Evidence map›Paper›PMID 23487423›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Fibrin facilitates both innate and T cell-mediated defense against Yersinia pestis.

Deyan Luo, Jr-Shiuan Lin, Michelle A Parent, Isis Mullarky-Kanevsky, Frank M Szaba, Lawrence W Kummer, Debra K Duso, Michael Tighe, Jim Hill, Andras Gruber and 3 more

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Interacting Effects of Sea Louse (Frontiers in immunology · 2022
    Article
  3. Review
  4. Article
  5. Infection and immunity · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Factor XII in inflammation and wound healing.Current opinion in hematology · 2018
    Review
  10. Article
  11. Tissue dual RNA-seq allows fast discovery of infection-specific functions and riboregulators shaping host-pathogen transcriptomes.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Fibrinolytic and coagulative activities of Yersinia pestis.Frontiers in cellular and infection microbiology · 2013
    Review
  18. 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

13 authors at 6 institutions in 2 countries.

Deyan LuoTrudeau Institute, Saranac Lake, NY 12983, USA.
Jr-Shiuan Lin
Michelle A Parent
Isis Mullarky-Kanevsky
Frank M Szaba
Lawrence W Kummer
Debra K Duso
Michael Tighe
Jim Hill
Andras Gruber
Nigel Mackman
David Gailani
Stephen T Smiley
Trudeau Institute · USDefence Science and Technology Laboratory · GBOregon Health & Science University · USUniversity of North Carolina Hospitals · USVanderbilt University · USVirginia Tech · US

Funding

Cell-mediated protection against pneumonic plagueR01AI061577 · NIAID · TRUDEAU INSTITUTE, INC. · PI LIN, JR-SHIUAN · 2004 to 2013
$3.8M
Factor Xl in Vascular ThrombosisR01HL081326 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GAILANI, DAVID · 2007 to 2017
$3.5M
Therapeutic factor XI blockade for sepsisR44AI088937 · NIAID · ARONORA, INC. · PI GRUBER, ANDRAS, TUCKER, ERIK IAN · 2012 to 2014
$3.0M
Roles for coagulation in immunityR01AI071295 · NIAID · TRUDEAU INSTITUTE, INC. · PI SMILEY, STEPHEN T · 2008 to 2011
$1.8M
NHLBI NIH HHS R01 HL081326NIAID NIH HHS R01 AI061577NIAID NIH HHS R01-AI061577NIAID NIH HHS R01 AI071295NIAID NIH HHS R01-AI071295NIAID NIH HHS R44 AI088937NIAID NIH HHS R44-AI088937
6 · The paper itself

Abstract

The Gram-negative bacterium Yersinia pestis causes plague, a rapidly progressing and often fatal disease. The formation of fibrin at sites of Y. pestis infection supports innate host defense against plague, perhaps by providing a nondiffusible spatial cue that promotes the accumulation of inflammatory cells expressing fibrin-binding integrins. This report demonstrates that fibrin is an essential component of T cell-mediated defense against plague but can be dispensable for Ab-mediated defense. Genetic or pharmacologic depletion of fibrin abrogated innate and T cell-mediated defense in mice challenged intranasally with Y. pestis. The fibrin-deficient mice displayed reduced survival, increased bacterial burden, and exacerbated hemorrhagic pathology. They also showed fewer neutrophils within infected lung tissue and reduced neutrophil viability at sites of liver infection. Depletion of neutrophils from wild-type mice weakened T cell-mediated defense against plague. The data suggest that T cells combat plague in conjunction with neutrophils, which require help from fibrin to withstand Y. pestis encounters and effectively clear bacteria.

Indexed as

Immunity, InnateAnimalsBacterial ProteinsFibrinFibrinogenMiceMice, Inbred C57BLMice, KnockoutPlaguePlasminogen ActivatorsT-Lymphocyte SubsetsYersinia pestisBacterial ProteinsFibrinFibrinogenPla protease, Yersinia pestisPlasminogen Activators

Identifiers

PMID23487423
PMCPMC3622124
OpenAlexW2104629425

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.