Evidence map›Paper›PMID 27124393›Full record

ArticlePloS one2016

Novel Tissue Level Effects of the Staphylococcus aureus Enterotoxin Gene Cluster Are Essential for Infective Endocarditis.

Christopher S Stach, Bao G Vu, Joseph A Merriman, Alfa Herrera, Michael P Cahill, Patrick M Schlievert, Wilmara Salgado-Pabón

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 48 citations in OpenAlex.

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  12. TSST-1The Journal of investigative dermatology · 2022
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  14. Review
  15. Vegetation Formation inFrontiers in cellular and infection microbiology · 2022
    Article
  16. Article
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  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Christopher S StachDepartment of Microbiology, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, United States of America.
Bao G VuDepartment of Microbiology, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, United States of America.
Joseph A MerrimanDepartment of Microbiology, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, United States of America.
Alfa HerreraDepartment of Microbiology, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, United States of America.
Michael P CahillDepartment of Microbiology, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, United States of America.
Patrick M SchlievertDepartment of Microbiology, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, United States of America.
Wilmara Salgado-PabónDepartment of Microbiology, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, United States of America.
University of Iowa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSuperantigens are indispensable virulence factors for Staphylococcus aureus in disease causation. Superantigens stimulate massive immune cell activation, leading to toxic shock syndrome (TSS) and contributing to other illnesses. However, superantigens differ in their capacities to induce body-wide effects. For many, their production, at least as tested in vitro, is not high enough to reach the circulation, or the proteins are not efficient in crossing epithelial and endothelial barriers, thus remaining within tissues or localized on mucosal surfaces where they exert only local effects. In this study, we address the role of TSS toxin-1 (TSST-1) and most importantly the enterotoxin gene cluster (egc) in infective endocarditis and sepsis, gaining insights into the body-wide versus local effects of superantigens.

methodsWe examined S. aureus TSST-1 gene (tstH) and egc deletion strains in the rabbit model of infective endocarditis and sepsis. Importantly, we also assessed the ability of commercial human intravenous immunoglobulin (IVIG) plus vancomycin to alter the course of infective endocarditis and sepsis.

resultsTSST-1 contributed to infective endocarditis vegetations and lethal sepsis, while superantigens of the egc, a cluster with uncharacterized functions in S. aureus infections, promoted vegetation formation in infective endocarditis. IVIG plus vancomycin prevented lethality and stroke development in infective endocarditis and sepsis.

conclusionsOur studies support the local tissue effects of egc superantigens for establishment and progression of infective endocarditis providing evidence for their role in life-threatening illnesses. In contrast, TSST-1 contributes to both infective endocarditis and lethal sepsis. IVIG may be a useful adjunct therapy for infective endocarditis and sepsis.

Indexed as

AnimalsAnti-Bacterial AgentsBacterial ToxinsDisease Models, AnimalDrug Therapy, CombinationEndocarditis, BacterialEnterotoxinsFemaleImmunoglobulins, IntravenousImmunologic FactorsMaleRabbitsSepsisShock, SepticStaphylococcal InfectionsStaphylococcus aureusAnti-Bacterial AgentsBacterial Toxinsenterotoxin F, StaphylococcalEnterotoxinsImmunoglobulins, IntravenousImmunologic FactorsSuperantigensVancomycin

Identifiers

PMID27124393
PMCPMC4849672
OpenAlexW2344288750

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.