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Article Dans Une Revue Toxins Année : 2015

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

Résumé

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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Toxicologie
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hal-01909846 , version 1 (27-05-2021)

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Johan Courjon, Patrick Munro, Yvonne Benito, Orane Visvikis, Coralie Bouchiat, et al.. EDIN-B Promotes the Translocation of Staphylococcus aureus to the Bloodstream in the Course of Pneumonia. Toxins, 2015, 7 (10), pp.4131 - 4142. ⟨10.3390/toxins7104131⟩. ⟨hal-01909846⟩
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