Evidence map›Paper›PMID 21724997›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Protective roles for fibrin, tissue factor, plasminogen activator inhibitor-1, and thrombin activatable fibrinolysis inhibitor, but not factor XI, during defense against the gram-negative bacterium Yersinia enterocolitica.

Deyan Luo, Frank M Szaba, Lawrence W Kummer, Edward F Plow, Nigel Mackman, David Gailani, Stephen T Smiley

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Thrombin-Fibrin(ogen) Interactions, Host Defense and Risk of Thrombosis.International journal of molecular sciences · 2021
    Review
  9. Host fibrinogen drives antimicrobial function inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. Infection and immunity · 2019
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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 4 institutions in 1 country.

Deyan LuoTrudeau Institute, Saranac Lake, NY 12983, USA.
Frank M Szaba
Lawrence W Kummer
Edward F Plow
Nigel Mackman
David Gailani
Stephen T Smiley
Trudeau Institute · USCleveland Clinic · USUniversity of North Carolina Hospitals · USVanderbilt University · US

Funding

Cell-mediated protection against pneumonic plagueR01AI061577 · NIAID · TRUDEAU INSTITUTE, INC. · PI LIN, JR-SHIUAN · 2004 to 2013
$3.8M
Roles for coagulation in immunityR01AI071295 · NIAID · TRUDEAU INSTITUTE, INC. · PI SMILEY, STEPHEN T · 2008 to 2011
$1.8M
NIAID NIH HHS R01 AI061577NIAID NIH HHS R01-AI061577NIAID NIH HHS R01 AI071295NIAID NIH HHS R01-AI071295
6 · The paper itself

Abstract

Septic infections dysregulate hemostatic pathways, prompting coagulopathy. Nevertheless, anticoagulant therapies typically fail to protect humans from septic pathology. The data reported in this work may help to explain this discrepancy by demonstrating critical protective roles for coagulation leading to fibrin deposition during host defense against the Gram-negative bacterium Yersinia enterocolitica. After i.p. inoculation with Y. enterocolitica, fibrinogen-deficient mice display impaired cytokine and chemokine production in the peritoneal cavity and suppressed neutrophil recruitment. Moreover, both gene-targeted fibrinogen-deficient mice and wild-type mice treated with the anticoagulant coumadin display increased hepatic bacterial burden and mortality following either i.p. or i.v. inoculation with Y. enterocolitica. Mice with low tissue factor activity succumb to yersiniosis with a phenotype similar to fibrin(ogen)-deficient mice, whereas factor XI-deficient mice show wild-type levels of resistance. Mice deficient in plasminogen activator inhibitor-1 or thrombin-activatable fibrinolysis inhibitor display modest phenotypes, but mice deficient in both plasminogen activator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor succumb to yersiniosis with a phenotype resembling fibrin(ogen)-deficient mice. These findings demonstrate critical protective roles for the tissue factor-dependent extrinsic coagulation pathway during host defense against bacteria and caution that therapeutics targeting major thrombin-generating or antifibrinolytic pathways may disrupt fibrin-mediated host defense during Gram-negative sepsis.

Indexed as

Factor XIAnimalsCarboxypeptidase B2FibrinHumansLiverMiceMice, KnockoutSepsisSerpin E2ThromboplastinYersinia enterocoliticaYersinia InfectionsCarboxypeptidase B2Factor XIFibrinSerpin E2Serpine2 protein, mouseThromboplastin

Identifiers

PMID21724997
PMCPMC3150340
OpenAlexW1706591859

What OpenQuestion holds

Textmetadata
LicenceTDM
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.