Evidence map›Paper›PMID 23202729›Full record

ArticleThe Journal of clinical investigation2013

PAR1 contributes to influenza A virus pathogenicity in mice.

Khaled Khoufache, Fatma Berri, Wolfgang Nacken, Annette B Vogel, Marie Delenne, Eric Camerer, Shaun R Coughlin, Peter Carmeliet, Bruno Lina, Guus F Rimmelzwaan and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
5.2field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  17. Article
  18. Targeting coagulation activation in severe COVID-19 pneumonia: lessons from bacterial pneumonia and sepsis.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  19. COVID-19: A collision of complement, coagulation and inflammatory pathways.Journal of thrombosis and haemostasis : JTH · 2020
    Review
  20. Antiviral anticoagulation.Research and practice in thrombosis and haemostasis · 2020
    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

13 authors at 9 institutions in 5 countries.

Khaled KhoufacheVirologie et Pathologie Humaine, EA 4610, Université Lyon1, Faculté de Médecine RTH Laennec, Lyon, France.
Fatma Berri
Wolfgang Nacken
Annette B Vogel
Marie Delenne
Eric Camerer
Shaun R Coughlin
Peter Carmeliet
Bruno Lina
Guus F Rimmelzwaan
Oliver Planz
Stephan Ludwig
Béatrice Riteau
Virologie et Pathologies Humaines · FRFriedrich-Loeffler-Institut · DEUniversity of Münster · DEDélégation Paris 5 · FRErasmus MC · NLInfectiologie Animale et Santé Publique · FRKU Leuven · BEUniversité Claude Bernard Lyon 1 · FRUniversity of California, San Francisco · US

Funding

PROTEASE-ACTIVATED RECEPTORS IN EMBRYONIC DEVELOPMENTR01HL065590 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI COUGHLIN, SHAUN R. · 2000 to 2013
$5.9M
NHLBI NIH HHS R01 HL065590
6 · The paper itself

Abstract

Influenza causes substantial morbidity and mortality, and highly pathogenic and drug-resistant strains are likely to emerge in the future. Protease-activated receptor 1 (PAR1) is a thrombin-activated receptor that contributes to inflammatory responses at mucosal surfaces. The role of PAR1 in pathogenesis of virus infections is unknown. Here, we demonstrate that PAR1 contributed to the deleterious inflammatory response after influenza virus infection in mice. Activating PAR1 by administering the agonist TFLLR-NH2 decreased survival and increased lung inflammation after influenza infection. Importantly, both administration of a PAR1 antagonist and PAR1 deficiency protected mice from infection with influenza A viruses (IAVs). Treatment with the PAR1 agonist did not alter survival of mice deficient in plasminogen (PLG), which suggests that PLG permits and/or interacts with a PAR1 function in this model. PAR1 antagonists are in human trials for other indications. Our findings suggest that PAR1 antagonism might be explored as a treatment for influenza, including that caused by highly pathogenic H5N1 and oseltamivir-resistant H1N1 viruses.

Indexed as

AnimalsDogsHumansInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H5N1 SubtypeInfluenza, HumanMiceMice, KnockoutNIH 3T3 CellsOligopeptidesOrthomyxoviridae InfectionsPlasminogenPlatelet Aggregation InhibitorsReceptor, PAR-1OligopeptidesPAR-1-activating peptidePlasminogenPlatelet Aggregation InhibitorsReceptor, PAR-1

Identifiers

PMID23202729
PMCPMC3533265
OpenAlexW2092311461

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.