Mammalian host-signals influence bacterial dispersal in Methicillin Resistant Staphylococcus aureus biofilms
Cardiff Metropolitan University
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Methicillin Resistant Staphylococcus aureus (MRSA) is a human commensal that has been well known for decades of causing re-current and almost untreatable infections due to their capability of forming biofilms in order to evade the effects of antimicrobials, generating a tolerance against them. A major cause of death in patients infected with Influenza A virus is due to the development of secondary bacteria pneumonia caused by S. aureus. It has been unclear how certain human commensal organisms transform from being harmless and asymptomatic to becoming invasive and capable of causing harmful disease until interkingdom signalling was discovered. However, despite awareness of existence of this type of signalling, the apparatus of how it functions in pathogens such as MRSA is currently relatively limited. The aim of this project was to investigate the host-signals that trigger biofilm dispersal in MRSA via interkingdom signalling. S. aureus strain EMRSA-15 was cultured and 24 h biofilms were grown in TSB, TSB + 2% NaCl and TSB + 1% glucose solution. Determination of optimum conditions for growth of MRSA biofilms was measured using 0.25% crystal violet staining. Following determination, 24 h static biofilms were all formed and varying dilutions of CACO-2 cell lysate (1 in 10, 1 in 100 and 1 in 1000) were added to the biofilms and incubated at 37°C and 39°C, with planktonic bacteria then quantified at 620nm and biomass measured following addition of host-signals. In this report, it’s demonstrated that growing MRSA in TSB + 1% glucose produces the greatest biomass over TSB and TSB + 2% NaCl. Additionally, this report shows the MRSA biofilms dispersed in response to the treatment of cell lysate and a febrile-range temperature – representing a host response to a viral infection - in some cases, with each dilution of cell lysate and different incubation temperatures causing varied effects on biofilm dispersal. These results reveal a certain level of insight into MRSA’s behaviour towards the presence of host-signals, and offer a baseline knowledge for future interkingdom signalling investigations to be carried out involving MRSA. There was a high level of variability in the data, with the addition of different dilutions of cell lysate and a febrile-range temperature showing mixed trends.
BSc Biomedical Sciences
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