Avaliação de mediadores inflamatórios no modelo de asma experimental induzida por ovalbumina em camundongos BALB/c submetidos a hiperóxia

Abstract

Asthma is considered a worldwide public health problem that involves a chain of pathophysiological events of difficult control and treatment. Therapeutic strategies have been studied so that the disease can be stabilized and controlled. However, the pathophysiological events involving the disease are not yet fully understood. In view of this premise, experimental studies are necessary and are under increasing development in the scientific community in order to clarify the pattern of inflammatory response triggered in the process. Both in humans and in BALB/c mice the pathophysiological process of asthma triggers classical cell response via helper T (T 2) cells with release of inflammatory interleukins (IL). In addition, macrophage infiltrates, eosinophils, mast cells. Studies evidence a shift in the pathway of triggering this response to IL-2 and interferon gamma-mediated helper 1 (Th1) via pathway. Activation of the Th17 cell pathway is also cited, but not fully elucidated as to the immunoregulation process. The objective of our study was to verify the immunological mechanisms by which hyperoxia leads to lesions in the lower airways and pulmonary parenchyma in a model of experimental asthma induced by OVA in BALB / c mice. We performed the histopathological analysis of the inflammatory infiltrate, collagen and mucus, by histochemical staining, in lung tissue samples, and quantification of interleukin-10 (IL-10), interleukin-22 (IL-22) and interleukin-17 IL-17), by the ELISA method, and nitrite (NO2), by the method of Greiss, in bronchoalveolar lavage. The data suggest that the polarization for the Th17 phenotype induced by hyperoxia is accompanied by highest levels in the BAL of IL-17, NO2, IL-10 and IL-22.