Immune evasion in Staphylococcus aureus infection
Staphylococcus aureus (S. aureus) is a commensal bacterium, which has the potential to cause a broad range of conditions from minor skin infections to invasive and potentially fatal systemic infections [1, 2]. Infection with resistant Staphylococcus aureus is a growing challenge worldwide and the need for novel therapeutics is evident.
Upon infection of the host, S. aureus initiate classical innate immune responses, which have been well established [3, 4]. A scientific gap, on the other hand, exists in the knowledge of T- and NK cell-mediated responses to S. aureus.
A critical role for NK cells in host defense against pulmonary S. aureus infection has been suggested , and T-cell memory has been detected in mice challenged repeatedly with S. aureus . However, little remains known regarding the underlying molecular mechanisms.
Treatment of S. aureus is now relying on “last-line” of therapeutics due to development of therapy-resistance, methicillin- and daptomycin-resistant S. aureus strains are becoming more frequent [3, 7]. The emergence of these new resistant S. aureus strains and their interaction with the human immune system is poorly understood. However, the consequences they have for human health underlines the need for development of novel therapeutics for treatment.
The aim of this project is to investigate the activity of human T- and NK cells upon co-cultivation with different methicillin- and daptomycin-resistant/sensitive S. aureus strains.
We expect that this project will contribute to the fundamental understanding of the human T- and NK cell-mediated immune response to S. aureus. Since pathogenicity of bacteria is highly dependent on immune evasion we anticipate that this expanding knowledge will set the stage for development of future novel therapeutics for treatment of S. aureus infection.
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