Evidence map›Paper›PMID 24875883›Full record

ArticlePLoS pathogens2014

Bacterial superantigens promote acute nasopharyngeal infection by Streptococcus pyogenes in a human MHC Class II-dependent manner.

Katherine J Kasper, Joseph J Zeppa, Adrienne T Wakabayashi, Stacey X Xu, Delfina M Mazzuca, Ian Welch, Miren L Baroja, Malak Kotb, Ewa Cairns, P Patrick Cleary and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 108 citations in OpenAlex.

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  14. The germ theory revisited: A noncentric view on infection outcome.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  15. Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024
    Review
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  20. Review

6 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 2 countries.

Katherine J KasperDepartment of Microbiology and Immunology and the Centre for Human Immunology, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada.
Joseph J ZeppaDepartment of Microbiology and Immunology and the Centre for Human Immunology, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada.
Adrienne T WakabayashiDepartment of Microbiology and Immunology and the Centre for Human Immunology, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada.
Stacey X XuDepartment of Microbiology and Immunology and the Centre for Human Immunology, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada.
Delfina M MazzucaDepartment of Microbiology and Immunology and the Centre for Human Immunology, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada.
Ian WelchDepartment of Animal Care and Veterinary Services, Western University, London, Ontario, Canada.
Miren L BarojaDepartment of Microbiology and Immunology and the Centre for Human Immunology, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada; Lawson Health Research Institute, London, Ontario, Canada.
Malak KotbDepartment of Basic Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota, United States of America.
Ewa CairnsDepartment of Microbiology and Immunology and the Centre for Human Immunology, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada; Department of Medicine, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada.
P Patrick ClearyDepartment of Microbiology, University of Minnesota, Minneapolis, Minnesota, United States of America.
S M Mansour HaeryfarDepartment of Microbiology and Immunology and the Centre for Human Immunology, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada; Lawson Health Research Institute, London, Ontario, Canada.
John K McCormickDepartment of Microbiology and Immunology and the Centre for Human Immunology, Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada; Lawson Health Research Institute, London, Ontario, Canada.
Western University · CALawson Health Research Institute · CAUniversity of Minnesota · USUniversity of North Dakota · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Establishing the genetic determinants of niche adaptation by microbial pathogens to specific hosts is important for the management and control of infectious disease. Streptococcus pyogenes is a globally prominent human-specific bacterial pathogen that secretes superantigens (SAgs) as 'trademark' virulence factors. SAgs function to force the activation of T lymphocytes through direct binding to lateral surfaces of T cell receptors and class II major histocompatibility complex (MHC-II) molecules. S. pyogenes invariably encodes multiple SAgs, often within putative mobile genetic elements, and although SAgs are documented virulence factors for diseases such as scarlet fever and the streptococcal toxic shock syndrome (STSS), how these exotoxins contribute to the fitness and evolution of S. pyogenes is unknown. Here we show that acute infection in the nasopharynx is dependent upon both bacterial SAgs and host MHC-II molecules. S. pyogenes was rapidly cleared from the nasal cavity of wild-type C57BL/6 (B6) mice, whereas infection was enhanced up to ∼10,000-fold in B6 mice that express human MHC-II. This phenotype required the SpeA superantigen, and vaccination with an MHC -II binding mutant toxoid of SpeA dramatically inhibited infection. Our findings indicate that streptococcal SAgs are critical for the establishment of nasopharyngeal infection, thus providing an explanation as to why S. pyogenes produces these potent toxins. This work also highlights that SAg redundancy exists to avoid host anti-SAg humoral immune responses and to potentially overcome host MHC-II polymorphisms.

Indexed as

Acute DiseaseAnimalsBacterial ProteinsExotoxinsHistocompatibility Antigens Class IIHumansMembrane ProteinsMice, Inbred C57BLNasopharynxReceptors, Antigen, T-CellStreptococcal InfectionsStreptococcus pyogenesSuperantigensT-LymphocytesBacterial ProteinsExotoxinsHistocompatibility Antigens Class IIMembrane ProteinsReceptors, Antigen, T-CellSpeA protein, Streptococcus pyogenesSuperantigens

Identifiers

PMID24875883
PMCPMC4038607
OpenAlexW2048086790

What OpenQuestion holds

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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.