The role of physical training in the pulmonary pro and anti-fibrotic responses of asthmatic individuals

• Grant number: 19/11008-9
• Support Opportunities: Scholarships in Brazil - Master
• Effective date (Start): October 01, 2019
• Effective date (End): August 31, 2021
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal Investigator: Rodolfo de Paula Vieira
• Grantee: Renilson Moraes Ferreira
• Host Institution: Instituto de Saúde e Sociedade (ISS). Universidade Federal de São Paulo (UNIFESP). Campus Baixada Santista. Santos , SP, Brazil

Abstract

Asthma is a bronchial chronic inflammatory disease, which limits the practice of physical activity and results in worsening of the quality of life of the patient. In addition, one of the main components of the asthma is the bronchial remodeling, which is featured by hypertrophy and hyperplasia of the epithelium and of the bronchial smooth muscle, and accumulation of extracellular matrix proteins in the bronchial wall. The bronchial remodeling results in a progressive bronchoconstriction which can be reflected in the reduction of pulmonary function parameters, such as VEF1, VEF1/CVF e FEF25%-75%. However, these parameters of the pulmonary function test (spirometry), often does not adequately reflect the degree of remodeling of the bronchi. In this sense, the measurement of pulmonary mechanics using impulse oscillometry has become a method that more precisely reflects the resistance of the respiratory system as a whole (R5Hz), of the central airways (R20Hz) and of the lower airways (R5Hz - R20Hz). Experimental studies in mice have shown that aerobic physical training (TFA) is able to inhibit both the development of remodeling as well as reverse remodeling in experimental models of asthma. Thus, the present study aims to investigate whether TFA is able to inhibits and / or reverse functional bronchial remodeling, assessed by impulse oscillometry, in patients with persistent mild, moderate and severe asthma. In addition, the possible effects of TFA on the levels of pro-fibrotic (VEGF, TGF-beta, IGF-1) and anti-fibrotic mediators (Relaxin 1, Relaxin 3 and Klotho) in the lungs (through the measurement in breath condensed air) and also systemically (through the measurement in the serum) will be performed. For this, asthmatic patients classified as mild (n = 25), moderate (n = 25) and severe (n = 25) persistent asthma and non-asthmatic individuals (control; n = 25) will be recruited and evaluated before and after 12 weeks of TFA. In addition to pulmonary function (spirometry) pre and post bronchodilator (CVF, VEF1, VEF1/CVF, FEF25-75%, FEF85%, VEF3, VEF6), the analysis of pulmonary mechanics by impulse oscillometry will be performed to evaluate the resistance and elastance of the respiratory system and of the airways and peripheral pulmonary tissue (R5Hz, R20Hz, R5hz - R20Hz, Z5Hz, X5Hz e resonant frequency (Fres). Finally, pulmonary (induced sputum) and systemic inflammation (whole blood count) and quality of life of these patients will also be evaluated. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

RODRIGUES BRANDAO-RANGEL, MAYSA ALVES; MORAES-FERREIRA, RENILSON; OLIVEIRA-JUNIOR, MANOEL CARNEIRO; SANTOS-DIAS, ALANA; LACERDA BACHI, ANDRE LUIS; GABRIELA-PEREIRA, GIOVANA; FREITAS, SIMONE DE OLIVEIRA; ARAUJO-ROSA, AMANDA CRISTINA; FRANCO OLIVEIRA, LUIS VICENTE; FRISON, CLAUDIO RICARDO; et al. Pulmonary function changes in older adults with and without metabolic syndrome. SCIENTIFIC REPORTS, v. 11, n. 1, AUG 30 2021. (12/15165-2, 19/05739-0, 19/11008-9)

EL-MAFARJEH, ELIAS; MARTINS, GISELE HENRIQUE CARDOSO; PROBST, JESSICA JORGE; SANTOS-DIAS, ALANA; OLIVEIRA-JUNIOR, MANOEL CARNEIRO; DE BARROS, MARCELO PAES; DE OLIVEIRA, LUIS VICENTE FRANCO; DE ANDRADE, LEANDRO DAMAS; DA PALMA, RENATA KELLY; MORAES-FERREIRA, RENILSON; et al. Exercise Improves Lung Inflammation, but Not Lung Remodeling and Mechanics in a Model of Bleomycin-Induced Lung Fibrosis. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, v. 2020, OCT 17 2020. (19/14115-0, 17/06032-2, 14/14604-8, 16/04845-3, 12/51464-4, 15/20562-9, 12/15165-2, 19/11008-9)