Evidence map›Paper›PMID 19074616›Full record

ReviewThe American journal of pathology2009

Where asthma and hypersensitivity pneumonitis meet and differ: noneosinophilic severe asthma.

Pieter Bogaert, Kurt G Tournoy, Thomas Naessens, Johan Grooten

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-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

19 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. A comprehensive summary of disease variants implicated in metal allergy.Journal of toxicology and environmental health. Part B, Critical reviews · 2022
    Review
  4. Ginger-derived compounds exertExperimental and therapeutic medicine · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Physiological reports · 2017
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Innate immunity and the pathogenicity of inhaled microbial particles.International journal of biological sciences · 2011
    Review
  19. 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

4 authors at 3 institutions in 1 country.

Pieter BogaertDepartment of Molecular Biomedical Research, Ghent University, Ghent, Belgium.
Kurt G Tournoy
Thomas Naessens
Johan Grooten
Vlaams Instituut voor Biotechnologie · BEGhent University · BEGhent University Hospital · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a type-I allergic airway disease characterized by Th(2) cells and IgE. Episodes of bronchial inflammation, eosinophilic in nature and promoting bronchoconstriction, may become chronic and lead to persistent respiratory symptoms and irreversible structural airway changes. Representative mostly of mild to moderate asthma, this clinical definition fails to account for the atypical and often more severe phenotype found in a considerable proportion of asthmatics who have increased neutrophil cell counts in the airways as a distinguishing trait. Neutrophilic inflammation is a hallmark of another type of allergic airway pathology, hypersensitivity pneumonitis. Considered as an immune counterpart of asthma, hypersensitivity pneumonitis is a prototypical type-III allergic inflammatory reaction involving the alveoli and lung interstitium, steered by Th(1) cells and IgG and, in its chronic form, accompanied by fibrosis. Although pathologically very different and commonly approached as separate disorders, as discussed in this review, clinical studies as well as data from animal models reveal undeniable parallels between both airway diseases. Danger signaling elicited by the allergenic agent or by accompanying microbial patterns emerges as critical in enabling immune sensitization and in determining the type of sensitization and ensuing allergic disease. On this basis, we propose that asthma allergens cause severe noneosinophilic asthma because of sensitization in the presence of hypersensitivity pneumonitis-promoting danger signaling.

Indexed as

Alveolitis, Extrinsic AllergicAnimalsAsthmaEosinophilsHumansInflammation

Identifiers

PMID19074616
PMCPMC2631313
OpenAlexW129386045

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.