Evidence map›Paper›PMID 25675292›Full record

ArticleCell death & disease2015

Induction of eosinophil apoptosis by hydrogen peroxide promotes the resolution of allergic inflammation.

A C Reis, A L Alessandri, R M Athayde, D A Perez, J P Vago, T V Ávila, T P T Ferreira, A C S de Arantes, D de Sá Coutinho, M A Rachid and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Different bacterial cargo in apoptotic cells drive distinct macrophage phenotypes.Apoptosis : an international journal on programmed cell death · 2024
    Article
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  14. Redistribution of EC-SOD resolves bleomycin-induced inflammationFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  15. Article
  16. Review
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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

16 authors at 4 institutions in 2 countries.

A C Reis1] Laboratório de Resolução da Resposta Inflamatória, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil [2] Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
A L AlessandriMedical Research Council Centre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, Scotland, UK.
R M Athayde1] Laboratório de Resolução da Resposta Inflamatória, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil [2] Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
D A Perez1] Laboratório de Resolução da Resposta Inflamatória, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil [2] Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
J P VagoLaboratório de Sinalização na Inflamação, Departamento de Análises Clínicas e Toxicológicas, Faculdade de Farmácia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
T V ÁvilaDepartamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
T P T FerreiraLaboratório de Inflamação, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
A C S de ArantesLaboratório de Inflamação, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
D de Sá CoutinhoLaboratório de Inflamação, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
M A RachidLaboratório de Patologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
L P SousaLaboratório de Sinalização na Inflamação, Departamento de Análises Clínicas e Toxicológicas, Faculdade de Farmácia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
M A MartinsLaboratório de Inflamação, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
G B MenezesLaboratório de Resolução da Resposta Inflamatória, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
A G RossiMedical Research Council Centre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, Scotland, UK.
M M TeixeiraLaboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
V Pinho1] Laboratório de Resolução da Resposta Inflamatória, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil [2] Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Universidade Federal de Minas Gerais · BRFundação Oswaldo Cruz · BRCentre for Inflammation Research · GBUniversity of Edinburgh · GB

Funding

Chief Scientist Office ETM/86Medical Research Council G0601481Medical Research Council MR/K013386/1
6 · The paper itself

Abstract

Eosinophils are effector cells that have an important role in the pathogenesis of allergic disease. Defective removal of these cells likely leads to chronic inflammatory diseases such as asthma. Thus, there is great interest in understanding the mechanisms responsible for the elimination of eosinophils from inflammatory sites. Previous studies have demonstrated a role for certain mediators and molecular pathways responsible for the survival and death of leukocytes at sites of inflammation. Reactive oxygen species have been described as proinflammatory mediators but their role in the resolution phase of inflammation is poorly understood. The aim of this study was to investigate the effect of reactive oxygen species in the resolution of allergic inflammatory responses. An eosinophilic cell line (Eol-1) was treated with hydrogen peroxide and apoptosis was measured. Allergic inflammation was induced in ovalbumin sensitized and challenged mouse models and reactive oxygen species were administered at the peak of inflammatory cell infiltrate. Inflammatory cell numbers, cytokine and chemokine levels, mucus production, inflammatory cell apoptosis and peribronchiolar matrix deposition was quantified in the lungs. Resistance and elastance were measured at baseline and after aerosolized methacholine. Hydrogen peroxide accelerates resolution of airway inflammation by induction of caspase-dependent apoptosis of eosinophils and decrease remodeling, mucus deposition, inflammatory cytokine production and airway hyperreactivity. Moreover, the inhibition of reactive oxygen species production by apocynin or in gp91(phox-/-) mice prolonged the inflammatory response. Hydrogen peroxide induces Eol-1 apoptosis in vitro and enhances the resolution of inflammation and improves lung function in vivo by inducing caspase-dependent apoptosis of eosinophils.

Indexed as

AnimalsApoptosisAsthmaBlotting, WesternCell LineEosinophilsHumansHydrogen PeroxideInflammationLeukocytesLungMaleMiceMice, Inbred C57BLPleurisyReactive Oxygen SpeciesHydrogen PeroxideReactive Oxygen Species

Identifiers

PMID25675292
PMCPMC4669804
OpenAlexW1966652499

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.