Avaliação da secreção salivar em modelo de asma alérgica em ratos

Abstract

Allergic asthma is a disease with high prevalence and morbidity, and a huge public health problem, characterized as a chronic disease of the airways that is characterized by variable and recurring symptoms such as airflow limitation, bronchial hyperresponsiveness and inflammation. Oral health in individuals with asthma, even controlled, is impaired, with increased levels of caries, teeth decayed, missing and filled (DMF). These disorders in the oral cavity is probably caused by the decrease in salivary secretion. Prolonged use of a range of drugs can trigger hyposalivation, a side effect that generates a discomfort. The drugs useful for the asthma treatment, such as corticosteroids and β-2 agonists do not reverse the decrease in salivary secretion in asthmatic patients. The major drug used for the treatment of hyposalivation is pilocarpine, but this drug is contraindicated for asthmatics for promoting smooth muscle constriction of the airway, making it more difficult to breathing in asthmatic patients. Given these facts, the aim of this study was to evaluate the hyposalivation in animals with allergic asthma induced by ovalbumin. This study was approved by the Ethics Committee on Animal Use (CEUA) of the Federal University of Alagoas (UFAL) under protocol 03/2014. Wistar rats were used (n=6 per group) non-asthmatic treated with saline (SAL), asthmatic treated with saline (OVA) and asthmatic treated with dexamethasone (OVA+DEXA). Asthma was induced by sensitization to ovalbumin and aluminum hydroxide - AL(OH)3 (50 μg + 5mg, each animal received 200 μl; s.c.) on days 0, 7 and 14. On days 21, 22 and 23 the animals received one antigen challenge per day, SAL group was challenged with saline (0.9%) OVA+OVA groups and DEXA with Ovalbumin (1mg/ml, 100 ul was placed in each animal; i.n.), the last one was treated 1h before challenge with dexamethasone (2 mg/kg, i.p.). 48h after the last challenge, the animals were anesthetized with sodium pentobarbital (60 mg/kg, i.p.), and then, the unstimulated saliva collection and stimulated by pilocarpine (2mg/kg, ip) was performed and then collecting bronchoalveolar lavage (BAL) and dissection of the chest and the neck to remove the lung tissue and submandibular gland respectively. Thus, the procedures of total and differential count of cells were performed and, measurement of salivary volume, total protein concentration, histological examination (HE and PAS). In another set of animals subjected to the same protocol induction of allergic asthma, were realized the respiratory electrophysiological analyze. The results were expressed as mean ± SEM and compared with ANOVA/Newman-Keuls test (p <0.05). The bronchial epithelium of asthmatics animal has an inflammatory infiltrate and an increase in mucus production, which is partially reversed by the treatment with dexamethasone. The minute volume at baseline was reduced in asthmatics compared to SAL animals, which was reversed by treatment with dexamethasone. For the first time, it was observed that the induction of asthma promotes a decrease in salivary secretion, both stimulated and non stimulated with pilocarpine and this was not reversed by treatment with dexamethasone. The protein concentration in saliva showed that DEXA+OVA group showed a decrease in total protein. The submandibular gland of OVA and OVA+DEXA animals showed a gap in the glandular parenchyma, which is not observed in SAL. Thus, it is concluded that, asthma may promote a decrease in salivary secretion. In addition, it is clear that treatment with dexamethasone can improve respiratory function, but it is not efficient to treat hyposalivation.