association of novel streptococcus sanguinis virulence factors with pathogenesis in a native valve infective endocarditis model
Clicks: 323
ID: 158345
2020
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
30.0
/100
323 views
52 readers
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #132 of 875 articles by views in journal of magnetic resonance (san diego, calif : 1997)
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 875 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
Streptococcus sanguinis (S. sanguinis) is an abundant oral commensal which can cause disseminated human infection if it gains access to the bloodstream. The most important among these diseases is infective endocarditis (IE). While virulence phenotypes of S. sanguinis have been correlated to disease severity, genetic factors mediating these phenotypes, and contributing to pathogenesis are largely uncharacterized. In this report, we investigate the roles of 128 genes in virulence-related phenotypes of S. sanguinis and characterize the pathogenic potential of two selected mutants in a left-sided, native valve IE rabbit model. Assays determining the ability of our mutant strains to produce a biofilm, bind to and aggregate platelets, and adhere to or invade endothelial cells identified sixteen genes with novel association to these phenotypes. These results suggest the presence of many uncharacterized genes involved in IE pathogenesis which may be relevant for disease progression. Two mutants identified by the above screening process – SSA_1099, encoding an RTX-like protein, and mur2, encoding a peptidoglycan hydrolase – were subsequently evaluated in vivo. Wild type (WT) S. sanguinis reliably induced cardiac vegetations, while the SSA_1099 and mur2 mutants produced either no vegetation or vegetations of small size. Splenomegaly was reduced in both mutant strains compared to WT, while pathology of other distal organs was indistinguishable. Histopathology analyses suggest the cardiac lesions and vegetations in this model resemble those observed in humans. These data indicate that SSA_1099 and mur2 encode virulence factors in S. sanguinis which are integral to pathogenesis of IE.
| Reference Key |
martini2020frontiersassociation
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | ;Anthony M. Martini;Bridget S. Moricz;Allison K. Ripperger;Phuong M. Tran;Molly E. Sharp;Ana N. Forsythe;Katarina Kulhankova;Wilmara Salgado-Pabón;Bradley D. Jones;Bradley D. Jones |
| Journal | journal of magnetic resonance (san diego, calif : 1997) |
| Year | 2020 |
| DOI |
10.3389/fmicb.2020.00010
|
| URL | |
| Keywords |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.