<i>Staphylococcus epidermidis</i> ST2 strains associated with bloodstream infections contain a unique mobile genetic element encoding a plasmin inhibitor

This study uncovers a new virulence mechanism in <i>Staphylococcus epidermidis</i> ST2 bloodstream isolates. We identify a mobile genetic element (MGE) characteristic of an integrated conjugated element (ICE). pICE-Sepi-ST2 carries the genetic information needed to produce a cell wall-anchored (CWA) protein called SesY. The results indicate that SesY binds to plasminogen (Plg) and plasmin (Pln) and inhibits Pln's degradation of fibrin clots. Genetic analysis showed that all ST2 bloodstream isolates can express the plasmin inhibitor SesY and carry a mutation in the SdrG gene, resulting in the expression of inactive SdrG. Thus, we describe a molecular pathway targeting the coagulation pathway that may be required for <i>S. epidermidis</i> ST2 to cause bloodstream infections.

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Publication Details

Journal
mBio
Published
2024-11-19
DOI
https://doi.org/10.1128/mbio.01907-24
Citations
1
Primary Topic
Antimicrobial Resistance in Staphylococcus
Type
article
Field-Weighted Citation Impact
0.39

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article

Staphylococcus epidermidis ST2 strains associated with bloodstream infections contain a unique mobile genetic element encoding a plasmin inhibitor

Kelly Churion, Holger Rohde, Sheila Thomas, Amy A. Gomez et al.
1 citations
mBio
Antimicrobial Resistance in Staphylococcus
0.39
article

Staphylococcus epidermidis ST2 strains associated with bloodstream infections contain a unique mobile genetic element encoding a plasmin inhibitor

Kelly Churion, Holger Rohde, Sheila Thomas, Amy A. Gomez, Jon T. Skare, Srishtee Arora, Samuel A. Shelburne, Wen Liu, Minseo Choi, Magnus Höök, Clara Kjerfve
article en
1 citations

Abstract

This study uncovers a new virulence mechanism in <i>Staphylococcus epidermidis</i> ST2 bloodstream isolates. We identify a mobile genetic element (MGE) characteristic of an integrated conjugated element (ICE). pICE-Sepi-ST2 carries the genetic information needed to produce a cell wall-anchored (CWA) protein called SesY. The results indicate that SesY binds to plasminogen (Plg) and plasmin (Pln) and inhibits Pln's degradation of fibrin clots. Genetic analysis showed that all ST2 bloodstream isolates can express the plasmin inhibitor SesY and carry a mutation in the SdrG gene, resulting in the expression of inactive SdrG. Thus, we describe a molecular pathway targeting the coagulation pathway that may be required for <i>S. epidermidis</i> ST2 to cause bloodstream infections.

mBioVol. 15(12)
Texas A&M Health Science Center (US), United States Department of Health and Human Services (US), The University of Texas MD Anderson Cancer Center (US), Universität Hamburg (DE), Texas A&M Health Science Center (US), University Medical Center Hamburg-Eppendorf (DE), Bryan College (US)
Hamill Foundation
Openalex Percentile: Top 35%
Antimicrobial Resistance in Staphylococcus
0.39
DOIOpen Access PDFOpenAlex
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<i>Staphylococcus epidermidis</i> ST2 strains associated with bloodstream infections contain a unique mobile genetic element encoding a plasmin inhibitor — Kelly Churion, Holger Rohde, et al. · mBio (2024) | TGRS Research Map | TGRS