Evidence map›Paper›PMID 11686879›Full record

ReviewRespiratory research2001

Eotaxin and the attraction of eosinophils to the asthmatic lung.

D M Conroy, T J Williams

Abstract readReview
In one paragraph

Review in Respiratory research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
–field-weighted citation impact
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

94 citing papers in PubMed.

  1. Trial
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  15. Article
  16. Inflammatory Patterns Associated withPathogens (Basel, Switzerland) · 2024
    Article
  17. Review
  18. Article
  19. Article
  20. Review

34 more citing papers are in PubMed but not listed here.

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.

D M ConroyLeukocyte Biology Section, Biomedical Sciences Division, Imperial College School of Medicine, London, UK. d.conroy@ic.ac.uk
T J Williams

Funding

Wellcome Trust
6 · The paper itself

Abstract

Eosinophilic leukocytes accumulate in high numbers in the lungs of asthmatic patients, and are believed to be important in the pathogenesis of asthma. A potent eosinophil chemoattractant is produced in the asthmatic lung. This small protein, the chemokine eotaxin, is synthesized by a number of different cell types, and is stimulated by interleukin-4 and interleukin-13, which are produced by T-helper (Th)2 lymphocytes. Low molecular weight compounds have been developed that can block the eotaxin receptor C-C chemokine receptor (CCR)3, and prevent stimulation by eotaxin. This provides the potential for orally available drugs that can prevent eosinophil recruitment into the lung and the associated damage and dysfunction.

Indexed as

AnimalsAsthmaBone MarrowChemokine CCL11Chemokines, CCEosinophilsHumansLungReceptors, CCR3Receptors, ChemokineTh2 CellsCCL11 protein, humanCCR3 protein, humanChemokine CCL11Chemokines, CCReceptors, CCR3Receptors, Chemokine

Identifiers

PMID11686879
PMCPMC2002069

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.