Evidence map›Paper›PMID 23733338›Full record

ArticleBlood2013

Bacillus anthracis peptidoglycan activates human platelets through FcγRII and complement.

Dawei Sun, Narcis I Popescu, Brent Raisley, Ravi S Keshari, George L Dale, Florea Lupu, K Mark Coggeshall

Open access · greenAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Induced pluripotent stem cell-derived platelets kill multidrug-resistantResearch and practice in thrombosis and haemostasis · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Sepsis - it is all about the platelets.Frontiers in immunology · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. Article
  17. Article
  18. Article
  19. Inhibition of complement C5 protects against organ failure and reduces mortality in a baboon model ofProceedings of the National Academy of Sciences of the United States of America · 2017
    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

7 authors at 2 institutions in 1 country.

Dawei SunDepartment of Cell Biology, University of Oklahoma, Oklahoma City, OK, USA.
Narcis I Popescu
Brent Raisley
Ravi S Keshari
George L Dale
Florea Lupu
K Mark Coggeshall
Oklahoma Medical Research Foundation · USUniversity of Oklahoma · US

Funding

Translation of immunologic technologies from basic research into pre-clinical nonU19AI062629 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI COGGESHALL, KENNETH MARK · 2004 to 2023
$56.2M
Complement inhibition as sepsis therapyR01GM097747 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI LAMBRIS, JOHN D, LUPU, FLOREA · 2011 to 2014
$2.1M
NIAID NIH HHS U19 AI062629NIGMS NIH HHS GM097747NIGMS NIH HHS R01 GM097747
6 · The paper itself

Abstract

Platelet activation frequently accompanies sepsis and contributes to the sepsis-associated vascular leakage and coagulation dysfunction. Our previous work has implicated peptidoglycan (PGN) as an agent causing systemic inflammation in gram-positive sepsis. We used flow cytometry and fluorescent microscopy to define the effects of PGN on the activation of human platelets. PGN induced platelet aggregation, expression of the activated form of integrin αIIbβ3, and exposure of phosphatidylserine (PS). These changes were dependent on immunoglobulin G and were attenuated by the Fcγ receptor IIa-blocking antibody IV.3, suggesting they are mediated by PGN-anti-PGN immune complexes signaling through Fcγ receptor IIa. PS exposure was not blocked by IV.3 but was sensitive to inhibitors of complement activation. PGN was a potent activator of the complement cascade in human plasma and caused deposition of C5b-9 on the platelet surface. Platelets with exposed PS had greatly accelerated prothrombinase activity. We conclude that PGN derived from gram-positive bacteria is a potent platelet agonist when complexed with anti-PGN antibody and could contribute to the coagulation dysfunction accompanying gram-positive infections.

Indexed as

Platelet ActivationBacillus anthracisBlood PlateletsComplement System ProteinsHumansImmunoglobulin GPeptidoglycanPhosphatidylserinesPlasmaPlatelet Glycoprotein GPIIb-IIIa ComplexProtein BindingReceptors, IgGComplement System ProteinsImmunoglobulin GPeptidoglycanPhosphatidylserinesPlatelet Glycoprotein GPIIb-IIIa ComplexReceptors, IgG

Identifiers

PMID23733338
PMCPMC3724192
OpenAlexW2018147541

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.