Evidence map›Paper›PMID 22871757›Full record

ArticleChest2012

Cysteinyl leukotriene 1 receptor expression associated with bronchial inflammation in severe exacerbations of COPD.

Jie Zhu, Venkata Bandi, Shengyang Qiu, David J Figueroa, Jilly F Evans, Neil Barnes, Kay K Guntupalli, Peter K Jeffery

Open access · bronzeAbstract read
In one paragraph

Article in Chest, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Baicalin Ameliorates Radiation-Induced Lung Injury by Inhibiting the CysLTs/CysLT1 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. 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

8 authors at 5 institutions in 2 countries.

Jie ZhuLung Pathology Unit, Department of Respiratory Medicine, Imperial College London, London, England.
Venkata BandiDepartment of Medicine, Baylor College of Medicine, Ben Taub General Hospital, Houston, TX.
Shengyang QiuLung Pathology Unit, Department of Respiratory Medicine, Imperial College London, London, England.
David J FigueroaDepartment of Pharmacology, Merck & Co Inc, West Point, PA.
Jilly F EvansDepartment of Pharmacology, Merck & Co Inc, West Point, PA.
Neil BarnesDepartment of Respiratory Medicine, Barts and The London Hospital, London, England.
Kay K GuntupalliDepartment of Medicine, Baylor College of Medicine, Ben Taub General Hospital, Houston, TX.
Peter K JefferyLung Pathology Unit, Department of Respiratory Medicine, Imperial College London, London, England. Electronic address: p.jeffery@imperial.ac.uk.
Imperial College London · GBUnited States Military Academy · USBaylor College of Medicine · USBen Taub Hospital · USRoyal London Hospital · GB

Funding

RESPIRATORY PATHOGENS RESEARCH UNIT-266965298N01AI065298 · NIAID · BAYLOR COLLEGE OF MEDICINE · 1996 to 2003
$0k
NIAID NIH HHS N01 AI065298
6 · The paper itself

Abstract

backgroundCysteinyl leukotriene 1 (CysLT1) receptor expression is known to be increased in the airway mucosa of patients with asthma, especially during exacerbations; however, nothing is known of its expression in COPD.

methodsWe applied immunohistochemistry and in situ hybridization to endobronchial biopsies to determine inflammatory cell CysLT1 receptor protein and mRNA expression in the following: (1) 15 nonsmoker control subjects (NSC), (2) 16 smokers with moderate to severe COPD in its stable phase (S-COPD), and (3) 15 smokers with COPD hospitalized for a severe exacerbation (SE-COPD).

resultsThe total number of bronchial mucosal inflammatory cells (CD45+) and those expressing CysLT1 receptor protein were significantly greater in SE-COPD (CysLT1 receptor protein: median [range] = 139 [31-634]) as compared with S-COPD (32 [6-114]) or NSC (16 [4-66]) (P < .001 for both). CysLT1 receptor gene expression showed similar differences. A greater proportion of CD451 cells expressed CysLT1 receptor protein in SE-COPD (median [range] = 22% [8-81]) compared with S-COPD (10% [4-32]) (P < .03) or NSC (7% [1-19]) (P < .002). In SE-COPD, the relative frequencies of CysLT1 receptor-expressing cells were as follows: tryptase1 mast cells > CD681 monocytes/macrophage > neutrophils > CD201 B lymphocytes = EG21 eosinophils. Moreover, there were positive correlations between the numbers of cells expressing CysLT1 receptor protein and the numbers of CD451 cells (r = 0.78; P < .003) and tryptase1 mast cells (r = 0.62; P < .02).

conclusionsBronchial mucosal CysLT1 receptor-positive inflammatory cells are present in the bronchial mucosa in COPD in greatest number in those experiencing a severe exacerbation.

Indexed as

AdultAgedBronchiCase-Control StudiesCohort StudiesFemaleHumansMaleMiddle AgedPulmonary Disease, Chronic ObstructiveReceptors, LeukotrieneRespiratory MucosaRNA, MessengerSmokingleukotriene D4 receptorReceptors, LeukotrieneRNA, Messenger

Identifiers

PMID22871757
PMCPMC3425162
OpenAlexW2011071012

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.