Evidence map›Paper›PMID 8551223›Full record

ArticleThe Journal of experimental medicine1996

Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model.

P S Foster, S P Hogan, A J Ramsay, K I Matthaei, I G Young

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 318 papers.

0numbers the graph read from it
0cells of the map it votes in
318citing papers in PubMed
52.3field-weighted citation impact, top 1% 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

318 citing papers in PubMed, 1,370 citations in OpenAlex.

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  14. Impact of TNF and IL-33 Cytokines on Mast Cells in Neuroinflammation.International journal of molecular sciences · 2024
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258 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

P S FosterDivision of Biochemistry and Molecular Biology, John Curtin School of Medical Research, Australian National University, Canberra, Australia.
S P Hogan
A J Ramsay
K I Matthaei
I G Young
Australian National University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airways inflammation is thought to play a central role in the pathogenesis of asthma. However, the precise role that individual inflammatory cells and mediators play in the development of airways hyperreactivity and the morphological changes of the lung during allergic pulmonary inflammation is unknown. In this investigation we have used a mouse model of allergic pulmonary inflammation and interleukin (IL) 5-deficient mice to establish the essential role of this cytokine and eosinophils in the initiation of aeroallergen-induced lung damage and the development of airways hyperreactivity. Sensitization and aerosol challenge of mice with ovalbumin results in airways eosinophilia and extensive lung damage analogous to that seen in asthma. Aeroallergen-challenged mice also display airways hyperreactivity to beta-methacholine. In IL-5-deficient mice, the eosinophilia, lung damage, and airways hyperreactivity normally resulting from aeroallergen challenge were abolished. Reconstitution of IL-5 production with recombinant vaccinia viruses engineered to express this factor completely restored aeroallergen-induced eosinophilia and airways dysfunction. These results indicate that IL-5 and eosinophils are central mediators in the pathogenesis of allergic lung disease.

Indexed as

Disease Models, AnimalAerosolsAnimalsAsthmaBronchoalveolar Lavage FluidBronchoconstrictor AgentsDose-Response Relationship, DrugEosinophiliaInterleukin-5LungMethacholine ChlorideMiceMice, Inbred C57BLOvalbuminRespiratory SystemAerosolsBronchoconstrictor AgentsInterleukin-5Methacholine ChlorideOvalbumin

Identifiers

PMID8551223
PMCPMC2192412
OpenAlexW2140686309

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.