Staphylococcus aureus is a major human opportunistic pathogen and a frequent cause of hospital-acquired infections. Staphylococcal disease ranges from minor skin infections to life-threatening conditions, such as endocarditis and sepsis. S. aureus has traditionally been considered as an extracellular pathogen, but importantly, it has recently become known that parasitism of phagocytic host immune cells by S. aureus bacteria is a key phase of the disease. Such infected phagocytes can act as reservoirs of disseminated infection. However, the mechanisms by which S. aureus subverts the host immune system during this phase remain unknown.

The Staphylomics project is supported by a Marie Curie Fellowship to Dr. Tomacz Prajsnar, who aims to identify novel phagocyte components important in Staphylococcus aureus disease progression. This is achieved using an established zebrafish model for S. aureus infection and RNA deep sequencing technology to analyze the transcriptome of neutrophils and macrophages isolated from infected zebrafish larvae. The central hypothesis is that staphylococcal infection of phagocytes causes a distinct change in the transcriptional profile of these host immune cells, which promotes the creation of a favourable environment for phagocyte parasitism by S. aureus. In the longer run a better understanding of the innate immune response to staphylococci could provide immunomodulatory strategies to enhance the host's immune response against this versatile pathogen.

• development & disease
• drug resistance
• host-microbe interactions
• host-pathogen interaction
• infectious disease
• innate immunity
• staphylococcus
• zebrafish