Evidence map›Paper›PMID 28034602›Full record

ArticleThe American journal of pathology2017

Contribution of Secreted NADase and Streptolysin O to the Pathogenesis of Epidemic Serotype M1 Streptococcus pyogenes Infections.

Luchang Zhu, Randall J Olsen, Jessica D Lee, Adeline R Porter, Frank R DeLeo, James M Musser

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 63 citations in OpenAlex.

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  16. Structure of the Streptococcus pyogenes NADJournal of bacteriology · 2022
    Article
  17. Article
  18. Article
  19. Population Genomics ofmSystems · 2021
    Article
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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

6 authors at 5 institutions in 1 country.

Luchang ZhuCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas; Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Randall J OlsenCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas; Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas.
Jessica D LeeDepartment of Biosciences, Rice University, Houston, Texas.
Adeline R PorterLaboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana.
Frank R DeLeoLaboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana.
James M MusserCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas; Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas. Electronic address: jmmusser@houstonmethodist.org.
Methodist Hospital · USHouston Methodist · USNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · USRice University · US

Funding

Interaction of pathogenic bacteria with human phagocytic leukocytesZIAAI000900 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DELEO, FRANK · 2009 to 2023
$3.6M
6 · The paper itself

Abstract

Streptococcus pyogenes secretes many toxins that facilitate human colonization, invasion, and dissemination. NADase (SPN) and streptolysin O (SLO) are two toxins that play important roles in pathogenesis. We previously showed that increased production of SPN and SLO in epidemic serotype M1 and M89 S. pyogenes strains is associated with rapid intercontinental spread and enhanced virulence. The biological functions of SPN and SLO have been extensively studied using eukaryotic cell lines, but the relative contribution of each of these two toxins to pathogenesis of epidemic M1 or M89 strains remains unexplored. Herein, using a genetically representative epidemic M1 strain and a panel of isogenic mutant derivative strains, we evaluated the relative contributions of SPN and SLO toxins to virulence in mouse models of necrotizing myositis, bacteremia, and skin and soft tissue infection. We found that isogenic mutants lacking SPN, SLO, and both toxins are equally impaired in ability to cause necrotizing myositis. In addition, mutants lacking either SPN or SLO are significantly attenuated in the bacteremia and soft tissue infection models, and the mutant strain lacking production of both toxins is further attenuated. The mutant strain lacking both SPN and SLO production is severely attenuated in ability to resist killing by human polymorphonuclear leukocytes. We conclude that both SPN and SLO contribute significantly to S. pyogenes pathogenesis in these virulence assays.

Indexed as

AnimalsBacterial ProteinsDisease Models, AnimalHumansImmune EvasionMicrobial ViabilityMutationNAD+ NucleosidaseNeutrophilsPhenotypeSerotypingStreptococcal InfectionsStreptococcus pyogenesStreptolysinsVirulenceBacterial ProteinsNAD+ Nucleosidasestreptolysin OStreptolysins

Identifiers

PMID28034602
PMCPMC5397666
OpenAlexW2561814558

What OpenQuestion holds

Textmetadata
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.