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EDIN-B Promotes the Translocation of Staphylococcus aureus to the Bloodstream in the Course of Pneumonia.

Toxins (2015-10-27)
Johan Courjon, Patrick Munro, Yvonne Benito, Orane Visvikis, Coralie Bouchiat, Laurent Boyer, Anne Doye, Hubert Lepidi, Eric Ghigo, Jean-Philippe Lavigne, François Vandenesch, Emmanuel Lemichez
ABSTRACT

It is crucial to define risk factors that contribute to host invasion by Staphylococcus aureus. Here, we demonstrate that the chromosomally encoded EDIN-B isoform from S. aureus contributes to the onset of bacteremia during the course of pneumonia. Deletion of edinB in a European lineage community-acquired methicillin resistant S. aureus (CA-MRSA) strain (ST80-MRSA-IV) dramatically decreased the frequency and magnitude of bacteremia in mice suffering from pneumonia. This deletion had no effect on the bacterial burden in both blood circulation and lung tissues. Re-expression of wild-type EDIN-B, unlike the catalytically inactive mutant EDIN-R185E, restored the invasive characteristics of ST80-MRSA-IV.

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