Resumo

Introduction: Asthma is a chronic inflammatory disease characterized by bronchial hyperreactivity with elevated levels of eosinophils and immunoglobulin E (IgE). Epidemiologic studies afirm that in the last decade it has been enhanced prevalence of alergic diseases, like asthma. One of the accepted explanations for this phenomenon is the Hygiene Hypothesis, in which the lower exposure to infectious disease, the overuse of antibiotics and the mass vaccination would facilitate the occurrence of allergies. Immunologicals mechanism that explain this phenomenon is related with absence of microbial stimulus and this leads an unbalance of T helper responses or regulatory mechanism. Studies have shown that Mycobacterium tuberculosis or members of Mycobacterium tuberculosis complex are able to protect against the development of allergic responses. Previous work performed in our laboratory showed that rBCG-S1PT mycobacteria administrated before allergen-induced protocols supresses the allergic parameters. Objective: In this work we analysed the effect of treatment with rBCG-S1PT intranasal (i.n.) or subcutaneous (s.c.) administered after allergic airway inflammation induced by OVA. Methods and Results: C57Bl/6 mice were sensitized with OVA/Alum s.c. on days 1 and 7 and were i.n. challenged on days 14 and 21. Mice were i.n. or s.c. administrated with rBCG-S1PT on day 28 and after two more challenges with OVA they were analysed 24h after the last one. Were verified that the number of total cells in bronchoalveolar lavage (BAL) decreased when compared with allergic group. The count number of eosinophils in BAL exhibited statistical difference when compared treated group with allergic group (p<0,05). The IgE levels measured by ELISA were in rBCG-S1PT treated group analysed after thirty days of rBCG-S1PT i.n. or s.c. administration and did not decrease levels statistically. IgE anti-OVA did not have difference between groups. Conclusion: Our results indicate that treatment with rBCG-S1PT i.n. or s.c. attenuates eosinophilic airways inflammation but with slight achievement on IgE production.