Evidence map›Paper›PMID 25165887›Full record

ReviewPLoS pathogens2014

Host responses to group a streptococcus: cell death and inflammation.

James A Tsatsaronis, Mark J Walker, Martina L Sanderson-Smith

Open access · goldAbstract readReview
In one paragraph

Review in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 60 citations in OpenAlex.

  1. Virulence · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. The Shr receptor fromProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Article
  14. Group A Streptococcal Septic Hip Arthritis in a Child With Spastic Triplegic Cerebral Palsy.Journal of the American Academy of Orthopaedic Surgeons. Global research & reviews · 2021
    Article
  15. Article
  16. Review
  17. Evaluation of IL-17D in Host Immunity to Group AJournal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  18. Article
  19. Frontiers in cellular and infection microbiology · 2020
    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

3 authors at 2 institutions in 1 country.

James A TsatsaronisIllawarra Health and Medical Research Institute (IHMRI), School of Biological Sciences, University of Wollongong, Wollongong, New South Wales, Australia.
Mark J WalkerAustralian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, University of Queensland, St. Lucia, Queensland, Australia.
Martina L Sanderson-SmithIllawarra Health and Medical Research Institute (IHMRI), School of Biological Sciences, University of Wollongong, Wollongong, New South Wales, Australia.
Illawarra Health and Medical Research Institute · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infections caused by group A Streptococcus (GAS) are characterized by robust inflammatory responses and can rapidly lead to life-threatening disease manifestations. However, host mechanisms that respond to GAS, which may influence disease pathology, are understudied. Recent works indicate that GAS infection is recognized by multiple extracellular and intracellular receptors and activates cell signalling via discrete pathways. Host leukocyte receptor binding to GAS-derived products mediates release of inflammatory mediators associated with severe GAS disease. GAS induces divergent phagocyte programmed cell death responses and has inflammatory implications. Epithelial cell apoptotic and autophagic components are mobilized by GAS infection, but can be subverted to ensure bacterial survival. Examination of host interactions with GAS and consequences of GAS infection in the context of cellular receptors responsible for GAS recognition, inflammatory mediator responses, and cell death mechanisms, highlights potential avenues for diagnostic and therapeutic intervention. Understanding the molecular and cellular basis of host symptoms during severe GAS disease will assist the development of improved treatment regimens for this formidable pathogen.

Indexed as

AnimalsCell DeathHost-Parasite InteractionsHumansInflammationStreptococcal InfectionsStreptococcus pyogenes

Identifiers

PMID25165887
PMCPMC4148426
OpenAlexW2025769429

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.