Evidence map›Paper›PMID 25058417›Full record

ArticlePloS one2014

Mycoplasma pneumoniae CARDS toxin exacerbates ovalbumin-induced asthma-like inflammation in BALB/c mice.

Jorge L Medina, Jacqueline J Coalson, Edward G Brooks, Claude Jourdan Le Saux, Vicki T Winter, Adriana Chaparro, Molly F R Principe, Laura Solis, T R Kannan, Joel B Baseman and 1 more

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Immune dysregulation inFrontiers in immunology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Frontiers in immunology · 2021
    Article
  13. Review
  14. Current perspectives on atypical pneumonia in children.Clinical and experimental pediatrics · 2020
    Article
  15. Article
  16. TheBioscience reports · 2019
    Article
  17. Journal of clinical medicine research · 2018
    Review
  18. Review
  19. Article
  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

11 authors at 1 institution in 1 country.

Jorge L MedinaDepartment of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America; Center for Airway Inflammation Research, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Jacqueline J CoalsonDepartment of Pathology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Edward G BrooksDepartment of Pediatrics, Division of Allergy and Infectious Diseases, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America; Center for Airway Inflammation Research, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Claude Jourdan Le SauxDepartment of Medicine, Division of Cardiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Vicki T WinterDepartment of Pathology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Adriana ChaparroDepartment of Pediatrics, Division of Allergy and Infectious Diseases, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America; Center for Airway Inflammation Research, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Molly F R PrincipeDepartment of Pediatrics, Division of Allergy and Infectious Diseases, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Laura SolisDepartment of Medicine, Division of Cardiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
T R KannanDepartment of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America; Center for Airway Inflammation Research, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Joel B BasemanDepartment of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America; Center for Airway Inflammation Research, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Peter H DubeDepartment of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America; Center for Airway Inflammation Research, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
The University of Texas Health Science Center at San Antonio · US

Funding

The role of CARDS toxin in genesis and exacerbation of allergic inflammationU19AI070412 · NIAID · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BASEMAN, JOEL BARRY · 2006 to 2015
$19.7M
NIAID NIH HHS NIH AI 070412NIAID NIH HHS U19 AI070412
6 · The paper itself

Abstract

Mycoplasma pneumoniae causes a range of airway and extrapulmonary pathologies in humans. Clinically, M. pneumoniae is associated with acute exacerbations of human asthma and a worsening of experimentally induced asthma in mice. Recently, we demonstrated that Community Acquired Respiratory Distress Syndrome (CARDS) toxin, an ADP-ribosylating and vacuolating toxin synthesized by M. pneumoniae, is sufficient to induce an asthma-like disease in BALB/cJ mice. To test the potential of CARDS toxin to exacerbate preexisting asthma, we examined inflammatory responses to recombinant CARDS toxin in an ovalbumin (OVA) murine model of asthma. Differences in pulmonary inflammatory responses between treatment groups were analyzed by histology, cell differentials and changes in cytokine and chemokine concentrations. Additionally, assessments of airway hyperreactivity were evaluated through direct pulmonary function measurements. Analysis of histology revealed exaggerated cellular inflammation with a strong eosinophilic component in the CARDS toxin-treated group. Heightened T-helper type-2 inflammatory responses were evidenced by increased expression of IL-4, IL-13, CCL17 and CCL22 corresponding with increased airway hyperreactivity in the CARDS toxin-treated mice. These data demonstrate that CARDS toxin can be a causal factor in the worsening of experimental allergic asthma, highlighting the potential importance of CARDS toxin in the etiology and exacerbation of human asthma.

Indexed as

AnimalsAsthmaBacterial ProteinsBacterial ToxinsBronchial HyperreactivityBronchoalveolar Lavage FluidChemokine CCL17Chemokine CCL22EosinophilsHumansInflammationInterleukin-13Interleukin-4MiceMice, Inbred BALB COvalbuminBacterial ProteinsBacterial ToxinsCARDS toxin, Mycoplasma pneumoniaeCcl17 protein, mouseCcl22 protein, mouseChemokine CCL17Chemokine CCL22Interleukin-13Interleukin-4OvalbuminRecombinant Proteins

Identifiers

PMID25058417
PMCPMC4109942
OpenAlexW2154347724

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.