Abstract
Staphylococcus aureus is the cause of serious vascular infections such as sepsis and endocarditis. These infections are notoriously difficult to treat, and it is believed that the ability of S. aureus to invade endothelial cells and persist intracellularly is a key mechanism for persistence despite ongoing antibiotic treatment. Here, we used dual RNA sequencing to study the simultaneous transcriptional response of S. aureus and human endothelial cells during in vitro infections. We revealed discrete and shared differentially expressed genes for both host and pathogen at the different stages of infection. While the endothelial cells upregulated genes involved in interferon signalling and antigen presentation during late infection, S. aureus downregulated toxin expression while upregulating genes related to iron scavenging. In conclusion, the presented data provide an important resource to facilitate functional investigations into host–pathogen interaction during S. aureus invasive infection and a basis for identifying novel drug target sites.
Highlights
Staphylococcus aureus is the cause of serious vascular infections such as sepsis and endocarditis
This behaviour has since been linked to the pathogenesis of S. aureus, in particular its ability to spread via the blood to o rgans[3] and its resilience against host response and antibiotic treatment e.g. in bloodstream infections such as endocarditis[4]
Bacteria from an exponential phase broth culture was used at a multiplicity of infection (MOI) of 16 to infect the human umbilical vein endothelial cells (HUVECs), and bacteriaHUVEC contact synchronized by centrifugation
Summary
Staphylococcus aureus is the cause of serious vascular infections such as sepsis and endocarditis. S. aureus has been viewed solely as an extracellular pathogen, but research conducted during the past decades has demonstrated a pronounced ability for this bacterium to invade and colonize both professional and non-professional phagocytes such as endothelial cells This behaviour has since been linked to the pathogenesis of S. aureus, in particular its ability to spread via the blood to o rgans[3] and its resilience against host response and antibiotic treatment e.g. in bloodstream infections such as endocarditis[4]. A global genetic analysis is lacking which maps the expression of genes, essential as well as non-essential, for both the bacterium and the human cell simultaneously during invasive endothelial infection This is important to understand the fundamental interactions between host and pathogen, and from a treatment perspective, to identify new targets for intervention. These data could indicate the importance of toxin repression and improved iron scavenging for intracellular survival of S. aureus during infection
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