The effects of Interkingdom signalling on biofilm dispersal in Staphylococcus epidermidis
Cardiff Metropolitan University
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Staphylococcus epidermidis is a common commensal bacteria and has now become the most common source of nosocomial infection due to its ability to form biofilms on indwelling medical devices. Though not a particularly pathogenic bacterial species its population wide coverage and proximity to insertion of medical devices means infections are commonplace leading to massive cost to public health systems around the world. While the nature of S.epidermidis biofilm formation and initial infection is established dissemination to other sterile sites and the factors involved remain poorly understood. Improved understanding of the increased virulence seen through biofilm dispersal is needed to attempt to alleviate the burden and financial cost of treatment on public health systems. Through the cultivation of static biofilms in wells of 96 microtitre plate this study enabled the replication of environmental changes closely associated with viral infection of the human host and investigation into the effects of interkingdom signalling on virulence through the analysis of biofilm dispersal. Two measurements were performed which included first the analysis of supernatant density post incubation in variable conditions and secondly remaining biomass post washing and staining. This study found that in vitro biofilm dispersal in S.epidermidis is triggered in response to environmental changes closely associated with viral infection. Cell lysate addition in combination with temperature increase from 37°C to 40°C was shown to significantly increase supernatant density and significantly reduce remaining biomass. These results indicate that dispersal of biofilm population and in turn virulence is directly affected by host induced environmental changes. Findings from this study were closely supported by findings from a number of comprehensive studies into interkingdom signalling on a range of other bacteria. These studies went further by analysing the effects of environmental changes on live epithelial cells in vitro and on mice in vivo. One study also analysed virulence gene expression of dispersed cell against sessile and planktonic cells. The nature of these further investigations mean these studies findings carry more significance, but offer direction for further study into the effects of interkingdom signalling on S.epidermidis virulence.
BSc (Hons) Biomedical Science
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