Evidence map›Paper›PMID 26919641›Full record

ArticleMicrobiologyOpen2016

The Caenorhabditis elegans p38 MAPK Gene plays a key role in protection from mycobacteria.

Thushara Galbadage, Tonya F Shepherd, Suat L G Cirillo, Tina L Gumienny, Jeffrey D Cirillo

Open access · goldAbstract read
In one paragraph

Article in MicrobiologyOpen, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Frontiers in tuberculosis · 2025
    Review
  3. Review
  4. Article
  5. Review
  6. Structure and biological evaluation ofAdvances in redox research · 2022
    Article
  7. The p38 MAPK/PMK-1 Pathway Is Required for Resistance toPathogens (Basel, Switzerland) · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Global Proteomics RevealedFrontiers in cellular and infection microbiology · 2017
    Article
  15. 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

5 authors at 3 institutions in 1 country.

Thushara GalbadageDepartments of Microbial Pathogenesis and Immunology, Texas A&M Health Science Center, Bryan, Texas, 77807-3260.
Tonya F ShepherdDepartments of Microbial Pathogenesis and Immunology, Texas A&M Health Science Center, Bryan, Texas, 77807-3260.
Suat L G CirilloDepartments of Microbial Pathogenesis and Immunology, Texas A&M Health Science Center, Bryan, Texas, 77807-3260.
Tina L GumiennyDepartment of Biology, Texas Woman's University, Denton, Texas, 76204-5799.
Jeffrey D CirilloDepartments of Microbial Pathogenesis and Immunology, Texas A&M Health Science Center, Bryan, Texas, 77807-3260.
Texas A&M Health Science Center · USTexas A&M Health Science Center · USTexas Woman's University · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
Application of Imaging to Development of Tuberculosis InterventionsR01AI104960 · NIAID · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CIRILLO, JEFFREY D. · 2014 to 2018
$1.9M
Molecular Mechanisms Regulating Intercellular Transit of TGF-betaR01GM097591 · NIGMS · TEXAS WOMAN'S UNIVERSITY · PI GUMIENNY, TINA L · 2011 to 2015
$1.0M
NIAID NIH HHS R01 AI104960NIGMS NIH HHS R01 GM097591NIH HHS P40 OD010440
6 · The paper itself

Abstract

Mitogen-activated protein kinases (MAPK) are critical mediators of cellular responses to pathogens and are activated in response to infection, but investigation is difficult in multi-cell hosts due to developmental lethality of mutations. Mycobacterium marinum (Mm) is an established model for tuberculosis, a disease afflicting nearly one-third of the world's population. We found that Mm-infected Caenorhabditis elegans display >80% mortality, but nonpathogenic M. smegmatis cause <15% mortality. C. elegans display pathological changes when infected with Mm, whereas Mm mutants produce lower mortality, suggesting that C. elegans is a promising virulence model for detailed genetic analysis. C. elegans MAPK mutants are hypersusceptible to mycobacterial infection; however, the C. elegans TOL-like, TGF-β and insulin-like pathway genes do not play important roles in susceptibility. We show that pathogenic mycobacteria inhibit MAPK-mediated protection through the MAPK phosphatase gene and demonstrate that C. elegans provide a genetically tractable pathogenicity model of both the host and pathogen.

Indexed as

AnimalsBacterial LoadCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA-Binding ProteinsDual-Specificity PhosphatasesForkhead Transcription FactorsIntestinesMitogen-Activated Protein KinasesMycobacterium marinumMycobacterium smegmatisNerve Tissue ProteinsNeuropeptidesp38 Mitogen-Activated Protein KinasesRNA InterferenceRNA, Small InterferingCaenorhabditis elegans Proteinsdaf-16 protein, C elegansDbl-1 protein, C elegansDNA-Binding ProteinsDual-Specificity PhosphatasesForkhead Transcription FactorsMitogen-Activated Protein KinasesNerve Tissue ProteinsNeuropeptidesp38 Mitogen-Activated Protein KinasesPmk-1 protein, C elegansRNA, Small Interferingskn-1 protein, C elegansTol-1 protein, C elegansTranscription FactorsTransforming Growth Factor betaVHP-1 protein, C elegansC. elegansinnate immunityMycobacterium

Identifiers

PMID26919641
PMCPMC4905996
OpenAlexW2280866505

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.