Evidence map›Paper›PMID 25309880›Full record

ReviewFrontiers in cellular and infection microbiology2014

The role of coagulation/fibrinolysis during Streptococcus pyogenes infection.

Torsten G Loof, Christin Deicke, Eva Medina

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2014. 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
4.8field-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

43 citing papers in PubMed, 84 citations in OpenAlex.

  1. The Antimicrobial Activity ofMolecules (Basel, Switzerland) · 2021
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  6. mBio · 2024
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  14. Evolutionary Insight into Immunothrombosis as a Healing Mechanism.International journal of molecular sciences · 2022
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  16. Review
  17. Review
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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

3 authors at 1 institution in 1 country.

Torsten G LoofInfection Immunology Research Group, Helmholtz Centre for Infection Research Braunschweig, Germany.
Christin DeickeInfection Immunology Research Group, Helmholtz Centre for Infection Research Braunschweig, Germany.
Eva MedinaInfection Immunology Research Group, Helmholtz Centre for Infection Research Braunschweig, Germany.
Helmholtz Centre for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hemostatic system comprises platelet aggregation, coagulation and fibrinolysis and is a host defense mechanism that protects the integrity of the vascular system after tissue injury. During bacterial infections, the coagulation system cooperates with the inflammatory system to eliminate the invading pathogens. However, pathogenic bacteria have frequently evolved mechanisms to exploit the hemostatic system components for their own benefit. Streptococcus pyogenes, also known as Group A Streptococcus, provides a remarkable example of the extraordinary capacity of pathogens to exploit the host hemostatic system to support microbial survival and dissemination. The coagulation cascade comprises the contact system (also known as the intrinsic pathway) and the tissue factor pathway (also known as the extrinsic pathway), both leading to fibrin formation. During the early phase of S. pyogenes infection, the activation of the contact system eventually leads to bacterial entrapment within a fibrin clot, where S. pyogenes is immobilized and killed. However, entrapped S. pyogenes can circumvent the antimicrobial effect of the clot by sequestering host plasminogen on the bacterial cell surface that, after conversion into its active proteolytic form, plasmin, degrades the fibrin network and facilitates the liberation of S. pyogenes from the clot. Furthermore, the surface-localized fibrinolytic activity also cleaves a variety of extracellular matrix proteins, thereby enabling S. pyogenes to migrate across barriers and disseminate within the host. This review summarizes the knowledge gained during the last two decades on the role of coagulation/fibrinolysis in host defense against S. pyogenes as well as the strategies developed by this pathogen to evade and exploit these host mechanisms for its own benefit.

Indexed as

Blood CoagulationFibrinolysisAnimalsFibrinogenHost-Pathogen InteractionsHumansImmunity, InnateStreptococcal InfectionsStreptococcus pyogenesFibrinogencoagulation systemcontact systemfibrinogenfibrinolysisplasminogenStreptococcus pyogenes

Identifiers

PMID25309880
PMCPMC4161043
OpenAlexW2140977850

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.