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Role of bronchial epithelium in the regulation of inflammation in asthma and COPD: new findings and state of art

Abstract

Asthma is a disease characterized by reversible airflow limitation, chronic airway inflammation and remodeling. Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow limitation, chronic airway inflammation and remodeling (mainly of small/distal airways), beyond destruction of airspaces (alveoli and alveolar septa). Airway epithelium is not only a physical barrier in the airways, but actively contributes for the pathogenesis of asthma and COPD through the release of mediators of inflammatory and fibrotic process. Beyond that, the bronchial epithelium also corresponds to the first line of defense against virus, bacterial and other pathogens involved in the exacerbation of asthma and COPD. In the context, in vivo and in vitro models of exacerbation have been developed to allow us to study the effects and the mechanisms underlying exacerbation in these diseases. Therefore, the present project for visiting professorship for Prof. Dr. Pieter S. Hiemstra aims to establish a first bridge for scientific collaboration, where our research group (Pulmonary and Exercise Immunology) will benefit a lot from the knowledge of Prof. Pieter S. Hiemstra in developing and studying in vivo and in vitro models of exacerbation of asthma and COPD. Beyond that, Prof. Pieter also will teach us how to isolate and culture primary mouse bronchial epithelial cells in air liquid interface system and also how to properly activate these cells to study mechanisms of exacerbation of both asthma and COPD and further to also study if the exercise physical training can inhibit asthma and COPD exacerbation. For the studies of asthma exacerbation (in vivo and in vitro), house dust mite (Dermatophagoides pteronyssinus) will be used as a primary agent (for induction of allergic inflammatory response), while for the COPD exacerbation studies (in vivo and in vitro), cigarrete smoke extract will be used as a primary agent (since smoke exposure is the main inductor agent of COPD development). In both cases (asthma and COPD), the exacerbation will be induced using bacterial (Staphylococcus aureus) and viral (Rhinovirus and Respiratory Syncytial Virus) stimuli. (AU)

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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)
DURIGON, THOMAS STRAVINSKAS; MACKENZIE, BREANNE; OLIVEIRA-JUNIOR, MANOEL CARNEIRO; SANTOS-DIAS, ALANA; DE ANGELIS, KATIA; MALFITANO, CHRISTIANO; DA PALMA, RENATA KELLY; GUERRA, JULIANA MORENO; DAMACENO-RODRIGUES, NILSA REGINA; CALDINI, ELIA GARCIA; DE ALMEIDA, FRANCINE MARIA; AQUINO-SANTOS, HELIDA CRISTINA; RIGONATO-OLIVEIRA, NICOLE CRISTINE; LEAL DE OLIVEIRA, DANIELLE BRUNA; AIMBIRE, FLAVIO; LIGEIRO DE OLIVEIRA, ANA PAULA; FRANCO DE OLIVEIRA, LUIZ VICENTE; DURIGON, EDISON LUIZ; HIEMSTRA, PIETER S.; VIEIRA, RODOLFO P. Aerobic Exercise Protects from Pseudomonas aeruginosa-Induced Pneumonia in Elderly Mice. JOURNAL OF INNATE IMMUNITY, v. 10, n. 4, p. 279-290, 2018. Web of Science Citations: 2.

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