CONICET | Buscador de Institutos y Recursos Humanos

Resistance to corticosteroids in patients with severe asthma and with chronic obstructive pulmonary disease (COPD) is an important barrier to an effective treatment. Different lines of evidence indicate that glucocorticoids(GCs) resistance in inflammatory diseases is the result of significant changes in the cellular microenvironment that occur over time during disease progression. Several factors have been involved in this process and recent findings indicate that miRNAs may also be playing a role in the development of GC resistance during chronic inflammatory states. In this work we contribute to the characterization of the immunoendocrine interactions observed in patients with both asthma and COPD as a preliminary approach to subsequent studies on the role of sRNA in the development of GC resistance in these diseases. Both sputum and blood samples from COPD patients were employed to compare the events occurring at the lung with what happens in the peripheral compartments. As expected, most asthmatic patients, and some with COPD showed abnormally high IgE blood levels and mild leukocytosis, with elevated eosinophils. Interestingly, in many of these patients sputum cytology did not show an eosinophilic infiltrate and neither of these findings correlated with the severity/stage of the diseases. Levels of endogenous cortisol were also quantified to evaluate the HPA axis functions in these patients.Also, RNA was purified from both sputum and blood samples from patients and controls and transcripts were quantified by RT-qPCR, being able to detect miRNAs in all analyzed samples, including extracellular fractions. In summary, these results provide a first approach for the better understanding of the immunoendocrine alterations associated with pulmonary obstructive diseases and presenta useful experimental design for the study of regulatory mechanisms mediated by miRNAs in secretions of patients with asthma and COPD.

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