Evidence map›Paper›PMID 12657158›Full record

ArticleRespiratory research2003

Dissociation by steroids of eosinophilic inflammation from airway hyperresponsiveness in murine airways.

Mark A Birrell, Cliff H Battram, Paul Woodman, Kerryn McCluskie, Maria G Belvisi

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2003. 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
1.1field-weighted citation impact, top 23% 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, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Corticosteroid insensitivity persists in the absence of STAT1 signaling in severe allergic airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2021
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  9. Wogonin induces eosinophil apoptosis and attenuates allergic airway inflammation.American journal of respiratory and critical care medicine · 2015
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  12. Review
  13. Cytochrome c oxidase subunit 4 isoform 2-knockout mice show reduced enzyme activity, airway hyporeactivity, and lung pathology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
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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.

Mark A BirrellImperial College School of Medicine, London, UK.
Cliff H Battram
Paul Woodman
Kerryn McCluskie
Maria G Belvisi
Imperial College London · GBBayer (United Kingdom) · GBEast Sussex County Council · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe link between eosinophils and the development of airway hyperresponsiveness (AHR) in asthma is still controversial. This question was assessed in a murine model of asthma in which we performed a dose ranging study to establish whether the dose of steroid needed to inhibit the eosinophil infiltration correlated with that needed to block AHR.

methodsThe sensitised BALB/c mice were dosed with vehicle or dexamethasone (0.01-3 mg/kg) 2 hours before and 6 hours after each challenge (once daily for 6 days) and 2 hours before AHR determination by whole-body plethysmography. At 30 minutes after the AHR to aerosolised methacholine the mice were lavaged and differential white cell counts were determined. Challenging with antigen caused a significant increase in eosinophils in the bronchoalveolar lavage (BAL) fluid and lung tissue, and increased AHR.

resultsDexamethasone reduced BAL and lung tissue eosinophilia (ED50 values of 0.06 and 0.08 mg/kg, respectively), whereas a higher dose was needed to block AHR (ED50 of 0.32 mg/kg at 3 mg/ml methacholine. Dissociation was observed between the dose of steroid needed to affect AHR in comparison with eosinophilia and suggests that AHR is not a direct consequence of eosinophilia.

conclusionThis novel pharmacological approach has revealed a clear dissociation between eosinophilia and AHR by using steroids that are the mainstay of asthma therapy. These data suggest that eosinophilia is not associated with AHR and questions the rationale that many pharmaceutical companies are adopting in developing low-molecular-mass compounds that target eosinophil activation/recruitment for the treatment of asthma.

Indexed as

Administration, InhalationAnimalsAnti-Inflammatory AgentsAsthmaBronchial HyperreactivityBronchoalveolar Lavage FluidBronchoconstrictor AgentsDexamethasoneDose-Response Relationship, DrugEosinophiliaImmunizationLungMaleMethacholine ChlorideMiceMice, Inbred BALB CAnti-Inflammatory AgentsBronchoconstrictor AgentsDexamethasoneMethacholine ChlorideOvalbumin

Identifiers

PMID12657158
PMCPMC152648
OpenAlexW2165663169

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.