Ponente
Descripción
Chronic obstructive pulmonary disease is one of the main causes of morbidity and mortality worldwide. Emphysema and chronic bronchitis constitute its two main phenotypes, which occur due to pathological
structural changes of the lung. Existing treatments so far reduce the severity of clinical symptoms, but do not cure. The evaluation of new therapeutic candidates requires the use of animal models that mimic the pathological scenario of the disease. The present work begins the path toward the development of a model of pulmonary emphysema in C57BL/6 mice, induced by intratracheal administration of two U of pancreatic porcine elastase (PPE) to each animal, alone or in combination with LPS from E. coli. A protocol for the administration of products through the intratracheal route was stablished, and dexamethasone was successfully used as control of lung damage recovery due to its anti-inflammatory effect. Histomorphometric techniques revealed structural changes in the lung of animals treated with PPE ± LPS in comparison with control animals. However, neither hemolysis nor enzymatic activity of neutrophil elastase were detected in the bronchoalveolar lavages of treated animals. Results indicate that, even though pathological mechanisms behind the disease were initiated, lung tissue damage was only detectable by histomorphometric studies. Future work will be directed toward the administration of larger amounts of PPE and the use of a different source of LPS, with the objective to assess the development of the pulmonary emphysema through indicators detectable in bronchoalveolar lavages.
