Evidence map›Paper›PMID 30629626›Full record

ArticlePloS one2019

Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model.

Juliana Tiyaki Ito, Daniela Aparecida de Brito Cervilha, Juliana Dias Lourenço, Natália Gomes Gonçalves, Rildo Aparecido Volpini, Elia Garcia Caldini, Gilles Landman, Chin Jia Lin, Ana Paula Pereira Velosa, Walcy Paganelli Rosolia Teodoro and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  11. Reduced frequencies of Foxp3Respiratory research · 2022
    Article
  12. Psoriasis and Systemic Inflammatory Disorders.International journal of molecular sciences · 2022
    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

15 authors at 2 institutions in 1 country.

Juliana Tiyaki ItoDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.ORCID 0000-0002-9438-5292
Daniela Aparecida de Brito CervilhaDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Juliana Dias LourençoDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Natália Gomes GonçalvesDepartment of Pathology, Laboratory of Molecular Pathology, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Rildo Aparecido VolpiniDepartment of Clinical Medicine, Basic Research Laboratory on Kidney Diseases, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Elia Garcia CaldiniDepartment of Pathology, Laboratory of Cell Biology, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Gilles LandmanDepartment of Pathology, Multi-purpose Laboratory of Molecular Pathology, Federal University of São Paulo, São Paulo, Brazil.
Chin Jia LinDepartment of Pathology, Laboratory of Molecular Pathology, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Ana Paula Pereira VelosaDepartment of Clinical Medicine, Laboratory of Extracellular Matrix, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Walcy Paganelli Rosolia TeodoroDepartment of Clinical Medicine, Laboratory of Extracellular Matrix, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Iolanda de Fátima Lopes Calvo TibérioDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Thais MauadDepartment of Pathology, Experimental Air Pollution Laboratory, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Milton de Arruda MartinsDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Mariangela MacchioneDepartment of Pathology, Experimental Air Pollution Laboratory, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Fernanda Degobbi Tenorio Quirino Dos Santos LopesDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Universidade de São Paulo · BRUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe imbalance between pro- and anti-inflammatory immune responses plays a pivotal role in chronic obstructive pulmonary disease (COPD) development and progression. To clarify the pathophysiological mechanisms of this disease, we performed a temporal analysis of immune response-mediated inflammatory progression in a cigarette smoke (CS)-induced mouse model with a focus on the balance between Th17 and Treg responses.

methodsC57BL/6 mice were exposed to CS for 1, 3 or 6 months to induce COPD, and the control groups were maintained under filtered air conditions for the same time intervals. We then performed functional (respiratory mechanics) and structural (alveolar enlargement) analyses. We also quantified the NF-κB, TNF-α, CD4, CD8, CD20, IL-17, IL-6, FOXP3, IL-10, or TGF-β positive cells in peribronchovascular areas and assessed FOXP3 and IL-10 expression through double-label immunofluorescence. Additionally, we evaluated the gene expression of NF-κB and TNF in bronchiolar epithelial cells.

resultsOur CS-induced COPD model exhibited an increased proinflammatory immune response (increased expression of the NF-κB, TNF-α, CD4, CD8, CD20, IL-17, and IL-6 markers) with a concomitantly decreased anti-inflammatory immune response (FOXP3, IL-10, and TGF-β markers) compared with the control mice. These changes in the immune responses were associated with increased alveolar enlargement and impaired lung function starting on the first month and third month of CS exposure, respectively, compared with the control mice.

conclusionOur results showed that the microenvironmental stimuli produced by the release of cytokines during COPD progression lead to a Th17/Treg imbalance.

Indexed as

AnimalsBiomarkersCellular MicroenvironmentCytokinesDisease Models, AnimalDisease ProgressionInflammation MediatorsLungMaleMiceMice, Inbred C57BLPulmonary Disease, Chronic ObstructiveRespiratory MechanicsSmokingTh17 CellsTime FactorsBiomarkersCytokinesInflammation Mediators

Identifiers

PMID30629626
PMCPMC6328193
OpenAlexW2909926438

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.