Evidence map›Paper›PMID 29451705›Full record

ReviewJournal of leukocyte biology2018

Modeling asthma: Pitfalls, promises, and the road ahead.

Helene F Rosenberg, Kirk M Druey

Open access · greenAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. The Enigma of Eosinophil Degranulation.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. ImmunoHorizons · 2019
    Article
  15. T cells in severe childhood asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019
    Review
  16. 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

2 authors at 1 institution in 1 country.

Helene F RosenbergInflammation Immunobiology Section and Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Kirk M DrueyMolecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
National Institutes of Health · US

Funding

Eosinophils, Inflammation and ImmunityZIAAI000941 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI ROSENBERG, HELENE · 2009 to 2020
$8.0M
Inflammation and Therapy for Respiratory Virus InfectionZIAAI000943 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI ROSENBERG, HELENE · 2009 to 2020
$7.4M
Regulation of Normal and Asthmatic Lung Function by G-Protein-Coupled ReceptorsZIAAI000939 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DRUEY, KIRK M · 2009 to 2025
$7.3M
Biology of the Eosinophilic LeukocyteZ01AI000941 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI ROSENBERG, HELENE · 2004 to 2008
$1.6M
Ribonucleases A in Health and DiseaseZIAAI000942 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI ROSENBERG, HELENE · 2009 to 2018
$1.5M
Regulation of Normal and Asthmatic Lung Function by G-Protein-Coupled ReceptorsZ01AI000939 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DRUEY, KIRK M · 2004 to 2008
$832k
Intramural NIH HHS Z01 AI000939Intramural NIH HHS Z01 AI000941Intramural NIH HHS ZIA AI000941
6 · The paper itself

Abstract

Asthma is a chronic, heterogeneous, and recurring inflammatory disease of the lower airways, with exacerbations that feature airway inflammation and bronchial hyperresponsiveness. Asthma has been modeled extensively via disease induction in both wild-type and genetically manipulated laboratory mice (Mus musculus). Antigen sensitization and challenge strategies have reproduced numerous important features of airway inflammation characteristic of human asthma, notably the critical roles of type 2 T helper cell cytokines. Recent models of disease induction have advanced to include physiologic aeroallergens with prolonged respiratory challenge without systemic sensitization; others incorporate tobacco, respiratory viruses, or bacteria as exacerbants. Nonetheless, differences in lung size, structure, and physiologic responses limit the degree to which airway dynamics measured in mice can be compared to human subjects. Other rodent allergic airways models, including those featuring the guinea pig (Cavia porcellus) might be considered for lung function studies. Finally, domestic cats (Feline catus) and horses (Equus caballus) develop spontaneous obstructive airway disorders with clinical and pathologic features that parallel human asthma. Information on pathogenesis and treatment of these disorders is an important resource.

Indexed as

AsthmaDisease Models, AnimalAnimalsHumansairwayseosinophilsinflammationleukocytesveterinary

Identifiers

PMID29451705
PMCPMC6134392
OpenAlexW2793544174

What OpenQuestion holds

Textmetadata
LicenceTDM
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.