Evidence map›Paper›PMID 28957360›Full record

ArticlePloS one2017

Human platelet interaction with E. coli O111 promotes tissue-factor-dependent procoagulant activity, involving Toll like receptor 4.

Valeria Matus, J Guillermo Valenzuela, Patricia Hidalgo, L María Pozo, Olga Panes, Aniela Wozniak, Diego Mezzano, Jaime Pereira, Claudia G Sáez

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Beyond hemostasis, the immunomodulatory nature of platelets.Research and practice in thrombosis and haemostasis · 2025
    Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Platelets andBiomedicines · 2022
    Review
  7. Article
  8. Review
  9. Effect of antiplatelet agents onFrontiers in microbiology · 2022
    Review
  10. Review
  11. Review
  12. Procoagulant Phosphatidylserine-Exposing PlateletsFrontiers in cardiovascular medicine · 2020
    Review
  13. Review
  14. 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

9 authors at 1 institution in 1 country.

Valeria MatusDepartment of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.ORCID http://orcid.org/0000-0001-7183-1491
J Guillermo ValenzuelaDepartment of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Patricia HidalgoDepartment of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
L María PozoDepartment of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Olga PanesDepartment of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Aniela WozniakDepartment of Clinical Laboratory, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Diego MezzanoDepartment of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Jaime PereiraDepartment of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Claudia G SáezDepartment of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Pontificia Universidad Católica de Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platelets have a major role in clotting activation and contribute to the innate immune response during systemic infections. Human platelets contain tissue factor (TF) and express functional Toll-like receptor 4 (TLR4). However, the role of TLR4 in triggering the procoagulant properties of platelets, upon challenge with bacteria, is yet unknown. Our hypothesis is that E. coli O111-TLR4 interaction activates platelets and elicits their procoagulant activity. We demonstrated that the strain, but not ultrapure LPS, increased surface P-selectin expression, platelet dependent TF procoagulant activity (TF-PCA) and prompted a faster thrombin generation (TG). Blockade of TLR4 resulted in decreased platelet activation, TF-PCA and TG, revealing the participation of this immune receptor on the procoagulant response of platelets. Our results provide a novel mechanism by which individuals with bacterial infections would have an increased incidence of blood clots. Furthermore, the identification of platelet TF and TLR4 as regulators of the effect of E. coli O111 might represent a novel therapeutic target to reduce the devastating consequences of the hemostatic disorder during sepsis.

Indexed as

Blood CoagulationAdultAgedAntibodies, MonoclonalBlood PlateletsEscherichia coliHumansLipoproteinsMiddle AgedPlatelet ActivationPlatelet-Rich PlasmaP-SelectinThrombinThromboplastinToll-Like Receptor 4Young AdultAntibodies, Monoclonallipoprotein-associated coagulation inhibitorLipoproteinsP-SelectinThrombinThromboplastinTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID28957360
PMCPMC5619753
OpenAlexW2758324084

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.