Evidence map›Paper›PMID 20123717›Full record

ArticleInfection and immunity2010

Toll-like receptor 3 agonist protection against experimental Francisella tularensis respiratory tract infection.

Richard B Pyles, G Eric Jezek, Tonyia D Eaves-Pyles

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Formulation of host-targeted therapeutics against bacterial infections.Translational research : the journal of laboratory and clinical medicine · 2020
    Review
  4. Article
  5. Article
  6. Review
  7. Mitogen-activated protein kinases (MAPKs) are modulated during Francisella tularensis infection, but inhibition of extracellular-signal-regulated kinases (ERKs) is of limited therapeutic benefit.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. New therapeutic approaches for treatment of tularaemia: a review.Frontiers in cellular and infection microbiology · 2014
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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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

3 authors at 1 institution in 1 country.

Richard B PylesDepartment of Pediatrics, University of Texas Medical Branch, Galveston, Texas 77555-0436, USA.
G Eric Jezek
Tonyia D Eaves-Pyles
The University of Texas Medical Branch at Galveston · US

Funding

Franciscella Tularensis: Characterizing Lung Innate ImmunityR21AI068774 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI EAVES-PYLES, TONYIA D · 2007 to 2009
$633k
NIAID NIH HHS R21 AI068774
6 · The paper itself

Abstract

We investigated whether Toll-like receptor 3 (TLR3) stimulation would protect the host from inhaled Francisella tularensis. TLR3 is expressed by respiratory epithelial cells and macrophages and can be activated by a synthetic double-stranded RNA ligand called polyinosine-polycytosine [poly(I:C)]. Thus, we evaluated poly(I:C) as a novel treatment against inhaled F. tularensis. In vivo, BALB/c mice intranasally (i.n.) treated with poly(I:C) (100 microg/mouse) 1 h before or after Schu 4 or LVS (100 CFU) i.n. challenge showed that poly(I:C) treatment significantly reduced bacterial load in the lungs (P < 0.05). Bronchoalveolar lavage from poly(I:C)-treated mice alone or combined with F. tularensis infection significantly increased cytokine secretion and enhanced neutrophil influx to lung tissues. Poly(I:C) responses were transient but significantly prolonged the survival of treated mice after i.n. F. tularensis challenge relative to mock treated animals. This prolonged survival providing a longer window for initiation of levofloxacin (LEVO) treatment (40 mg/kg). Animals treated with poly(I:C), challenged with F. tularensis, and then treated with LEVO 5 days later had 100% survival relative to 0% survival in animals receiving LEVO alone. Mechanistically, poly(I:C) given to human monocyte-derived macrophages before or after Schu 4 or LVS challenge (multiplicity of infection, 20:1) had significantly reduced intracellular bacterial replication (P < 0.05). These data suggest that poly(I:C) may represent a potential therapeutic agent against inhaled F. tularensis that prolongs survival and the opportunity to initiate standard antibiotic therapy (i.e., LEVO).

Indexed as

AnimalsAnti-Bacterial AgentsBronchoalveolar Lavage FluidCells, CulturedColony Count, MicrobialCytokinesFemaleFrancisella tularensisHumansImmunologic FactorsLevofloxacinLungMiceMice, Inbred BALB CMonocytesNeutrophilsAnti-Bacterial AgentsCytokinesImmunologic FactorsLevofloxacinOfloxacinPoly I-CToll-Like Receptor 3

Identifiers

PMID20123717
PMCPMC2849393
OpenAlexW2163440400

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.