Evaluation of inflammation, remodeling, hyperresponsiveness and oxidative stress in experimental models of asthma-COPD overlap

<bold>Background:</bold> Asthma-COPD Overlapping Syndrome (OCP) is characterized by fixed obstruction to airflow. Patients have a higher number of exacerbations, low quality of life, more pronounced decline in respiratory function, frequent use of medical resources, increased morbidity and mortality. <bold>Objective:</bold> To compare the evolution of the inflammatory profile, oxidative stress and pulmonary tissue remodeling in a model of Asthma-COPD Overlapping Syndrome (OCP) in two different periods of exposure. <bold>Methods:</bold> Male Balb/c mice were divided into Control, Asthma, COPD and OC groups, submitted to short (28 days) and long (54 days) exposure, sensitized (intraperitoneal) and exposed (inhalation) to ovoalbumine (Asthma and ACO) and instillation (intratracheal) the porcine pancreatic elastase. Data were collected from oxidative stress (NO), lung function (Gtis, Htis, Rrs, Ers and Raw) and materials for analysis of BALF and Histology (HE, Picrossirius and Immunohistochemistry). <bold>Results:</bold> in the short phase, changes in pulmonary resistance and elastance were observed, increased inflammatory cells, edema, collagen, IL-4, IL-13, IL-17, TNF-α, IL-10, MMP-12, TGF-β, TIMP-1, 8-iso-PGF-2 and INOS in the air septolar and alveolar pathways mononuclear and polymorphonuclear. The long model showed an increase: exhaled NO, inflammatory cells, edema, mononuclear and polymorphonuclear cells, collagen, IL-4, IL-13, IL-17, IL-5, IL-6, TNF-α, IL-10, MMP-9, MMP-12, TGF-β, IL-8, PGO-1, PGO-2, and ISO-2. <bold>Conclusion:</bold> the lung function was altered, remodeling was induced, and inflammation and oxidative stress were increased by the short and long models.