Evidence map›Paper›PMID 24967596›Full record

ArticlePloS one2014

Mycobacteria counteract a TLR-mediated nitrosative defense mechanism in a zebrafish infection model.

Philip M Elks, Michiel van der Vaart, Vincent van Hensbergen, Esther Schutz, Michael J Redd, Emi Murayama, Herman P Spaink, Annemarie H Meijer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
1.8field-weighted citation impact, top 16% 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, 41 citations in OpenAlex.

  1. mBio · 2026
    Article
  2. Journal of bacteriology · 2025
    Review
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  7. Review
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  12. Article
  13. Hypoxia Induces MacrophageFrontiers in immunology · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

8 authors at 4 institutions in 4 countries.

Philip M ElksInstitute of Biology, Leiden University, Leiden, South Holland, The Netherlands; The Bateson Centre, University of Sheffield, Sheffield, South Yorkshire, United Kingdom; Department of Infection and Immunity, University of Sheffield, Sheffield, South Yorkshire, United Kingdom.
Michiel van der VaartInstitute of Biology, Leiden University, Leiden, South Holland, The Netherlands.
Vincent van HensbergenInstitute of Biology, Leiden University, Leiden, South Holland, The Netherlands.
Esther SchutzInstitute of Biology, Leiden University, Leiden, South Holland, The Netherlands.
Michael J ReddDepartment of Oncological Sciences, University Of Utah, Salt Lake City, Utah, United States of America.
Emi MurayamaUnité Macrophages et Développement de l'Immunité, Institut Pasteur, Paris, France; Centre National de la Recherche Scientifique-Unité de Recherche Associée 2578, Institut Pasteur, Paris, France.
Herman P SpainkInstitute of Biology, Leiden University, Leiden, South Holland, The Netherlands.
Annemarie H MeijerInstitute of Biology, Leiden University, Leiden, South Holland, The Netherlands.
Leiden University · NLInstitut Pasteur · FRUniversity of Sheffield · GBUniversity of Utah · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary tuberculosis (TB), caused by the intracellular bacterial pathogen Mycobacterium tuberculosis (Mtb), is a major world health problem. The production of reactive nitrogen species (RNS) is a potent cytostatic and cytotoxic defense mechanism against intracellular pathogens. Nevertheless, the protective role of RNS during Mtb infection remains controversial. Here we use an anti-nitrotyrosine antibody as a readout to study nitration output by the zebrafish host during early mycobacterial pathogenesis. We found that recognition of Mycobacterium marinum, a close relative of Mtb, was sufficient to induce a nitrosative defense mechanism in a manner dependent on MyD88, the central adaptor protein in Toll like receptor (TLR) mediated pathogen recognition. However, this host response was attenuated by mycobacteria via a virulence mechanism independent of the well-characterized RD1 virulence locus. Our results indicate a mechanism of pathogenic mycobacteria to circumvent host defense in vivo. Shifting the balance of host-pathogen interactions in favor of the host by targeting this virulence mechanism may help to alleviate the problem of infection with Mtb strains that are resistant to multiple drug treatments.

Indexed as

AnimalsAnimals, Genetically ModifiedDisease Models, AnimalInterleukin-8MycobacteriumMycobacterium InfectionsMyeloid Differentiation Factor 88NeutrophilsPeroxidaseReactive Nitrogen SpeciesReceptors, Interleukin-1Receptors, Interleukin-8BSignal TransductionToll-Like ReceptorsTyrosineZebrafishInterleukin-8Myeloid Differentiation Factor 88PeroxidaseReactive Nitrogen SpeciesReceptors, Interleukin-1Receptors, Interleukin-8BToll-Like ReceptorsTyrosine

Identifiers

PMID24967596
PMCPMC4072692
OpenAlexW2035647297

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.