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

Toxins (Basel). 2015 Oct 15;7(10):4131-42. doi: 10.3390/toxins7104131.

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.

Keywords: bacteremia; methicillin-resistant Staphylococcus aureus; toxins; virulence factor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bacteremia / microbiology*
  • Bacterial Proteins / genetics*
  • Bacterial Translocation* / genetics
  • Disease Models, Animal
  • Female
  • Gene Deletion
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • Pneumonia, Bacterial / microbiology*
  • Staphylococcal Infections / microbiology*
  • Staphylococcus aureus / genetics*
  • Staphylococcus aureus / isolation & purification
  • Virulence

Substances

  • Bacterial Proteins
  • epidermal cell differentiation inhibitor, Staphylococcus aureus