Evaluation of the expression of the proteins suppressor of cytokine signaling (SOCS) in the anti-inflammatory effects of physical training in an experimental model of Asthma

• Grant number: 14/23086-0
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: June 01, 2015
• End date: May 31, 2016
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal Investigator: Rodolfo de Paula Vieira
• Grantee: Daniel Hungerbuhler Paiva
• Host Institution: Universidade Nove de Julho (UNINOVE). Campus Vergueiro. São Paulo , SP, Brazil
• Associated research grant: 12/15165-2 - Role of purinergic signaling and of SOCS-JAK-STAT signaling in the antiinflammatory effects of aerobic training in experimental models of asma and in asthmatic individuals, AP.JP

Abstract

Asthma is a chronic airway inflammatory disease that results in impairment of quality of life. In the last years, several studies have demonstrated that aerobic training (AT) performed properly results in anti-inflammatory effects to the airways, either in experimental models of asthma and to asthmatic individuals. However, although few cellular effects have been investigated (still only in animals' models), the possible extra and intracellular mediators underlying the effects of AT on asthma never were investigated, except to NF-kB. Thus, the present project aims to evaluate the effects of AT on SOCS (SOCS1, SOCS2 and SOCS3) proteins signaling on the lungs as possible modulators of the anti-inflammatory effects of aerobic training in an experimental model of asthma (by using house dust mite - HDM). For this purpose, the animals will receive intra-tracheal administration of HDM (100ug) on days 0, 7, 14, 21, 28, 35 e 42 and will be submitted to AT (for evaluation of therapeutic effect) begining on day 17 during 5 weeks. Twenty-four hours after the last session of training and allergen challenge, the animals will be assessed to the inflammatory profile in the broncho alveolar lavage and in the lung tissue, to the levels of pro-inflammatory cytokines (IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-12, IL-13, IL-17, IL-23) and to the levels of anti-inflammatory cytokines (IL-10, IL-1ra) and also for the expression of SOCS1, SOCS2 and SOCS3 in the lungs, as well as for the airway remodeling, and bronchial hyper responsiveness.