Evidence map›Paper›PMID 24768603›Full record

Trial reportProstaglandins, leukotrienes, and essential fatty acids2014

Biological effects of leukotriene E4 on eosinophils.

John W Steinke, Julie Negri, Spencer C Payne, Larry Borish

Abstract readClinical Trial
In one paragraph

Trial report in Prostaglandins, leukotrienes, and essential fatty acids, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Trial
  2. Article
  3. Frontiers in aging · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. 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

4 authors at 1 institution in 1 country.

John W SteinkeCarter Immunology Center Asthma and Allergic Disease Center Departments of Medicine, University of Virginia Health Systems, Charlottesville, VA 22908-1355, USA.
Julie NegriCarter Immunology Center Asthma and Allergic Disease Center Departments of Medicine, University of Virginia Health Systems, Charlottesville, VA 22908-1355, USA.
Spencer C PayneCarter Immunology Center Asthma and Allergic Disease Center Departments of Medicine, University of Virginia Health Systems, Charlottesville, VA 22908-1355, USA; Carter Immunology Center Asthma and Allergic Disease Center Departments of Otolaryngology, University of Virginia Health Systems, Charlottesville, VA 22908-1355, USA.
Larry BorishCarter Immunology Center Asthma and Allergic Disease Center Departments of Microbiology, University of Virginia Health Systems, Charlottesville, VA 22908-1355, USA. Electronic address: lb4m@virginia.edu.
University of Virginia Health System · US

Funding

DUST MITE, COCKROACH AND CAT ALLERGENS IN HOUSES/ASTHMAR01AI020565 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI PLATTS-MILLS, THOMAS A. · 1985 to 2017
$7.1M
An Evaluation of Treatment with Omalizumab to Improve the Asthmatic Response to aU01AI100799 · NIAID · UNIVERSITY OF VIRGINIA · PI HEYMANN, PETER W, PLATTS-MILLS, THOMAS A. · 2012 to 2015
$5.3M
Interplay between LTE4/LTE4 receptors and IFN-y with mast cells and eosinophils iR01AI057438 · NIAID · UNIVERSITY OF VIRGINIA · PI BORISH, LARRY C · 2006 to 2015
$3.7M
NIAID NIH HHS AI057438NIAID NIH HHS AI1090413NIAID NIH HHS R01 AI020565NIAID NIH HHS R01 AI057438NIAID NIH HHS U01 AI100799
6 · The paper itself

Abstract

Studies demonstrate the existence of novel receptors for cysteinyl leukotrienes (CysLTs) that are responsive to leukotriene (LT) E4 and might be pathogenic in asthma. Given the eosinophilic infiltration in this disorder, we investigated eosinophil expression of P2Y12 and gpr99 and their capacity to respond to LTE4. Receptor transcript expression was investigated via quantitative PCR and surface protein expression via flow cytometry. We investigated LTE4 influences on eosinophils including Ca(+2) flux, cAMP induction, modulation of adhesion molecule expression, apoptosis and degranulation. Eosinophils displayed both transcript and surface protein expression of P2Y12 and gpr99. We could not find evidence of LTE4 activation of eosinophils, however, LTE4 induced cAMP expression, and preincubation of eosinophils with LTE4 inhibited degranulation. Even though eosinophils are an important source of CysLTs in AERD, eosinophils are not themselves the pro-inflammatory biological target and, in contrast, LTE4 via cAMP primarily elicits anti-inflammatory responses.

Indexed as

ApoptosisCell Adhesion MoleculesCell DegranulationCyclic AMPEosinophilsFemaleFlow CytometryGene Expression RegulationHumansLeukotriene E4MalePolymerase Chain ReactionReceptors, G-Protein-CoupledReceptors, Purinergic P2Receptors, Purinergic P2Y12Cell Adhesion MoleculesCyclic AMPLeukotriene E4OXGR1 protein, humanP2RY12 protein, humanReceptors, G-Protein-CoupledReceptors, Purinergic P2Receptors, Purinergic P2Y12Aspirin-exacerbated respiratory diseaseCalciumcAMPCysteinyl leukotrienesEosinophils

Identifiers

PMID24768603
PMCPMC4127125
OpenAlexW2098373052

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.