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

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Courjon, Johan | Munro, Patrick | Benito, Yvonne | Visvikis, Orane | Bouchiat, Coralie | Boyer, Laurent | Doye, Anne | Lepidi, Hubert | Ghigo, Eric | Lavigne, Jean-Philippe | Vandenesch, François | Lemichez, Emmanuel

Edité par CCSD ; MDPI -

International audience. 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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