Evidence map›Paper›PMID 21252304›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Gastrin-releasing peptide blockade as a broad-spectrum anti-inflammatory therapy for asthma.

Shutang Zhou, Erin N Potts, Frank Cuttitta, W Michael Foster, Mary E Sunday

RetractedOpen access · greenAbstract readValidation StudyRetracted Publication
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Regulatory Peptides in Asthma.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. ROCK insufficiency attenuates ozone-induced airway hyperresponsiveness in mice.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  11. Article
  12. Article
  13. Review
  14. Neural processing of itch.Neuroscience · 2013
    Review
  15. Article
  16. Gastrin-releasing peptide receptor (GRPR) mediates chemotaxis in neutrophils.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 1 country.

Shutang ZhouDepartment of Pathology, Duke University Medical Center, Durham, NC 27710, USA. shutang.zhou@duke.edu
Erin N Potts
Frank Cuttitta
W Michael Foster
Mary E Sunday
Duke Medical Center · USDuke University · USDuke University Hospital · USNational Cancer Institute · US

Funding

Surfactant Protein-A Regulation of Innate Immunityin AsthmaP01AI081672 · NIAID · DUKE UNIVERSITY · PI SUNDY, JOHN S · 2009 to 2013
$7.4M
Dependency of O-3 Induced Lung Mucus Hypersecretion on NQ01R01ES016347 · NIEHS · DUKE UNIVERSITY · PI FOSTER, W MICHAEL · 2008 to 2010
$1.0M
NIAID NIH HHS AI081672NIAID NIH HHS P01 AI081672NIEHS NIH HHS ES016347NIEHS NIH HHS R01 ES016347
6 · The paper itself

Abstract

Gastrin-releasing peptide (GRP) is synthesized by pulmonary neuroendocrine cells in inflammatory lung diseases, such as bronchopulmonary dysplasia (BPD). Many BPD infants develop asthma, a serious disorder of intermittent airway obstruction. Despite extensive research, early mechanisms of asthma remain controversial. The incidence of asthma is growing, now affecting >300 million people worldwide. To test the hypothesis that GRP mediates asthma, we used two murine models: ozone exposure for air pollution-induced airway hyperreactivity (AHR), and ovalbumin (OVA)-induced allergic airway disease. BALB/c mice were given small molecule GRP blocking agent 77427, or GRP blocking antibody 2A11, before exposure to ozone or OVA challenge. In both models, GRP blockade abrogated AHR and bronchoalveolar lavage (BAL) macrophages and granulocytes, and decreased BAL cytokines implicated in asthma, including those typically derived from Th1 (e.g., IL-2, TNFα), Th2 (e.g., IL-5, IL-13), Th17 (IL-17), macrophages (e.g., MCP-1, IL-1), and neutrophils (KC = IL-8). Dexamethasone generally had smaller effects on all parameters. Macrophages, T cells, and neutrophils express GRP receptor (GRPR). GRP blockade diminished serine phosphorylation of GRPR with ozone or OVA. Thus, GRP mediates AHR and airway inflammation in mice, suggesting that GRP blockade is promising as a broad-spectrum therapeutic approach to treat and/or prevent asthma in humans.

Indexed as

AnimalsAnti-Inflammatory AgentsAsthmaBronchoalveolar Lavage FluidFemaleGastrin-Releasing PeptideImmunohistochemistryMiceMice, Inbred BALB CAnti-Inflammatory AgentsGastrin-Releasing Peptide

Identifiers

PMID21252304
PMCPMC3033299
OpenAlexW1982831232

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.