomaterials currently in use in human patients. We conducted a thorough in vitro and in vivo investigation using titanium (Ti) and polyether-ether-ketone (PEEK) as both commercially available and as modified equivalents (surface polished Ti, and oxygen plasma treated PEEK). Complement activation and cytokine secretion of cell of the immune system was assessed in vitro for all materials in the absence and presence of bacterial stimulants. In a follow-up in vivo study, we monitored bacterial infection associated with clinically available and standard Ti and PEEK inoculated with Staphylococcus aureus. Complement activation was affected by material choice in the absence of bacterial stimulation, although the material based differences were largely lost upon bacterial stimulation. In the in vivo study, the bacterial burden, histological response and cytokine secretion suggests that there is no significant difference between both PEEK and Ti. In conclusion, the underlying material has a certain impact in the absence of bacterial stimulation, however, in the presence of bacterial stimulation, bacteria seem to dictate the responses in a manner that overshadows the influence of material surface properties.
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    Monitoring immune responses in a mouse model of fracture fixation with and without Staphylococcus aureus osteomyelitis
    (2016) Zeiter, S. (Stephan); Richards, R. G. (R. Geoff); Rochford, E. T. J. (Edward Thomas James); Sabaté-Brescó, M. (Marina); Moriarty, T. F. (T. Fintan); O'Mahony, L. (Liam); Ziegler, M. (Mario); Kluge, K. (Katharina); Poulsson, A. (Alexandra)
    Post-traumatic bone fractures are commonly fixed with implanted devices to restore the anatomical position of bone fragments and aid in the healing process. Bacterial infection in this situation is a challenge for clinicians due to the need for aggressive antibiotic therapy, debridement of infected tissues, and the need to maintain fracture stability. The aim of this study was to monitor immune responses that occur during healing and during Staphylococcus aureus infection, in a clinically relevant murine model of fracture fixation. Skeletally mature C57bl/6 mice received a transverse osteotomy of the femur, which was treated with commercially available titanium fracture fixation plates and screws. In the absence of infection, healing of the fracture was complete within 35 days and was characterized by elevated Interleukin (IL)-4 and Interferon-gamma secretion from bone-derived cells and expression of these same genes. In contrast, mice inoculated with S. aureus could not heal the fracture within the observation period and were found to develop typical signs of implant-associated bone infection, including biofilm formation on the implant and osteolysis of surrounding bone. The immune response to infection was characterized by a TH17-led bone response, and a pro-inflammatory cytokine-led Tumor necrosis factor (TNF)-α, Interleukin (IL)-1β) soft tissue response, both of which were ineffectual in clearing implant related bone and soft tissue infections respectively. In this murine model, we characterize the kinetics of pro-inflammatory responses to infection, secondary to bone trauma and surgery. A divergent local immune polarization is evident in the infected versus non-infected animals, with the immune response ultimately unable to clear the S. aureus infection.