Evidence map›Paper›PMID 38598121›Full record

ArticleMolecular biology reports2024

Aerobic physical training reduces severe asthma phenotype involving kinins pathway.

Maysa Alves Rodrigues Brandao-Rangel, Renilson Moraes-Ferreira, Anamei Silva-Reis, Victor Hugo Souza-Palmeira, Francine Maria Almeida, Fabiana Regina da Silva Olimpio, Carlos Rocha Oliveira, Nilsa Regina Damaceno-Rodrigues, João Bosco Pesquero, Leonardo Martin and 4 more

Abstract read
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In one paragraph

Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

14 authors at 5 institutions in 3 countries.

Maysa Alves Rodrigues Brandao-RangelPost-graduate Program in Sciences of Human Movement and Rehabilitation, Federal University of São Paulo (UNIFESP), Avenida Ana Costa 95, Santos, SP, 11060-001, Brazil.
Renilson Moraes-FerreiraPost-graduate Program in Sciences of Human Movement and Rehabilitation, Federal University of São Paulo (UNIFESP), Avenida Ana Costa 95, Santos, SP, 11060-001, Brazil.
Anamei Silva-ReisPost-graduate Program in Sciences of Human Movement and Rehabilitation, Federal University of São Paulo (UNIFESP), Avenida Ana Costa 95, Santos, SP, 11060-001, Brazil.
Victor Hugo Souza-PalmeiraPost-graduate Program in Sciences of Human Movement and Rehabilitation, Federal University of São Paulo (UNIFESP), Avenida Ana Costa 95, Santos, SP, 11060-001, Brazil.
Francine Maria AlmeidaLaboratory of Experimental Therapeutic (LIM 20), School of Medicine, University of São Paulo, Avenida Doutor Arnaldo 455, São Paulo, SP, 01246-903, Brazil.
Fabiana Regina da Silva OlimpioPost-graduate Program in Translational Medicine, Department of Medicine, Federal University of São Paulo (UNIFESP), Rua Pedro De Toledo 720, 2º Andar, São Paulo, SP, 04039-002, Brazil.
Carlos Rocha OliveiraSchool of Medicine, Anhembi Morumbi University, Avenida Deputado Benedito Matarazzo 6070, São José dos Campos, SP, 12230-002, Brazil.
Nilsa Regina Damaceno-RodriguesLaboratory of Cellular Biology (LIM 59 HCFMUSP), School of Medicine, University of São Paulo, Avenida Doutor Arnaldo 455, São Paulo, SP, 01246-903, Brazil.
João Bosco PesqueroDepartment of Biophysics, Federal University of São Paulo (UNIFESP), Rua Botucatu 740, São Paulo, SP, 04023-062, Brazil.
Leonardo MartinDepartment of Biophysics, Federal University of São Paulo (UNIFESP), Rua Botucatu 740, São Paulo, SP, 04023-062, Brazil.
Flavio AimbirePost-graduate Program in Translational Medicine, Department of Medicine, Federal University of São Paulo (UNIFESP), Rua Pedro De Toledo 720, 2º Andar, São Paulo, SP, 04039-002, Brazil.
Regiane AlbertiniPost-graduate Program in Sciences of Human Movement and Rehabilitation, Federal University of São Paulo (UNIFESP), Avenida Ana Costa 95, Santos, SP, 11060-001, Brazil.
Sara Socorro FariaPost-graduate Programs in Humam Movement and Rehabilitation and in Pharmaceutical Sciences, Evangelical University of Goias (UniEvavngelica), Avenida Universitária Km3,5, Anápolis, GO, 75083-515, Brazil.
Rodolfo P VieiraPost-graduate Program in Sciences of Human Movement and Rehabilitation, Federal University of São Paulo (UNIFESP), Avenida Ana Costa 95, Santos, SP, 11060-001, Brazil. rodrelena@yahoo.com.br.
Universidade Federal de São Paulo · BRUniversidade de São Paulo · BRUniversidade Evangelica de Goiás · BRAnhembi Morumbi University · BRInstitute for Medical Biology · PL

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo #2012/15165-2Fundação de Amparo à Pesquisa do Estado de São Paulo #2019/05739-0Fundação de Amparo à Pesquisa do Estado de São Paulo #2019/11008-9Fundação de Amparo à Pesquisa do Estado de São Paulo #2019/11244-4Fundação de Amparo à Pesquisa do Estado de São Paulo #2020/03994-0
6 · The paper itself

Abstract

introductionAerobic physical training (APT) reduces eosinophilic airway inflammation, but its effects and mechanisms in severe asthma remain unknown.

methodsAn in vitro study employing key cells involved in the pathogenesis of severe asthma, such as freshly isolated human eosinophils, neutrophils, and bronchial epithelial cell lineage (BEAS-2B) and lung fibroblasts (MRC-5 cells), was conducted. Additionally, an in vivo study using male C57Bl/6 mice, including Control (Co; n = 10), Trained (Exe; n = 10), house dust mite (HDM; n = 10), and HDM + Trained (HDM + Exe; n = 10) groups, was carried out, with APT performed at moderate intensity, 5x/week, for 4 weeks.

resultsHDM and bradykinin, either alone or in combination, induced hyperactivation in human neutrophils, eosinophils, BEAS-2B, and MRC-5 cells. In contrast, IL-10, the primary anti-inflammatory molecule released during APT, inhibited these inflammatory effects, as evidenced by the suppression of numerous cytokines and reduced mRNA expression of the B1 receptor and ACE-2. The in vivo study demonstrated that APT decreased bronchoalveolar lavage levels of bradykinin, IL-1β, IL-4, IL-5, IL-17, IL-33, TNF-α, and IL-13, while increasing levels of IL-10, klotho, and IL-1RA. APT reduced the accumulation of polymorphonuclear cells, lymphocytes, and macrophages in the peribronchial space, as well as collagen fiber accumulation, epithelial thickness, and mucus accumulation. Furthermore, APT lowered the expression of the B1 receptor and ACE-2 in lung tissue and reduced bradykinin levels in the lung tissue homogenate compared to the HDM group. It also improved airway resistance, tissue resistance, and tissue damping. On a systemic level, APT reduced total leukocytes, eosinophils, neutrophils, basophils, lymphocytes, and monocytes in the blood, as well as plasma levels of IL-1β, IL-4, IL-5, IL-17, TNF-α, and IL-33, while elevating the levels of IL-10 and IL-1RA.

conclusionThese findings indicate that APT inhibits the severe asthma phenotype by targeting kinin signaling.

Indexed as

AsthmaBradykininAnimalsHumansInterleukin-10Interleukin-17Interleukin 1 Receptor Antagonist ProteinInterleukin-33Interleukin-4Interleukin-5MaleMiceTumor Necrosis Factor-alphaBradykininInterleukin-10Interleukin-17Interleukin 1 Receptor Antagonist ProteinInterleukin-33Interleukin-4Interleukin-5Tumor Necrosis Factor-alphaBradykininExercise immunologyPulmonary rehabilitationSevere asthmaSTAT signaling

Identifiers

PMID38598121
OpenAlexW4394692297

What OpenQuestion holds

Textmetadata
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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.